Ask Dr. Sher- Open Forum

dr geoffrey sher ivf infertility You are not alone. Dr. Sher is here to answer your questions and support you.

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Dear Patients,

I created this forum to welcome any questions you have on the topic of infertility, IVF, conception, testing, evaluation, or any related topics. I do my best to answer all questions in less than 24 hours. I know your question is important and, in many cases, I will answer within just a few hours. Thank you for taking the time to trust me with your concern.

– Geoffrey Sher, MD

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22,544 Comments

Lauren

Dr Sher, I would really appreciate your opinion. I had 2 natural pregnancies and births, boy then girl, and got pregnant in the first month of trying with both. Did IVF with PGD for next pregnancy to test for recessive genetic condition. Got pregnant on the first try and delivered a healthy baby boy. Three years later I went back to do a FET, still with PGD embryos (24 chromosome testing). First FET ended with miscarriage at 5.5 weeks. Next FET the beta didn’t get above 5. My RE then recommended that I get immune testing. Based on the 2 FET cycles and the immune tests, would you recommend that I proceed with an immune protocol at all? Two high risk MFM doctors have advised against it. The one recommended includes prednisone, plaquenil, Lovenox, Neupogen, baby aspirin, and intralipids. Results were: negative for ANA, APA and ATAs. KIR AA haplotype, partial lack of class II allele mismatching (2 total class II mismatches out of 6), 1 HLA-DRB1 mismatch out of 2, 1 HLA-DR super type mismatch out of 2; positive for several class I anti-HLA antibodies, includeing three partner-specific anti-HLA antibodies (A2, A24, B51) that are all present at 6K MFI or greater. Testing is currently pending to determine if these antibodies fix complement (C1q). Also have elevated levels of TNFα positive, IFNγ positive, and IL-17 positive NKT cells, as well as elevated levels of IL-17 positive CD4+ T cells, CD8+ T cells, and NK cells (IL-17 positive CD8+ T cells in the 99th percentile). All NKT cell IC ratios are highly elevated, and almost all CD8+ T cell and NK cell IC ratios are also elevated. NKa is also elevated and I have elevated levels of total NKT cells and CD8+ T cells.

reply
Dr. Geoffrey Sher

To be honest, I personally would NOT have done such a barrage of expensive immunologic testing. I would have ordered a natural killer cell activity test by the K-562 target cell assay, a full antiphoispholipid antibody (APA) profile and an immunophenotype on your blood. More importantly, I would have had you and your husband tested for DQ alpha/HLA genetic similarities to look for an alloimmune implantation issue, which given that you and your husband have children together and that you subsequently conceived again, it is in my opinion not very likely that an autoimmune immunologic implantation dysfunction (IID) as a cause of activated NK cells or T-cells. It is far more likely. Alloimmune IID this is the type that can occur after having had natural conceptions. If I am correct, then in my opinion, the treatment you received would not have been likely to address your problem adequately. Please read the articles on IID, below.

Whenever a patient fails to achieve a viable pregnancy following embryo transfer (ET), the first question asked is why! Was it simply due to, bad luck?, How likely is the failure to recur in future attempts and what can be done differently, to avoid it happening next time?.
It is an indisputable fact that any IVF procedure is at least as likely to fail as it is to succeed. Thus when it comes to outcome, luck is an undeniable factor. Notwithstanding, it is incumbent upon the treating physician to carefully consider and address the causes of IVF failure before proceeding to another attempt:
1. Age: The chance of a woman under 35Y of age having a baby per embryo transfer is about 35-40%. From there it declines progressively to under 5% by the time she reaches her mid-forties. This is largely due to declining chromosomal integrity of the eggs with advancing age…”a wear and tear effect” on eggs that are in the ovaries from birth.
2. Embryo Quality/”competency (capable of propagating a viable pregnancy)”. As stated, the woman’s age plays a big role in determining egg/embryo quality/”competency”. This having been said, aside from age the protocol used for controlled ovarian stimulation (COS) is the next most important factor. It is especially important when it comes to older women, and women with diminished ovarian reserve (DOR) where it becomes essential to be aggressive, and to customize and individualize the ovarian stimulation protocol.
We used to believe that the uterine environment is more beneficial to embryo development than is the incubator/petri dish and that accordingly, the earlier on in development that embryos are transferred to the uterus, the better. To achieve this goal, we used to select embryos for transfer based upon their day two or microscopic appearance (“grade”). But we have since learned that the further an embryo has advanced in its development, the more likely it is to be “competent” and that embryos failing to reach the expanded blastocyst stage within 5-6 days of being fertilized are almost invariably “incompetent” and are unworthy of being transferred. Moreover, the introduction into clinical practice about a decade ago, (by Levent Keskintepe PhD and myself) of Preimplantation Genetic Sampling (PGS), which assesses for the presence of all the embryos chromosomes (complete chromosomal karyotyping), provides another tool by which to select the most “competent” embryos for transfer. This methodology has selective benefit when it comes to older women, women with DOR, cases of unexplained repeated IVF failure and women who experience recurrent pregnancy loss (RPL).
3. The number of the embryos transferred: Most patients believe that the more embryos transferred the greater the chance of success. To some extent this might be true, but if the problem lies with the use of a suboptimal COS protocol, transferring more embryos at a time won’t improve the chance of success. Nor will the transfer of a greater number of embryos solve an underlying embryo implantation dysfunction (anatomical molecular or immunologic).Moreover, the transfer of multiple embryos, should they implant, can and all too often does result in triplets or greater (high order multiples) which increases the incidence of maternal pregnancy-induced complications and of premature delivery with its serious risks to the newborn. It is for this reason that I rarely recommend the transfer of more than 2 embryos at a time and am moving in the direction of advising single embryo transfers …especially when it comes to transferring embryos derived through the fertilization of eggs from young women.
4. Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:
a. A“ thin uterine lining”
b. A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
c. Immunologic implantation dysfunction (IID)
d. Endocrine/molecular endometrial receptivity issues
Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).

I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach:
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!

Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691
 800-780-7437

Geoff Sher

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
Michelle

Hi Dr. Sher,

I have a quick question…something I’m concerned about. The night before egg retreival I had sexual intercourse with my husband. The next morning at the egg retrival procedure, my doctor couldn’t manage to retrieve many eggs on my right side, even though I had good follicles. In the end, he only managed to get three eggs in total, even though I had about eight good sized follicles. He tried two methods for retrieving the eggs – flushing it out, and another method that I forget what he called it.

My question is: did having sex ten hours before retrival somehow cause my eggs to be irretrievable? Did having sex make the eggs stuck or something, or shift them in such a way that my doctor couldn’t get them out? Your insight is greatly appreciated…

Michelle

reply
Dr. Geoffrey Sher

Absolutely not! More than likely this was a technical problem in accessing that ovary.

Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691
 800-780-7437

Geoff Sher

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

Geoff Sher

reply
Sarah

Hi Dr Sher, is it possible to take oral estrogen tablets alongside stimms to help lining growth or will it stop the follicles from growing?

reply
Dr. Geoffrey Sher

Although it probably will not reduce follicular growth in response to gonadotropins, in the vast majority of cases (except possibly for women with severely diminished ovarian reserve) estrogen priming is redundant, in my opinion.

Geoff Sher

reply
Sarah

So what’s the best way to increase the lining now? I never have that many follicles normally between 7-9 growing. My lining always used to be really good around 9-10mm at egg collection but since I had a hysteroscopy the last 2 cycles it has been slower to grow and is maybe 8-8.5mm at egg collection which compacts down a bit once progesterone is started. Is it worth taking estrogen after egg collection to try and maintain the thickness?

reply
Dr. Geoffrey Sher

Whatever you do after the trigger or after starting progesterone supplementation with embryo recipient cycles (such as with FET), will have NO abiloity to increase proliferation of endometrial cells and will thus not help. It is what you do up until thta point that might help.

About seventeen years ago, after reporting on the benefit of vaginal Sildenafil (Viagra) for to women who had implantation dysfunction due to thin endometrial linings I was proud to announce the birth of the world’s first “Viagra baby.” For those of you who aren’t familiar with the use of Viagra in IVF, allow me to provide some context.

It was as far back as 1989, when I first published a study that examined the correlation between the thickness of a woman’s uterine lining (the endometrium), and the subsequent successful implantation of embryos in IVF patients. This study revealed that when the uterine lining measured <8mm in thickness by the day of the “hCG trigger” (in fresh IVF cycles), or at the time of initiating progesterone therapy (in embryo recipient cycles, e.g. frozen embryo transfers, egg donation-IVF etc.) , pregnancy and birth rates were substantially improved. Currently, it is my opinion, that an ideal estrogen-promoted endometrial lining should ideally measure at least 9mm in thickness and that an endometrial lining measuring 8-9mm is “intermediate”. An estrogenic lining of <8mm is in most cases unlikely to yield a viable pregnancy.

A “poor” uterine lining is usually the result of the innermost layer of endometrium (the basal or germinal endometrium from which endometrium grows) ) not being able to respond to estrogen by propagating an outer, “functional” layer thick enough to support optimal embryo implantation and development of a healthy placenta (placentation). The “functional” layer ultimately comprises 2/3 of the full endometrial thickness and is the layer that sheds with menstruation in the event that no pregnancy occurs.

The main causes of a “poor” uterine lining are:

1. Damage to the basal endometrium as a result of:
a. Inflammation of the endometrium (endometritis) most commonly resulting from infected products left over following abortion, miscarriage or birth
b. Surgical trauma due to traumatic uterine scraping, (i.e. due to an over-aggressive D & C)
2. Insensitivity of the basal endometrium to estrogen due to:
a. Prolonged , over-use/misuse of clomiphene citrate
b. Prenatal exposure to diethylstilbestrol (DES). This is a drug that was given to pregnant women in the 1960’s to help prevent miscarriage
3. Over-exposure of the uterine lining to ovarian male hormones (mainly testosterone): Older women, women with diminished ovarian reserve (poor responders) and women with polycystic ovarian syndrome -PCOS tend to have raised LH biological activity.. This causes the connective tissue in the ovary (stroma/theca) to overproduce testosterone. The effect can be further exaggerated when certain methods for ovarian stimulation such as agonist (Lupron/Buserelin) “flare” protocols and high dosages of menotropins such as Menopur are used in such cases.
4. Reduced blood flow to the basal endometrium:
Examples include;
a. Multiple uterine fibroids - especially when these are present under the endometrium (submucosal)
b. Uterine adenomyosis (excessive, abnormal invasion of the uterine muscle by endometrial glands).

“The Viagra Connection”

Treatments such supplementary estrogen therapy, aspirin administration and/or administration of high dosage gonadotropin fertility drugs, aimed at improving endometrial development have all yielded disappointing results.

It was in the 90’s that Sildenafil (brand named Viagra) was gaining popularity as a treatment for erectile dysfunction. The mechanism by which it acted was through increasing penile blood flow through increasing nitric oxide activity. This prompted me to investigate whether Viagra administered vaginally, might similarly improve uterine blood flow and in the process cause more estrogen to be delivered to the basal endometrium and thereby increase endometrial thickening. We found that when Viagra was administered vaginally it did just that! However oral administration was without any significant benefit in this regard. We enlisted the services of a compound pharmacy to produce vaginal Viagra suppositories. Initially, four (4) women with chronic histories of poor endometrial development and failure to conceive following several advanced fertility treatments were evaluated for a period of 4-6 weeks and then underwent IVF with concomitant Viagra therapy. Viagra suppositories were administered four times daily for 8-11 days and were discontinued 5-7 days prior to embryo transfer in all cases.

Our findings clearly demonstrated that vaginal Viagra produced a rapid and profound improvement in uterine blood flow and that was followed by enhanced endometrial development in all four cases. Three (3) of the four women subsequently conceived. . I expanded the trial in 2002 and became the first to report on the administration of vaginal Viagra to 105 women with repeated IVF failure due to persistently thin endometrial linings. All of the women had experienced at least two (2) prior IVF failures attributed to intractably thin uterine linings. About 70% of these women responded to treatment with Viagra suppositories with a marked improvement in endometrial thickness. Forty five percent (45%) achieved live births following a single cycle of IVF treatment with Viagra The miscarriage rate was 9%. None of the women who had failed to show an improvement in endometrial thickness following Viagra treatment achieved viable pregnancies.
Following vaginal administration, Viagra is rapidly absorbed and quickly reaches the uterine blood system in high concentrations. Thereupon it dilutes out as it is absorbed into the systemic circulation. This probably explains why treatment is virtually devoid of systemic side effects

Since the introduction of this form of treatment, thousands of women with thin uterine linings have been reported treated and many have gone on to have babies after repeated prior IVF failure.

It is important to recognize that Viagra will NOT be effective in improving endometrial thickness in all cases. In fact, about one third of women treated fail to show any improvement. This is because in certain cases of thin uterine linings, the basal endometrium will have been permanently damaged and left unresponsive to estrogen. This happens in cases of severe endometrial damage due mainly to post-pregnancy endometritis (inflammation), chronic granulomatous inflammation due to uterine tuberculosis (hardly ever seen in the United States) and following extensive surgical injury to the basal endometrium (as sometimes occurs following over-zealous D&C’s).

To be effective, Viagra must be administered vaginally. It is NOT effective when taken orally. We prescribe 20mg vaginal suppositories to be inserted four times per day. Treatment is commenced soon after menstruation ceases and is continued until the day of the “hCG trigger.” While ideally the treatment should be sustained throughout the first half of the cycle, most women will respond within 48-72 hours. For this reason, Viagra can be used to “rescue” a poor lining after the cycle has already started, provided that there is enough time remaining prior to ovulation, egg retrieval or progesterone administration.

I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
• Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian
• Endometrial Thickness, Uterine Pathology and Immunologic Factors
• Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• The Role of Nutritional Supplements in Preparing for IVF
Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691
 800-780-7437

Geoff Sher

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
Sarah

Thanks Dr Sher I did once manage to increase the lining thickness between egg collection and transfer by 2.5mm!

reply
Dr. Geoffrey Sher

I am not saying that the lining wont thicken with a progesterone effect. What I am saying is that this is due to a build up of secretions in the endometrial glands and NOT due to a proliferation of endonmetrial cells…and it is the latter that counts. This is why we assess endometrial thickening before the hCG trigger of progesterone administration (in case of embryo recipient cycles).

Geoff Sher

reply
Sarah

Ok thanks Dr Sher, I can get hold of some vaginal viagara which my doctor is happy for me to try. I see from various reports its is successful in around 3/4 of women.

1. How much on average would you expect the lining to increase with this sort of supplementation?

2. what is the recommended dose per day? Is it 100mg of sildenafin?

3. Would it be sufficient to start from my first scan on a fresh cycle (around day 8) and continue until trigger (day 12)?

Dr. Geoffrey Sher

20mg Viagra vaginally 4 times a day from when menstruation stops until the hCG trigger.

About seventeen years ago, after reporting on the benefit of vaginal Sildenafil (Viagra) for to women who had implantation dysfunction due to thin endometrial linings I was proud to announce the birth of the world’s first “Viagra baby.” For those of you who aren’t familiar with the use of Viagra in IVF, allow me to provide some context.

It was as far back as 1989, when I first published a study that examined the correlation between the thickness of a woman’s uterine lining (the endometrium), and the subsequent successful implantation of embryos in IVF patients. This study revealed that when the uterine lining measured <8mm in thickness by the day of the “hCG trigger” (in fresh IVF cycles), or at the time of initiating progesterone therapy (in embryo recipient cycles, e.g. frozen embryo transfers, egg donation-IVF etc.) , pregnancy and birth rates were substantially improved. Currently, it is my opinion, that an ideal estrogen-promoted endometrial lining should ideally measure at least 9mm in thickness and that an endometrial lining measuring 8-9mm is “intermediate”. An estrogenic lining of <8mm is in most cases unlikely to yield a viable pregnancy.

A “poor” uterine lining is usually the result of the innermost layer of endometrium (the basal or germinal endometrium from which endometrium grows) ) not being able to respond to estrogen by propagating an outer, “functional” layer thick enough to support optimal embryo implantation and development of a healthy placenta (placentation). The “functional” layer ultimately comprises 2/3 of the full endometrial thickness and is the layer that sheds with menstruation in the event that no pregnancy occurs.

The main causes of a “poor” uterine lining are:

1. Damage to the basal endometrium as a result of:
a. Inflammation of the endometrium (endometritis) most commonly resulting from infected products left over following abortion, miscarriage or birth
b. Surgical trauma due to traumatic uterine scraping, (i.e. due to an over-aggressive D & C)
2. Insensitivity of the basal endometrium to estrogen due to:
a. Prolonged , over-use/misuse of clomiphene citrate
b. Prenatal exposure to diethylstilbestrol (DES). This is a drug that was given to pregnant women in the 1960’s to help prevent miscarriage
3. Over-exposure of the uterine lining to ovarian male hormones (mainly testosterone): Older women, women with diminished ovarian reserve (poor responders) and women with polycystic ovarian syndrome -PCOS tend to have raised LH biological activity.. This causes the connective tissue in the ovary (stroma/theca) to overproduce testosterone. The effect can be further exaggerated when certain methods for ovarian stimulation such as agonist (Lupron/Buserelin) “flare” protocols and high dosages of menotropins such as Menopur are used in such cases.
4. Reduced blood flow to the basal endometrium:
Examples include;
a. Multiple uterine fibroids - especially when these are present under the endometrium (submucosal)
b. Uterine adenomyosis (excessive, abnormal invasion of the uterine muscle by endometrial glands).

“The Viagra Connection”

Treatments such supplementary estrogen therapy, aspirin administration and/or administration of high dosage gonadotropin fertility drugs, aimed at improving endometrial development have all yielded disappointing results.

It was in the 90’s that Sildenafil (brand named Viagra) was gaining popularity as a treatment for erectile dysfunction. The mechanism by which it acted was through increasing penile blood flow through increasing nitric oxide activity. This prompted me to investigate whether Viagra administered vaginally, might similarly improve uterine blood flow and in the process cause more estrogen to be delivered to the basal endometrium and thereby increase endometrial thickening. We found that when Viagra was administered vaginally it did just that! However oral administration was without any significant benefit in this regard. We enlisted the services of a compound pharmacy to produce vaginal Viagra suppositories. Initially, four (4) women with chronic histories of poor endometrial development and failure to conceive following several advanced fertility treatments were evaluated for a period of 4-6 weeks and then underwent IVF with concomitant Viagra therapy. Viagra suppositories were administered four times daily for 8-11 days and were discontinued 5-7 days prior to embryo transfer in all cases.

Our findings clearly demonstrated that vaginal Viagra produced a rapid and profound improvement in uterine blood flow and that was followed by enhanced endometrial development in all four cases. Three (3) of the four women subsequently conceived. . I expanded the trial in 2002 and became the first to report on the administration of vaginal Viagra to 105 women with repeated IVF failure due to persistently thin endometrial linings. All of the women had experienced at least two (2) prior IVF failures attributed to intractably thin uterine linings. About 70% of these women responded to treatment with Viagra suppositories with a marked improvement in endometrial thickness. Forty five percent (45%) achieved live births following a single cycle of IVF treatment with Viagra The miscarriage rate was 9%. None of the women who had failed to show an improvement in endometrial thickness following Viagra treatment achieved viable pregnancies.
Following vaginal administration, Viagra is rapidly absorbed and quickly reaches the uterine blood system in high concentrations. Thereupon it dilutes out as it is absorbed into the systemic circulation. This probably explains why treatment is virtually devoid of systemic side effects

Since the introduction of this form of treatment, thousands of women with thin uterine linings have been reported treated and many have gone on to have babies after repeated prior IVF failure.

It is important to recognize that Viagra will NOT be effective in improving endometrial thickness in all cases. In fact, about one third of women treated fail to show any improvement. This is because in certain cases of thin uterine linings, the basal endometrium will have been permanently damaged and left unresponsive to estrogen. This happens in cases of severe endometrial damage due mainly to post-pregnancy endometritis (inflammation), chronic granulomatous inflammation due to uterine tuberculosis (hardly ever seen in the United States) and following extensive surgical injury to the basal endometrium (as sometimes occurs following over-zealous D&C’s).

To be effective, Viagra must be administered vaginally. It is NOT effective when taken orally. We prescribe 20mg vaginal suppositories to be inserted four times per day. Treatment is commenced soon after menstruation ceases and is continued until the day of the “hCG trigger.” While ideally the treatment should be sustained throughout the first half of the cycle, most women will respond within 48-72 hours. For this reason, Viagra can be used to “rescue” a poor lining after the cycle has already started, provided that there is enough time remaining prior to ovulation, egg retrieval or progesterone administration.

Geoff Sher
800-780-7437

Randy Kenan

Hello Doctor,

My wife and I just had a 2nd failed IVF cycle. Here is the details of each cycle:
My wife and I are both 35 years old

First IVF:
Antagonist Protocol
18 eggs retrieved
12 mature
8 fertilized
5 made it to day 3
All 5 arrested by day 5
Doctor indicated the eggs were poor quality

IVF 2:
Lupron Overlap Protocol

16 eggs retrieved
13 mature eggs + 4 eggs that were frozen from 1st IVF
12 eggs fertilized (6 from ejaculated sperm 6 from TESE sperm)
only 1 fertilized with ejaculated sperm made it to blast and FET
1st blood test was 10 HCG and 2nd blood test was 3 HCG
Doctor said the egg quality was poor as well

Sperm quality:
Sperm count: 22.1 million/ml
Motility: 27% rapid 4% slow
Morphology: 6% normal form, 83% abnormal head, 6% abnormal mid piece, 6% abnormal tail

Had two sperm DNA fragmentation tests; first test 45% fragmentation, after antioxidant therapy 2nd test showed 20% fragmentation.

We haven’t had a meeting with our current doctor about the 2nd failed IVF and why we had poor egg quality.

Met with a new RE doctor and based on IVF results (No lab results or our medical files were available) I mentioned above diagnosed my wife with polycystic ovaries, (Not PCOS) Although her sister does have PCOS. His recommendation was for my wife to exercise 30 minutes six days a week for 3 months and loose 5 pounds. This would reduce insulin in her ovaries. After 3 months, we would do the long-lupron protocol with HGH and he would try for maximum stimulation. He said that our case is rare and he sees our case 2-3 times a year and we got a 50% chance of having a good number of good embryos.

Does this sound like an appropriate diagnoses? Should we get a second opinion? What are the possible causes for our poor egg quality?
Age 33 tests results:
TSH: 2.56
FSH: 9.7
LH: 3.1
Prolactin: 20.6
Right ovary: 3.1 x 1.6 x 2.3 cm
Left ovary: 3.5 x 1.7 x 2.4 cm
HSG: Normal

reply
Dr. Geoffrey Sher

Very respectfully,

I do not think the advice given to improve egg quality is reasonable.

In my opinion, that the problem with egg/embryo quality could largely be due to the protocol(s) used for ovarian stimulation and the implementation thereof. I doubt that sperm quality has anything to do with it. In my opinion a DF! of 20% is adequate and the fact trhat sperm aspiration was needed is probably also not the main issue.

I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers Should be the Standard of Care in IVF
• Why did my IVF Fail
• Male Factor Infertility
• Routine Fertilization by Intracytoplasmic Sperm Injection (ICSI): An Argument in FavorHormonal Treatment of Male Infertility
• Testicular Sperm Extraction (TESE) and Testicular Sperm Aspiration (TESA): Surgical Approaches for Accessing Sperm from men who have no sperm in their ejaculates (Azoospermia)
• The Sperm Chromatin Structure Assay (SCSA): A Measure of the Potential of Sperm to Help Propagate a Viable Pregnancy

Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691
 800-780-7437

Geoff Sher

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
Kalli

Hi Dr. Sher,
I had my embryo transfer today and we were originally planning on two embryos however ultimately decided on a single embryo transfer due to the high quality of my embryos. I was given a report and it says that for Day 5 I have 3 Grade 1 EX BL, 1 Grade 2 EB, 3 Grade 2 EG BL, 5 Grade 2 EX BL, then 6 Grade 3. I don’t really understand the differences between these grades and what it means for us, can you explain it to me please?

reply
Dr. Geoffrey Sher

The grading systems used differ from center to center , but in general, Grade 1 or Grade 2 expanded blastocysts are good quality. Unexpanded day 5 embryos…less so and Grade 3’s are usually poorer quality.

Geoff Sher

reply
Sarah

Hi Dr. Sher,
I got pregnant at 36 on the first try and had a healthy baby who is now 4 years old. Then within a 1 year time span (age 38 and 39) I got pregnant naturally 3 times and miscarried each time in the first trimester. I decided to do ivf only for the purpose of doing PGS testing. I did 3 retrievals in a year and only 2 embryos came back normal. Also did Alan Beer immune testing but found nothing major just a few minor clotting disorders and Mthfr. My transfers were held off for a few months due to a thin uterine lining. A septum on my uterus was found which was removed. My first PGS embryo transfer in July failed (lining 7.7) pMy Dr was surprised as it was normal and I get pregnant so easily. My second PGS transfer a month later also failed. Again my Dr is very shocked as he hasnt really had 2 PGS failures before plus recurrent miscarriage. I also did IVIG with my second transfer snd Intralipids with the first transfer. With both transfer I did blood thinners, aspirin, neuprogen, progesterone) Today at my follow up he mentioned that there is the possibility that my husband and I are too “genetically similiar” which could be the cause of my losses and my implantation pgs failures. Do you think I have Alloimmume Implantation Dysfunction?
Thanks,
Sarah
Reply

reply
Dr. Geoffrey Sher

This really sounds like an alloimmune implantation dysfunction. I would love to see your immune testing profile (specifically the K-562 target cell test results for NKa; yous antiphospholipid profile, your immunophenotype and your and your husband’s DQ alpha HLA genetic profiles). I would wager a bet that you do bave NKa+ and possibly also a DQ alpha/HLA match with your husband. WE should talk…

I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers Should be the Standard of Care in IVF
• Why did my IVF Fail
• “Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
• Secondary Infertility: Addressing the Root Causes
• Recurrent Pregnancy Loss (RPL): Why do I keep losing my Pregnancies
• Blastocyst Embryo Transfers Done 5-6 Days Following Fertilization are Fast Replacing Earlier day 2-3 Transfers of Cleaved Embryos.
• Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
• Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
• IVF Failure and Implantation Dysfunction:
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Endometrial Thickness, Uterine Pathology and Immunologic Factors
• Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
• Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• The Role of Nutritional Supplements in Preparing for IVF
Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691
 800-780-7437

Geoff Sher

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
Sarah

Thanks for your reply. If it is
Alloimmume Implantation Dysfunction what is the treatment for this to fix it?

reply
Dr. Geoffrey Sher

See below!

I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly. :
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691
 800-780-7437

Geoff Sher

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
Krystle

Dr. Sher,
Does estrace affect embryo growth once pregnancy is confirmed? What is the time window for taking each dose if taking three times a day?

reply
Dr. Geoffrey Sher

I am not a fan of oral estrogen therapy…least of all estrace. But in general, estrogen in the first 8-10 weeks of pregnancy should not be harmful.

Geoff Sher

reply
Julia

Hello,
My husband and I did IVF with PGD and PGS screening and ended up with four high grade, chromosomally normal embryos. I am 35 and I’ve never been pregnant, but we haven’t had prior infertility issues (we only did IVF because of a genetic abnormality that we both carry.) I’ve had two chemical pregnancies so far, with the first two embryos. I’ve attributed this to lining issues (immune testing came back normal, but my lining only ever gets to just over 7 mm.) Yesterday, a RE suggested that despite the testing, the problem might lie with the embryos–that chromosomes aside, there might be something about the way they were handled in the lab that makes this batch less than ideal, and I will just need to try again with another cycle. I wonder if that sounds right to you, or if you think it’s more likely that the problem lies with the lining and I might still have a shot with the two remaining embryos. If the latter, what can be done about the fact that my lining never gets much above 7, even with all varieties of drugs/acupuncture etc.
Many thanks,
Julia

reply
Dr. Geoffrey Sher

Something about your case does not add up. Yes a lining of <8mm is rarely associated with a viable implantation and this MUST be reversed or you will keep spinning your wheels, but the issue is..WHY do you have an inadequate lining. I am also NOT convinced that you do not have an immune issue. I would need to see results of the immune tests done and need to know where they were performed as, in my opinion, fewer than a half dozen Reproductive Immunology Reference Laboratories in this country can do the required tests adequately?

Whenever a patient fails to achieve a viable pregnancy following embryo transfer (ET), the first question asked is why! Was it simply due to, bad luck?, How likely is the failure to recur in future attempts and what can be done differently, to avoid it happening next time?.
It is an indisputable fact that any IVF procedure is at least as likely to fail as it is to succeed. Thus when it comes to outcome, luck is an undeniable factor. Notwithstanding, it is incumbent upon the treating physician to carefully consider and address the causes of IVF failure before proceeding to another attempt:
1. Age: The chance of a woman under 35Y of age having a baby per embryo transfer is about 35-40%. From there it declines progressively to under 5% by the time she reaches her mid-forties. This is largely due to declining chromosomal integrity of the eggs with advancing age…”a wear and tear effect” on eggs that are in the ovaries from birth.
2. Embryo Quality/”competency (capable of propagating a viable pregnancy)”. As stated, the woman’s age plays a big role in determining egg/embryo quality/”competency”. This having been said, aside from age the protocol used for controlled ovarian stimulation (COS) is the next most important factor. It is especially important when it comes to older women, and women with diminished ovarian reserve (DOR) where it becomes essential to be aggressive, and to customize and individualize the ovarian stimulation protocol.
We used to believe that the uterine environment is more beneficial to embryo development than is the incubator/petri dish and that accordingly, the earlier on in development that embryos are transferred to the uterus, the better. To achieve this goal, we used to select embryos for transfer based upon their day two or microscopic appearance (“grade”). But we have since learned that the further an embryo has advanced in its development, the more likely it is to be “competent” and that embryos failing to reach the expanded blastocyst stage within 5-6 days of being fertilized are almost invariably “incompetent” and are unworthy of being transferred. Moreover, the introduction into clinical practice about a decade ago, (by Levent Keskintepe PhD and myself) of Preimplantation Genetic Sampling (PGS), which assesses for the presence of all the embryos chromosomes (complete chromosomal karyotyping), provides another tool by which to select the most “competent” embryos for transfer. This methodology has selective benefit when it comes to older women, women with DOR, cases of unexplained repeated IVF failure and women who experience recurrent pregnancy loss (RPL).
3. The number of the embryos transferred: Most patients believe that the more embryos transferred the greater the chance of success. To some extent this might be true, but if the problem lies with the use of a suboptimal COS protocol, transferring more embryos at a time won’t improve the chance of success. Nor will the transfer of a greater number of embryos solve an underlying embryo implantation dysfunction (anatomical molecular or immunologic).Moreover, the transfer of multiple embryos, should they implant, can and all too often does result in triplets or greater (high order multiples) which increases the incidence of maternal pregnancy-induced complications and of premature delivery with its serious risks to the newborn. It is for this reason that I rarely recommend the transfer of more than 2 embryos at a time and am moving in the direction of advising single embryo transfers …especially when it comes to transferring embryos derived through the fertilization of eggs from young women.
4. Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:
a. A“ thin uterine lining”
b. A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
c. Immunologic implantation dysfunction (IID)
d. Endocrine/molecular endometrial receptivity issues
Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).

I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• IVF Failure and Implantation Dysfunction:
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Endometrial Thickness, Uterine Pathology and Immunologic Factors
• Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
• Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• The Role of Nutritional Supplements in Preparing for IVF

Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691
 800-780-7437

Geoff Sher

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
Julia

Thank you so much for your reply. My immune testing was done at Cornell. (I’m not sure of everything they tested for, but I know there were 16 vials of blood.) Is this one of the labs you would trust? In any case, I am going to set up a Skype session with you. Thanks again for your wisdom on this!

reply
Dr. Geoffrey Sher

To my knowledge, the immune testing done at Cornell differs from that needed to evaluate for an immunologic implantation dysfunction.

Geoff Sher

reply
Raquel

Hola doc, yo llevo buscando embarazarme desde hace 4 años tenia las trompas tapadas me hice el estudio de salpincografia ya estan permeables le hicieron estudios a mi esposo y todo esta bien mi problema es q soy muy irregular ya tome ommifin que otra cosa puedo tomar para volverme regular

reply
Dr. Geoffrey Sher

Sorry Raquel,

You will need to post the question in English please.

Geoff Sher

reply
Lindsay

Hi- I just finished my first unsuccessful IVF cycle. I was on Lupron, low dose HCG, follistim and used ovidril to trigger. I’m only 31 and my fsh level is .7. My final ultrasound on Wednesday showed 3 follicles over 22mm and a 4th one which was a little smaller then on the left side I didn’t respond well and only had a few smaller follicles, all my levels were perfect and the uterine lining was nice and thick. My RE said she suspected we could get at 3 nice eggs. I had my retrieval this morning and all the follicles were empty and only cells were left. I’m devastated, any idea why this would happen and if it’s going to be preventable in the future?

reply
Dr. Geoffrey Sher

Hi Linsay,

It sounds from your post that in spite of your age you likely have diminished ovarian reserve. This means that the likely explanation for your few follicles not yielding eggs could be the protocol used for ovarian stimulation. This needs to be reviewed and revised if necessary. By the way there is no such thing as “empty follicles”. They may not release the eggs but they are never empty. Another fact is that in my opinion, the dosage of Ovidrel should ideally be 500mcg rather than 250mcg. The lower dosage is more likely to impact egg quality adversely…especially in women who have diminished ovarian reserve.

Women awho (regardless of age) have DOR have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production of LH biological activity which can result in excessive LH-induced ovarian male hormone (predominantly testosterone) production which in turn can have a deleterious effect on egg/embryo “competency”.

While it is presently not possible by any means, to reverse the age-related effect on the woman’s “biological clock, certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can make matters worse. Similarly, the amount/dosage of certain fertility drugs that contain LH/hCG (e.g. Menopur) can have a negative effect on the development of the eggs of older women and those who have DOR and should be limited.

I try to avoid using such protocols/regimes (especially) in older women and those with DOR, favoring instead the use of the agonist/antagonist conversion protocol (A/ACP), a modified, long pituitary down-regulation regime, augmented by adding supplementary human growth hormone (HGH). I further recommend that such women be offered access to embryo banking of PGS (next generation gene sequencing/NGS)-selected normal blastocysts, the subsequent selective transfer of which by allowing them to to capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” could significantly enhance the opportunity to achieve a viable pregnancy

Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
• A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
• Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
• Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers Should be the Standard of Care in IVF
• Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
• Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
• Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
• Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
• Preimplantation Genetic Testing (PGS) in IVF: It Should be Used Selectively and NOT be Routine.
• Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
• PGS in IVF: Are Some Chromosomally Abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
• PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
• Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• The Role of Nutritional Supplements in Preparing for IVF
• Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
• Empty Follicle syndrome.
I invite you to arrange to have a Skype or an in-person consultation with me to discuss your case in detail. If you are interested, please contact Julie Dahan, at:

Email: Julied@sherivf.com

OR

Phone: 702-533-2691
800-780-7437

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
Maria

Hello Doctor, I wrote you last week but still have some questions and Im not receiving answers in Germany. I was a low responder (only one egg retrieved, first Ivf) I’m 29 years old and an AMH of 1.93.
Should I also get a third day FSH exam?
Should I also get Antral follicle count?
My only egg fertilized and was transferred on day 3, it had 4 cells and I think it was fragmented, do I have a chance?
I would like to know your opinion because I don’t want to invest more money and emotions if things are unlikely to go well for me. With such a poor response I feel hopeless, I haven’t seen anywhere of someone with just one egg retrieved.
If you were to be my doctor would you continue trying?

reply
Dr. Geoffrey Sher

Frankly, I doubt that doing any more such testing will be of benefit. As I stated before, women who (regardless of age) have DOR have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production of LH biological activity which can result in excessive LH-induced ovarian male hormone (predominantly testosterone) production which in turn can have a deleterious effect on egg/embryo “competency”.

While it is presently not possible by any means, to reverse the age-related effect on the woman’s “biological clock, certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can make matters worse. Similarly, the amount/dosage of certain fertility drugs that contain LH/hCG (e.g. Menopur) can have a negative effect on the development of the eggs of older women and those who have DOR and should be limited.

I try to avoid using such protocols/regimes (especially) in older women and those with DOR, favoring instead the use of the agonist/antagonist conversion protocol (A/ACP), a modified, long pituitary down-regulation regime, augmented by adding supplementary human growth hormone (HGH). I further recommend that such women be offered access to embryo banking of PGS (next generation gene sequencing/NGS)-selected normal blastocysts, the subsequent selective transfer of which by allowing them to to capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” could significantly enhance the opportunity to achieve a viable pregnancy

Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
• A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
• Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
• Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers Should be the Standard of Care in IVF
• Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
• Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
• Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
• Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
• Preimplantation Genetic Testing (PGS) in IVF: It Should be Used Selectively and NOT be Routine.
• Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
• PGS in IVF: Are Some Chromosomally Abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
• PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
• Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• The Role of Nutritional Supplements in Preparing for IVF
• Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
• Empty Follicle syndrome.
I invite you to arrange to have a Skype or an in-person consultation with me to discuss your case in detail. If you are interested, please contact Julie Dahan, at:

Email: Julied@sherivf.com

OR

Phone: 702-533-2691
800-780-7437

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
Daisy Vatanan

Hi Dr. Sher,

What are your thoughts on the endometrial receptivity assay and endometrial scratching. It was suggested by our RE as we have only a few frozen blasts, although they are high quality. This would be the first time attempting to transfer and we want to do everything to make it a success, but also going through more painful and possibly unnecessary testing is not appealing. Thanks!

reply
Dr. Geoffrey Sher

Hi Daisy,

Very respectfully, In my opinion, neither of these techniques have any merit. I do not use them on my patients.

Geoff Sher

G

reply
Daisy Vatanan

Thank you! I have no known issues in this area, so was hoping this wasn’t necessary. Much appreciated!

reply
Zenman

Hello Doctor,
My Wife undergone IVF treatment and 5 day embryo got transferred on 20th July after 14 days HCG level came up to 73 and two day later it went up to 107 and again after 2 day it went up to 120 after 2 days it came down to 80 and again it went up to 90 (such a roller coaster), Yesterday she undergone Ultra Sound where they found very unclear SAC and they confirmed no ectopic pregnancy and our Dr asked my wife to be on Progesterone 2ml twice per day for one more week to check whether any improvement is there on HCG level . Do you think that there is any chance to become a viable pregnancy and does it make any sense to be on progesterone.
Thank You!
Zen

reply
Dr. Geoffrey Sher

Frankly it does not sound promising but “while there is life there is still hope”!

Good luck!

Geoff Sher

reply
Shirley

Dear Dr.Sher,
I’m very happy to find your website and reviewed many of patients questions and your answers. I’m also facing very difficult situation, lot of confuse and lack of confidence. I’m 39 years old, 5’4″, 128 lb. My husband and I we all like sports, we run 1-3 times a week, around 5-15 miles. We married 3 years, we really look forward a baby, but due to my problem I can’t get pregnant naturally. I have premature ovarian failure, high FSH 32.8 and low AMH 0.03. I have another issue is pituitary tumors, I did MRI on 2014 Oct, the tumor is very small, (I can’t remember exactly, it should be something like 3 mm.), I already had Bromocriptin around 3 years, half per day.My period is very abnormal these years, the new period didn’t come yet since last year Oct. My doctor suggest me to do donate egg if we really want a baby. Recently I’m start to looking for donor. Although donor egg is the way we can try, actually it might be the only we if we still want to have a baby, I don’t have other choices. But I am not sure how much possibility I will be successful if by donate egg IVF based on my situation? And what aspects I need to pay attention and concern? I really need help and advice to know what I should do? Can you kindly give me some help and advise? Look forward to hearing from you. Thanks!

reply
Dr. Geoffrey Sher

Shirly,

You are indeed a candidate for egg donation IVF. Your pituitary tumor is not likely to pose a problem (but discuss this with your endocrinologist).

I would be happy to discuss the oportunity with you but to do so we would need to connect.

Name: (F) Michelle Bleier Age: 41
Partner: Scott Bleier Age 38
Email Address: SUMROF75@YAHOO.COM; scottebleier@yahoo.com
Contact Phone # 602) 999-7596
Dear Michelle,
I really enjoyed meeting and interacting with you. Thank you kindly for your interest in my opinion and in my services.
Below, please find a summary of our consultation for your records. Also, please know that you will be contacted by an office administrator to help you understand the financial options, as well as by a clinical coordinator who will discuss clinical aspects of treatment with me in Las Vegas.
I typically schedule my IVF cycles 6 months in advance, for specific dates. The cycles last about two weeks, and I do limit the number of cases in each batch in order to make sure I can personally monitor the cycles, and dedicate special attention to each patient. Given my very busy schedule, it is always advisable for you to schedule possible treatment for the earliest convenient date. Both, the financial and clinical coordinators will help you work out logistic issues, and assist you in finalizing the ideal dates for your treatment. We require that all patients make a modest non-refundable deposit to secure the date. This deposit is deducted from the cost of the cycle of treatment.
We recognize that regardless of the nature of your reproductive issue both partners have a stake in the process and its outcome. Accordingly both would usually wish to be present throughout most of the 7-14 days of management. From a practical standpoint however, this might not always be possible (or even necessary). In such cases, we would be able to provide the male partner at least 3 days advance notice of when he would be to be present in Las Vegas for one day. In cases where frozen embryo transfers (FETs) are being done, the male partner will not even be required to be present in Las Vegas. Moreover, selectively when sperm is required from a fertile male partner, we can even arrange for frozen semen sample to be shipped timely for the fertilization process.
There is rarely a need for women undergoing controlled ovarian stimulation (COS) for IVF to begin serial monitoring by ultrasound and/or blood testing prior to the 7th day of stimulation. As such, the female partner is not needed to arrive in Las Vegas prior to the 7th day of fertility drug administration, All preliminary preparatory testing can thus be done at your home setting by your primary GP or OB/GYN, including (if needed) bloodwork and a baseline ultrasound examination with the start of the menstrual period that launches the cycle of ovarian stimulation. After treatment is completed, you can return home. We will follow up with you and/or your partner by phone or Skype communication. We will also interact as needed with your primary care OB/GYN to supervise post-treatment and early-pregnancy management.
While this process might at first glance seem somewhat complex, in reality with a dedicated Clinical Coordinator assisting you, we have developed over the past 30 years of providing infertility treatment to more than 70,000 patients a very easy, convenient, safe and effective method for treating local patients as well as those traveling to Las Vegas from out of state or from abroad.
I provide my cell phone number and email address (702) 281-7437 to all my patients and as such I invite you to call me if you have any questions or issues that need to be addressed. If I am not immediately available, leave your name and phone number and I will get back to you promptly.
Thank you again for your interest

CONSULTATION SUMMARY:
Date of Consultation: August 11th, 2016
Nature of The Reproductive Dysfunction:
Age: 41y
• G P M E G4 P0 M4 (10/2014-3/2016) all early
• Duration of infertility: 2Y
• Menstruation: Regular/normal flow/not very painful.
• Pain with deep penetration during intercourse: no
• Pain with ovulation: yes
• PAP Smears (10/2015)..: normal
• Previous pelvic inflammatory disease: no
• Prior abdominal-pelvic surgeries: no
• Systemic History: hypothyroid disease/heterozygous MTHFR mutation
• Current Medications: Levothyroxine 250mcg daily/Labetalol 400mg BID
• Allergic to: none
• Substances:
o Smoking: no
o Alcohol: no
o Substance abuse no
• Family History: Diabetes/hypertension
• Ovarian reserve: DOR…AMH=0.23ng/ml/basal FSH=11MIU/ml
• Prior immune tests for IID: No ATA done…aPS-+ve…no NK cell assessment or alloimmune profile done
• Previous hysterosalpingogram: no
• Previous hysterosonogram (HSN): no
• Male partner” ` normal sperm parameters
o Initiated pregnancies in the past 4 with partner
• Previous infertility treatments: #X3 IVF with one (1) FET with two (2) PGS-normal blastocysts : last fresh cycle was in April 20116. Launched off BCP and then Lupron (?flare)…….? Dosage gonadotropins…3 follicles observed…2 eggs harvested …2 transferred on day 3
SUMMATION: Age 41Y…RPL….DOR (AMH=0.23ng/ml), 3 X failed IVF/ WANTS IVF WITH OD…Probably done at a distance.. Probably has an IID. We need to evaluate for this. (autoimmune vs alloimmune).
PLAN:
• Immune tests: ATA/NKa/APA/RIP/DQa/HLA
• HSN
• BCP
• IVF with OD …I have referred them to FTF…aim for ER on OD in October cycle. Will need to get a specimen of husband’s sperm frozen here.
• CC/F consultation
¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬¬____________________________________
ADDITIONAL INFORMATION!
I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.

• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Recurrent Pregnancy Loss (RPL): Why do I keep losing my Pregnancies
• IVF Failure and Implantation Dysfunction:
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Endometrial Thickness, Uterine Pathology and Immunologic Factors
• Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
• Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• The Role of Nutritional Supplements in Preparing for IVF
• IVF with egg donation

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

Geoff Sher

reply
Sheena

Hi Dr Sher, does too much ivf drugs (eg LH for older women) and the wrong protocol impact on the quality of all eggs or just the eggs that grow in that particular cycle? Many thanks!

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Anonymous

Thanks. Why is it that the rest of the eggs aren’t exposed to the same drugs? Aren’t all eggs stored in the ovaries? … Sorry if this is a silly/basic question.

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Dr. Geoffrey Sher

They are likely most vulnerable during cyclical ovogenesis (development).

Geoff Sher

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Julie

Hi Dr Sher,
We are living in Italy and are attempting to do FET with donor eggs. The Italian doctors refuse to answer any questions and always say “Don’t worry” and “Everything is fine” instead of explaining to us what is going on.

This round of therapy entails taking the BCP Lestronete 2 August-16 August, along with taking Suprefact nasal spray 1 puff in each nostril 3 times daily from 10 August-indefinte. The first monitoring is scheduled for 26 August.

The leaflet with Suprefact says to take 1 puff in each nostril 6 times a day, but the doctors here have me only taking half as much. Do you think 3 puffs a day in each nostril is enough?

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Dr. Geoffrey Sher

I do not recommend the nasal preparation. My advice would be to use injectible agonist.

Geoff Sher

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Julie

unfortunately we don’t have a choice. We have absolutely no input concerning the treatment; they say “We’re the doctors, so do what we say”. So, even though you don’t recommend it, can you tell me if the 3 puffs per day per nostril is enough?

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Dr. Geoffrey Sher

Sorry, but that is sooo arrogant.
The reason I do not prescribe the nasal agonist is because absorbtion varies too widely in my opinion.

Geoff Sher

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Katy

Having failed to respond to a medicated FET or ovulation induction FET (cycles cancelled due to inadequate endometrial growth), we’re going to prepare my endometrium for another treatment cycle with extended oestrogen therapy, and 1-2 months of a copper IUD. We’ll be adding in pentoxifylline + vitamin E to the treatment protocol while priming the endometrium – would you recommend adding in vaginal viagra to the protocol, to support the oestrogen therapy?

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Katy

Great! Thank you very much. In that case, presumably it is safe to take the vaginal viagra over an extended period of time (ie a period of weeks, vs the usual way of taking it within a treatment cycle for a period of days up until hCG trigger or day of progesterone administration)?

Would you recommend the same dosage? We would be getting the pessaries made up to order, so would like to make sure we get the dose right!

Very many thanks in advance

Katy

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Dr. Geoffrey Sher

You should only use it during the treatment cycle…not over an extended period of time.

Geoff Sher

reply
Katy

Oh, OK, so you DON’T recommend the viagra be added into the protocol to support the extended estrogen therapy, pentoxifylline + vitamin E (during the 1-2 months of the copper IUD)?

We would add viagra into a treatment cycle, but my question was about whether we should add it in to an extended period of estrogen priming to prepare the endometrium *before* a treatment cycle.

Just so I have understood correctly, you recommend that viagra should *not* be used for this period of endometrial preparation, and only during the treatment cycle itself?

Dr. Geoffrey Sher

Yes! that is what I would recommend…only to use it during the cycle concerned.

Geoff Sher

Patty

Hello Dr. Sher, I have had 3 losses I’m a 28 yr old who has gone though 1 round of IVF so far with a missed miscarriag. My question is the first round was a very good grade embryo and I still had a miscarriage. I only have one embryo left which is a lower grade what are the chances of this becoming a successful pregnancy? All of my other losses have been blightum ovum and a eptopic.

reply
Dr. Geoffrey Sher

When it comes to reproduction, humans are the poorest performers of all mammals. In fact we are so inefficient that up to 75% of fertilized eggs do not produce live births, and up to 30% of pregnancies end up being lost within 10 weeks of conception (in the first trimester). RPL is defined as two (2) or more failed pregnancies. Less than 5% of women will experience two (2) consecutive miscarriages, and only 1% experience three or more.
Pregnancy loss can be classified by the stage of pregnancy when the loss occurs:
• Early pregnancy loss (first trimester)
• Late pregnancy loss (after the first trimester)
• Occult “hidden” and not clinically recognized, (chemical) pregnancy loss (occurs prior to ultrasound confirmation of pregnancy)
• Early pregnancy losses usually occur sporadically (are not repetitive).
In more than 70% of cases the loss is due to embryo aneuploidy (where there are more or less than the normal quota of 46 chromosomes). Conversely, repeated losses (RPL), with isolated exceptions where the cause is structural (e.g., unbalanced translocations), are seldom attributable to numerical chromosomal abnormalities (aneuploidy). In fact, the vast majority of cases of RPL are attributable to non-chromosomal causes such as anatomical uterine abnormalities or Immunologic Implantation Dysfunction (IID).
Since most sporadic early pregnancy losses are induced by chromosomal factors and thus are non-repetitive, having had a single miscarriage the likelihood of a second one occurring is no greater than average. However, once having had two losses the chance of a third one occurring is double (35-40%) and after having had three losses the chance of a fourth miscarriage increases to about 60%. The reason for this is that the more miscarriages a woman has, the greater is the likelihood of this being due to a non-chromosomal (repetitive) cause such as IID. It follows that if numerical chromosomal analysis (karyotyping) of embryonic/fetal products derived from a miscarriage tests karyotypically normal, then by a process of elimination, there would be a strong likelihood of a miscarriage repeating in subsequent pregnancies and one would not have to wait for the disaster to recur before taking action. This is precisely why we strongly advocate that all miscarriage specimens be karyotyped.
There is however one caveat to be taken into consideration. That is that the laboratory performing the karyotyping might unwittingly be testing the mother’s cells rather than that of the conceptus. That is why it is not possible to confidently exclude aneuploidy in cases where karyotyping of products suggests a “chromosomally normal” (euploid) female.
Late pregnancy losses (occurring after completion of the 1st trimester/12th week) occur far less frequently (1%) than early pregnancy losses. They are most commonly due to anatomical abnormalities of the uterus and/or cervix. Weakness of the neck of the cervix rendering it able to act as an effective valve that retains the pregnancy (i.e., cervical incompetence) is in fact one of the commonest causes of late pregnancy loss. So also are developmental (congenital) abnormalities of the uterus (e.g., a uterine septum) and uterine fibroid tumors. In some cases intrauterine growth retardation, premature separation of the placenta (placental abruption), premature rupture of the membranes and premature labor can also causes of late pregnancy loss.
Much progress has been made in understanding the mechanisms involved in RPL. There are two broad categories:
1. Problems involving the uterine environment in which a normal embryo is prohibited from properly implanting and developing. Possible causes include:
• Inadequate thickening of the uterine lining
• Irregularity in the contour of the uterine cavity (polyps, fibroid tumors in the uterine wall, intra-uterine scarring and adenomyosis)
• Hormonal imbalances (progesterone deficiency or luteal phase defects). This most commonly results in occult RPL.
• Deficient blood flow to the uterine lining (thin uterine lining).
• Immunologic implantation dysfunction (IID). A major cause of RPL. Plays a role in 75% of cases where chromosomally normal preimplantation embryos fail to implant.
• Interference of blood supply to the developing conceptus can occur due to a hereditary clotting disorder known as Thrombophilia.
2. Genetic and/or structural chromosomal abnormality of the embryo.Genetic abnormalities are rare causes of RPL. Structural chromosomal abnormalities are slightly more common but are also occur infrequently (1%). These are referred to as unbalanced translocation and they result from part of one chromosome detaching and then fusing with another chromosome. Additionally, a number of studies suggest the existence of paternal (sperm derived) effect on human embryo quality and pregnancy outcome that are not reflected as a chromosomal abnormality. Damaged sperm DNA can have a negative impact on fetal development and present clinically as occult or early clinical miscarriage. The Sperm Chromatin Structure Assay (SCSA) which measures the same endpoints are newer and possibly improved methods for evaluating.

IMMUNOLOGIC IMPLANTATION DYSFUNCTION
Autoimmune IID: Here an immunologic reaction is produced by the individual to his/her body’s own cellular components. The most common antibodies that form in such situations are APA and antithyroid antibodies (ATA).
But it is only when specialized immune cells in the uterine lining, known as cytotoxic lymphocytes (CTL) and natural killer (NK) cells, become activated and start to release an excessive/disproportionate amount of TH-1 cytokines that attack the root system of the embryo, that implantation potential is jeopardized. Diagnosis of such activation requires highly specialized blood test for cytokine activity that can only be performed by a handful of reproductive immunology reference laboratories in the United States.
Alloimmune IID, i.e., where antibodies are formed against antigens derived from another member of the same species, is believed to be a relatively common immunologic cause of recurrent pregnancy loss.
Autoimmune IID is often genetically transmitted. Thus it should not be surprising to learn that it is more likely to exist in women who have a family (or personal) history of primary autoimmune diseases such as lupus erythematosus (LE), scleroderma or autoimmune hypothyroidism (Hashimoto’s disease), autoimmune hyperthyroidism (Grave’s disease), rheumatoid arthritis, etc. Reactionary (secondary) autoimmunity can occur in conjunction with any medical condition associated with widespread tissue damage. One such gynecologic condition is endometriosis. Since autoimmune IID is usually associated with activated NK and T-cells from the outset, it usually results in such very early destruction of the embryo’s root system that the patient does not even recognize that she is pregnant. Accordingly the condition usually presents as “unexplained infertility” or “unexplained IVF failure” rather than as a miscarriage.

Alloimmune IID, on the other hand, usually starts off presenting as unexplained miscarriages (often manifesting as RPL). Over time as NK/T cell activation builds and eventually becomes permanently established the patient often goes from RPL to “infertility” due to failed implantation. RPL is more commonly the consequence of alloimmune rather than autoimmune implantation dysfunction.
However, regardless, of whether miscarriage is due to autoimmune or alloimmune implantation dysfunction the final blow to the pregnancy is the result of activated NK cells and CTL in the uterine lining that damage the developing embryo’s “root system” (trophoblast) so that it can no longer sustain the growing conceptus. This having been said, it is important to note that autoimmune IID is readily amenable to reversal through timely, appropriately administered, selective immunotherapy, and alloimmune IID is not. It is much more difficult to treat successfully, even with the use of immunotherapy. In fact, in some cases the only solution will be to revert to selective immunotherapy plus using donor sperm (provided there is no “match” between the donor’s DQa profile and that of the female recipient) or alternatively to resort to gestational surrogacy.
DIAGNOSING THE CAUSE OF RPL
In the past, women who miscarried were not evaluated thoroughly until they had lost several pregnancies in a row. This was because sporadic miscarriages are most commonly the result of embryo numerical chromosomal irregularities (aneuploidy) and thus not treatable. However, a consecutive series of miscarriages points to a repetitive cause that is non-chromosomal and is potentially remediable. Since RPL is most commonly due to a uterine pathology or immunologic causes that are potentially treatable, it follows that early chromosomal evaluation of products of conception could point to a potentially treatable situation. Thus I strongly recommend that such testing be done in most cases of miscarriage. Doing so will avoid a great deal of unnecessary heartache for many patients.
Establishing the correct diagnosis is the first step toward determining effective treatment for couples with RPL. It results from a problem within the pregnancy itself or within the uterine environment where the pregnancy implants and grows. Diagnostic tests useful in identifying individuals at greater risk for a problem within the pregnancy itself include:

• Karyotyping (chromosome analysis) both prospective parents
• Assessment of the karyotype of products of conception derived from previous miscarriage specimens
• Ultrasound examination of the uterine cavity after sterile water is injected or sonohysterogram, fluid ultrasound, etc.)
• Hysterosalpingogram (dye X-ray test)
• Hysteroscopic evaluation of the uterine cavity
• Full hormonal evaluation (estrogen, progesterone, adrenal steroid hormones, thyroid hormones, FSH/LH, etc.)
• Immunologic testing to include:
a) Antiphospholipid antibody (APA) panel
b) Antinuclear antibody (ANA) panel
c) Antithyroid antibody panel (i.e., antithyroglobulin and antimicrosomal antibodies)
d) Reproductive immunophenotype
e) Natural killer cell activity (NKa) assay (i.e., K562 target cell test)
f) Alloimmune testing of both the male and female partners
TREATMENT OF RPL
Treatment for Anatomic Abnormalities of the Uterus: This involves restoration through removal of local lesions such as fibroids, scar tissue, and endometrial polyps or timely insertion of a cervical cerclage (a stitch placed around the neck of the weakened cervix) or the excision of a uterine septum when indicated.
Treatment of Thin Uterine Lining: A thin uterine lining has been shown to correlate with compromised pregnancy outcome. Often this will be associated with reduced blood flow to the endometrium. Such decreased blood flow to the uterus can be improved through treatment with sildenafil and possibly aspirin.
Sildenafil (Viagra) Therapy. Viagra has been used successfully to increase uterine blood flow. However, to be effective it must be administered starting as soon as the period stops up until the day of ovulation and it must be administered vaginally (not orally). Viagra in the form of vaginal suppositories given in the dosage of 25 mg four times a day has been shown to increase uterine blood flow as well as thickness of the uterine lining. To date, we have seen significant improvement of the thickness of the uterine lining in about 70% of women treated. Successful pregnancy resulted in 42% of women who responded to the Viagra. It should be remembered that most of these women had previously experienced repeated IVF failures.

Use of Aspirin: This is an anti-prostaglandin that improves blood flow to the endometrium. It is administered at a dosage of 81 mg orally, daily from the beginning of the cycle until ovulation.
Treating Immunologic Implantation Dysfunction with Selective Immunotherapy: Modalities such as IL/IVIg, heparinoids (Lovenox/Clexane), and corticosteroids (dexamethasone, prednisone, prednisolone) can be used in select cases depending on autoimmune or alloimmune dysfunction.
The Use of IVF in the Treatment of RPL
In the following circumstances, IVF is the preferred option:
1. When in addition to a history of RPL, another standard indication for IVF (e.g., tubal factor, endometriosis, and male factor infertility) is superimposed.
2. In cases where selective immunotherapy is needed to treat an immunologic implantation dysfunction.
The reason for IVF being a preferred approach in such cases is that in order to be effective, the immunotherapy needs to be initiated well before spontaneous or induced ovulation. Given the fact that the anticipated birthrate per cycle of COS with or without IUI is at best about 15%, it follows that short of IVF, to have even a reasonable chance of a live birth, most women with immunologic causes of RPL would need to undergo immunotherapy repeatedly, over consecutive cycles. Conversely, with IVF, the chance of a successful outcome in a single cycle of treatment is several times greater and, because of the attenuated and concentrated time period required for treatment, IVF is far safer and thus represents a more practicable alternative
Since embryo aneuploidy is a common cause of miscarriage, the use of preimplantation genetic diagnosis (PGD), with tests such as CGH, can provide a valuable diagnostic and therapeutic advantage in cases of RPL. PGD requires IVF to provide access to embryos for testing.
There are a few cases of intractable alloimmune dysfunction due to absolute DQ alpha matching where Gestational Surrogacy or use of donor sperm could represent the only viable recourse, other than abandoning treatment altogether and/or resorting to adoption. Other non-immunologic factors such as an intractably thin uterine lining or severe uterine pathology might also warrant that last resort consideration be given to gestational surrogacy.
The good news is that if a couple with RPL is open to all of the diagnostic and treatment options referred to above, a live birthrate of 70%–80% is ultimately achievable.

I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
• Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• Why did my IVF Fail
• IVF Failure and Implantation Dysfunction:
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Endometrial Thickness, Uterine Pathology and Immunologic Factors
• Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
• Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• The Role of Nutritional Supplements in Preparing for IVF

Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691
 800-780-7437

Geoff Sher

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
Oana Stefanache

Hello Dr Sher,

What is the best level of testosterone for fertility and ivf? I had 0.4, 0.5, 0.6 and 1.44 (after taking a dhea supplement). My lab shows normal levels as somewhere between 0.22 – 2.9, so I guess I had normal levels of testosterone, but where exactly within this range should it be for best results?

Thank you!

reply
Brie

brie
August 11, 2016 at 6:20 am
hello,
I have a question regarding FET. I am thinking of having another baby. I have two pgd frozen embryos that I froze at 37. I am now 40.
Does the fact that these embryos are younger than my age put me at less of any sort of risk?
Or I am at risk regardless because of my current age?
Thank you

reply
Dr. Geoffrey Sher

The fact that these have been frozen for some time, will have no impact on their viability. And, provided that you check out as medically fit, you should still be OK at 40Y.

Geoff Sher

reply
Stephanie

Hello,
I had surgery back in 2008 to reopen my tubes, though I had severe scaring my tubes were not removed, I was also diagnosed with PCOS. What are my chances of conceiving with IVF? I’m also over weight, which I am currently working on and I just turned 38!
Thank you for your time.
Stephanie

reply
Dr. Geoffrey Sher

Hi Stephanie,

If your tubes are damaged but not distended with fluid (hydrosalpinx) , it should not affect your chance of IVF success. However, to be more specific in terms of potential success , I would need a great deal more information.

I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
• Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• The Role of Nutritional Supplements in Preparing for IVF
• The Basic Infertility Work-Up

Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691
 800-780-7437

Geoff Sher

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
Kalli

What are your recommendations for activity restrictions following embryo transfer? My clinic is recommending to stay in bed laying flat for 4 days as much as possible.
I had my egg retrieval a few days ago, 48 eggs retrieved 28 mature and 24 fertilized. How many should I expect to make it to blastocyst day 5? I am 29 years old, no prior pregnancies. We are going to have PGS testing performed on all blastocysts, and still do a fresh transfer.

reply
Dr. Geoffrey Sher

I advise my patients to try and be as still as possible for 6-8 hours and thereupon be a “couch potato” overnight. Ther next day…resume normal activity. It is worthwhile to mention that 6 hours after transfer, the embryos become wedged in the endometrial glands and thus are immobilized such that no activity can dislodge them.

Geoff Sher

reply
Kalli

Thank you. What is your opinion regarding Valium prior to the transfer? What about acupuncture?

Also what percentage of my embryos do you typically expect to make it to day 5?

reply
Dr. Geoffrey Sher

In women <35Y about 40% of cleaved embryos will make it to blastocyst by day-6. But this will likely vary depending on other factors such as male factor, ovarian reserve the protocol used for ovarian stimulation and laboratory prowes.

I routinely prescribe valium (or equivalent) about 10mn prior to ET. Acupuncture is also a good idea around the time of ET as it should improve uterine blood flow.

Good luck!

Geoff Sher

reply
Lauren

Hello Dr. Sher,

You mention using human growth hormone in patients with DOR. My RE indicated that human growth hormones could be used in the past for treatment, but are currently banned. Is this not true?

Thanks!

reply
Roz

I was wondering with my post et being day 12 today and my levels were 778 from day 10 which were 229… Is that a higher chance for multiples

reply
Sena R.

Hi. I am 35, with a history of pelvic surgeries. I underwent 1st for appendicitis when I was 15, right tube was erroneously removed in that procedure. The main reason for the surgery was pelvic pain that was happening due to a congenital mass engulfing my large intestine. The doctors later managed to diagnose it and I underwent my 2nd surgery after a month’s gap. At the age of 27 when I was married for 2 years the same pelvic pain reoccurred and it was diagnosed that some of the part of that membrane was not properly removed and I have developed a water sack accumulating water in the tummy. It was non malignant. After the three surgeries, one tube absent, I was asked to get my Hystero done and i was diagnosed with Bilateral Hydrosalpinx. I underwent 2 IUIs and 1 IVF with the same and it failed. Doctors told me that operating you for the 4th time and digging for the tube under so many adhesions is not a great idea and life threatening too. So they avoided it and went straight to IVF. My protocol was Gonal 150 IUs for 5 days(day 2 to day 7). Day 8: Injection Cetrotide(0.25mg) and Gonal F 225 IUs and Gonal F 300 and Pregnyl 10,000 units; 36 hours before retrieval. . I produced 10 eggs, 7 fertilized and 4 were of grade 1. They transferred 2 and the attempt failed.

In May 2016( i migrated to Canada, Toronto) and am a patient or Dr. Alfonso P. Del Valle. He did Hystero and observed that Hydrosalpinx is not there anymore, Further more he was not in the favour of operating me for complete tubal removal due to massive surgeries already done. I underwent my 2nd IVF(1st in Canada) based on the said protocol:

1. BCP for 24 days.
2. Gonal F 250 IUs and Menopur 75IUs each day for 10 days.
3. I was triggered with Orglutran 10,000 IUs 36 hours before egg retrieval.

On day of retrieval, I produced 6( i observed the count was low; as last year same dates in produced 10). 4 fertilized. 3 reached blastocyst stage and 1 was transferred on day 5. The transfer is made yesterday. I am on progestrone supp and oil injections. My endo was fine on transfer day.

The conclusion with the 2 attempts one back home and one in Canada is that my egg production is fine but with one failed attempt in 2015 I am super panic. Are the docs following the right protocol. Despite being given clean chit for Hydrosalpinx, should I still take risk of surgery?.

Thanks

reply
Dr. Geoffrey Sher

A HSG will reveal whether you have hydrosalpinx or not. If so the tube can be clipped rather than removed …with much less risk.

I do however feel that you should at the same time be assessed for an immunologic or anatomical implantation dysfunction.

Whenever a patient fails to achieve a viable pregnancy following embryo transfer (ET), the first question asked is why! Was it simply due to, bad luck?, How likely is the failure to recur in future attempts and what can be done differently, to avoid it happening next time?.
It is an indisputable fact that any IVF procedure is at least as likely to fail as it is to succeed. Thus when it comes to outcome, luck is an undeniable factor. Notwithstanding, it is incumbent upon the treating physician to carefully consider and address the causes of IVF failure before proceeding to another attempt:
1. Age: The chance of a woman under 35Y of age having a baby per embryo transfer is about 35-40%. From there it declines progressively to under 5% by the time she reaches her mid-forties. This is largely due to declining chromosomal integrity of the eggs with advancing age…”a wear and tear effect” on eggs that are in the ovaries from birth.
2. Embryo Quality/”competency (capable of propagating a viable pregnancy)”. As stated, the woman’s age plays a big role in determining egg/embryo quality/”competency”. This having been said, aside from age the protocol used for controlled ovarian stimulation (COS) is the next most important factor. It is especially important when it comes to older women, and women with diminished ovarian reserve (DOR) where it becomes essential to be aggressive, and to customize and individualize the ovarian stimulation protocol.
We used to believe that the uterine environment is more beneficial to embryo development than is the incubator/petri dish and that accordingly, the earlier on in development that embryos are transferred to the uterus, the better. To achieve this goal, we used to select embryos for transfer based upon their day two or microscopic appearance (“grade”). But we have since learned that the further an embryo has advanced in its development, the more likely it is to be “competent” and that embryos failing to reach the expanded blastocyst stage within 5-6 days of being fertilized are almost invariably “incompetent” and are unworthy of being transferred. Moreover, the introduction into clinical practice about a decade ago, (by Levent Keskintepe PhD and myself) of Preimplantation Genetic Sampling (PGS), which assesses for the presence of all the embryos chromosomes (complete chromosomal karyotyping), provides another tool by which to select the most “competent” embryos for transfer. This methodology has selective benefit when it comes to older women, women with DOR, cases of unexplained repeated IVF failure and women who experience recurrent pregnancy loss (RPL).
3. The number of the embryos transferred: Most patients believe that the more embryos transferred the greater the chance of success. To some extent this might be true, but if the problem lies with the use of a suboptimal COS protocol, transferring more embryos at a time won’t improve the chance of success. Nor will the transfer of a greater number of embryos solve an underlying embryo implantation dysfunction (anatomical molecular or immunologic).Moreover, the transfer of multiple embryos, should they implant, can and all too often does result in triplets or greater (high order multiples) which increases the incidence of maternal pregnancy-induced complications and of premature delivery with its serious risks to the newborn. It is for this reason that I rarely recommend the transfer of more than 2 embryos at a time and am moving in the direction of advising single embryo transfers …especially when it comes to transferring embryos derived through the fertilization of eggs from young women.
4. Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:
a. A“ thin uterine lining”
b. A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
c. Immunologic implantation dysfunction (IID)
d. Endocrine/molecular endometrial receptivity issues
Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).

I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
• Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers Should be the Standard of Care in IVF
• IVF Failure and Implantation Dysfunction:
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Endometrial Thickness, Uterine Pathology and Immunologic Factors
• Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
• Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• The Role of Nutritional Supplements in Preparing for IVF
• Pelvic Inflammatory Disease (PID), Tubal Damage and Hydrosalpinx: Preparing for IVF
Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691
 800-780-7437

Geoff Sher

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
Maria

Hi dr sher, just finished my first ivf cycle and yesterday i had my egg collection and failed to retrieve any eggs out of the 4 follicles. I was on the pill for six weeks, then I was told to start lucrin 10, got my period and started on gonal f 225 a day, as follicles were not growing fast they also asked me to inject Luveris at same time as gonal f. The whole time I was also injecting lucrin in the morning. On Monday I had my ovridel 250 trigger plus had to do final shot of gonal at 7:30 pm. I have endometriosis, and reserve level is 1.8, and I’m 39 years old. I was told that my no egg retrieval is mostly because my age and low reserve and follicles were empty. Can you let me know if I should try a different type of cycle? Doc said possible should try donor egg but I ding want to do that just yet. Thanks

reply
Dr. Geoffrey Sher

There is no such thing as “empty follicles”:. All follicles have eggs. They might not release them but they are trapped in the follicles …see below.

Also triggering with 250mcg Ovidrel is in my opinion too lw a dosage. Ideally you need 500mcg. This could also have contributed to the problem.

Finally, endometriosis is associated with an immunologic implantation dysfunction in about 1/3 of cases…regardless of its severity (see below).

Older women as well as those who (regardless of age) have diminished ovarian reserve (DOR) tend to produce fewer and less “competent” eggs, the main reason for reduced IVF success in such cases. The compromised outcome is largely due to the fact that such women tend to have increased LH biological activity which often results in excessive LH-induced ovarian testosterone production which in turn can have a deleterious effect on egg/embryo “competency”.
Certain ovarian stimulation regimes either promote excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), augment LH/hCG delivered through additional administration (e.g. high dosage menotropins such as Menopur), or fail to protect against body’s own/self-produced LH (e.g. late antagonist protocols where drugs such as Ganirelix/Cetrotide/Orgalutron that are first administered 6-7 days after ovarian stimulation has commenced).
I try to avoid using such protocols/regimes (especially) in older women and those with DOR, favoring instead the use of a modified, long pituitary down-regulation protocol (the agonist/antagonist conversion protocol-A/ACP) augmented by adding supplementary human growth hormone (HGH). I further recommend Staggered IVF with embryo banking of PGS (next generation gene sequencing/NGS)-normal blastocysts in such cases. This type of approach will in my opinion, optimize the chance of a viable pregnancy per embryo transfer procedure and provide an opportunity to capitalize on whatever residual ovarian reserve and egg quality still exists, allowing the chance to “make hay while the sun still shines”.

Older women as well as those who (regardless of age) have diminished ovarian reserve (DOR) tend to produce fewer and less “competent” eggs, the main reason for reduced IVF success in such cases. The compromised outcome is largely due to the fact that such women tend to have increased LH biological activity which often results in excessive LH-induced ovarian testosterone production which in turn can have a deleterious effect on egg/embryo “competency”.
Certain ovarian stimulation regimes either promote excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), augment LH/hCG delivered through additional administration (e.g. high dosage menotropins such as Menopur), or fail to protect against body’s own/self-produced LH (e.g. late antagonist protocols where drugs such as Ganirelix/Cetrotide/Orgalutron that are first administered 6-7 days after ovarian stimulation has commenced).
I try to avoid using such protocols/regimes (especially) in older women and those with DOR, favoring instead the use of a modified, long pituitary down-regulation protocol (the agonist/antagonist conversion protocol-A/ACP) augmented by adding supplementary human growth hormone (HGH). I further recommend Staggered IVF with embryo banking of PGS (next generation gene sequencing/NGS)-normal blastocysts in such cases. This type of approach will in my opinion, optimize the chance of a viable pregnancy per embryo transfer procedure and provide an opportunity to capitalize on whatever residual ovarian reserve and egg quality still exists, allowing the chance to “make hay while the sun still shines”.

reply
Lisa H

Hi Dr Sher,
I was wondering if I could get your opinion on my case. We have been trying to conceive for 2.5 years. I am 34 years old with a lower than average AMH of 10 and a slight increased FSH on day 3 of 11. My husband is 39 and semen analysis was normal the 3 occasions it has been tested. We have been diagnosed with “unexplained infertility”. However i think I have a luteal phase defect, from using a clearblue fertility monitor, OPK’s, and monitoring cervical mucous for last 18 months I consistently ovulate on day 18-21 and my period comes on around day 28. Some months I will only have a 6 day luteal phase. I have seen 2 specialists in the UK one privately and one on the NHS. One of them said that a luteal phase defect isn’t possible and everyone had 14 days after ovulation before period?? The other said there wasn’t enough evidence to say that a luteal phase defect could be an issue. Both said IVF only option. We had 1st round of IVF in May (short protocol 300mg menopur and certrotide -8 eggs retrieved 5 fertilised 3 made it blastocyst one transferred) which was successful but unfortunately I had a miscarriage at 7 weeks. I can’t help feeling that the IVF may have worked due to the progesterone pessaries rather than an actual conception issue. I was just wondering if this is possible or likely? And if so what would be best way to proceed? We have 2 frozen embryos and are considering FET.
Many thanks!

reply
Dr. Geoffrey Sher

Whenever a patient fails to achieve a viable pregnancy following embryo transfer (ET), the first question asked is why! Was it simply due to, bad luck?, How likely is the failure to recur in future attempts and what can be done differently, to avoid it happening next time?.
It is an indisputable fact that any IVF procedure is at least as likely to fail as it is to succeed. Thus when it comes to outcome, luck is an undeniable factor. Notwithstanding, it is incumbent upon the treating physician to carefully consider and address the causes of IVF failure before proceeding to another attempt:
1. Age: The chance of a woman under 35Y of age having a baby per embryo transfer is about 35-40%. From there it declines progressively to under 5% by the time she reaches her mid-forties. This is largely due to declining chromosomal integrity of the eggs with advancing age…”a wear and tear effect” on eggs that are in the ovaries from birth.
2. Embryo Quality/”competency (capable of propagating a viable pregnancy)”. As stated, the woman’s age plays a big role in determining egg/embryo quality/”competency”. This having been said, aside from age the protocol used for controlled ovarian stimulation (COS) is the next most important factor. It is especially important when it comes to older women, and women with diminished ovarian reserve (DOR) where it becomes essential to be aggressive, and to customize and individualize the ovarian stimulation protocol.
We used to believe that the uterine environment is more beneficial to embryo development than is the incubator/petri dish and that accordingly, the earlier on in development that embryos are transferred to the uterus, the better. To achieve this goal, we used to select embryos for transfer based upon their day two or microscopic appearance (“grade”). But we have since learned that the further an embryo has advanced in its development, the more likely it is to be “competent” and that embryos failing to reach the expanded blastocyst stage within 5-6 days of being fertilized are almost invariably “incompetent” and are unworthy of being transferred. Moreover, the introduction into clinical practice about a decade ago, (by Levent Keskintepe PhD and myself) of Preimplantation Genetic Sampling (PGS), which assesses for the presence of all the embryos chromosomes (complete chromosomal karyotyping), provides another tool by which to select the most “competent” embryos for transfer. This methodology has selective benefit when it comes to older women, women with DOR, cases of unexplained repeated IVF failure and women who experience recurrent pregnancy loss (RPL).
3. The number of the embryos transferred: Most patients believe that the more embryos transferred the greater the chance of success. To some extent this might be true, but if the problem lies with the use of a suboptimal COS protocol, transferring more embryos at a time won’t improve the chance of success. Nor will the transfer of a greater number of embryos solve an underlying embryo implantation dysfunction (anatomical molecular or immunologic).Moreover, the transfer of multiple embryos, should they implant, can and all too often does result in triplets or greater (high order multiples) which increases the incidence of maternal pregnancy-induced complications and of premature delivery with its serious risks to the newborn. It is for this reason that I rarely recommend the transfer of more than 2 embryos at a time and am moving in the direction of advising single embryo transfers …especially when it comes to transferring embryos derived through the fertilization of eggs from young women.
4. Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:
a. A“ thin uterine lining”
b. A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
c. Immunologic implantation dysfunction (IID)
d. Endocrine/molecular endometrial receptivity issues
Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).

Whenever a patient fails to achieve a viable pregnancy following embryo transfer (ET), the first question asked is why! Was it simply due to, bad luck?, How likely is the failure to recur in future attempts and what can be done differently, to avoid it happening next time?.
It is an indisputable fact that any IVF procedure is at least as likely to fail as it is to succeed. Thus when it comes to outcome, luck is an undeniable factor. Notwithstanding, it is incumbent upon the treating physician to carefully consider and address the causes of IVF failure before proceeding to another attempt:
1. Age: The chance of a woman under 35Y of age having a baby per embryo transfer is about 35-40%. From there it declines progressively to under 5% by the time she reaches her mid-forties. This is largely due to declining chromosomal integrity of the eggs with advancing age…”a wear and tear effect” on eggs that are in the ovaries from birth.
2. Embryo Quality/”competency (capable of propagating a viable pregnancy)”. As stated, the woman’s age plays a big role in determining egg/embryo quality/”competency”. This having been said, aside from age the protocol used for controlled ovarian stimulation (COS) is the next most important factor. It is especially important when it comes to older women, and women with diminished ovarian reserve (DOR) where it becomes essential to be aggressive, and to customize and individualize the ovarian stimulation protocol.
We used to believe that the uterine environment is more beneficial to embryo development than is the incubator/petri dish and that accordingly, the earlier on in development that embryos are transferred to the uterus, the better. To achieve this goal, we used to select embryos for transfer based upon their day two or microscopic appearance (“grade”). But we have since learned that the further an embryo has advanced in its development, the more likely it is to be “competent” and that embryos failing to reach the expanded blastocyst stage within 5-6 days of being fertilized are almost invariably “incompetent” and are unworthy of being transferred. Moreover, the introduction into clinical practice about a decade ago, (by Levent Keskintepe PhD and myself) of Preimplantation Genetic Sampling (PGS), which assesses for the presence of all the embryos chromosomes (complete chromosomal karyotyping), provides another tool by which to select the most “competent” embryos for transfer. This methodology has selective benefit when it comes to older women, women with DOR, cases of unexplained repeated IVF failure and women who experience recurrent pregnancy loss (RPL).
3. The number of the embryos transferred: Most patients believe that the more embryos transferred the greater the chance of success. To some extent this might be true, but if the problem lies with the use of a suboptimal COS protocol, transferring more embryos at a time won’t improve the chance of success. Nor will the transfer of a greater number of embryos solve an underlying embryo implantation dysfunction (anatomical molecular or immunologic).Moreover, the transfer of multiple embryos, should they implant, can and all too often does result in triplets or greater (high order multiples) which increases the incidence of maternal pregnancy-induced complications and of premature delivery with its serious risks to the newborn. It is for this reason that I rarely recommend the transfer of more than 2 embryos at a time and am moving in the direction of advising single embryo transfers …especially when it comes to transferring embryos derived through the fertilization of eggs from young women.
4. Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:
a. A“ thin uterine lining”
b. A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
c. Immunologic implantation dysfunction (IID)
d. Endocrine/molecular endometrial receptivity issues
Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).

reply
Roz

This is my first IVF not sure if all the terminology but I had a 5 day et and a day 10 hcg test the numbers were 229.. Is that good And today which is day 12 my levels were 778… Is that good

reply
Anonymous

Hi Dr Sher, My consultant has said blood tests do not show I have PCOS. However in 2009 PCOS blood tests were inconclusive and on one scan there were polycystic looking ovaries (but many other scans later do not show this). I have always had irregular periods but no other symptoms. Is it possible that due to my age (44) the blood tests are not reliable? My AMH is high at 17. Is there anyway to test conclusively for PCOS and if not would you modify my protocol as if I do have PCOS? Thanks so much!

reply
Dr. Geoffrey Sher

I would need to consult with you !

Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691
 800-780-7437

Geoff Sher

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
Elizabeth

Dear dr sher

If would want your opinion on two issues

2. How do proceed with ivf in a scenario where a corpus luteum cyst found on day 21 of the cycle is resolving but still there on first day of new cycle (memstration) . On day 21 it as 5cm and now 4cm. Are my options wait or aspirate. Will birth control pills help . ? I am 41
2. So on the same day 21 when I saw the corpus luteum cyst I run a progesterone tests. This came back low at 1.5 . My doctor seems to think I am not ovulating or having annuvulatory cycle or cycles with low progesterone observed in another cycle. Would this be a sound assertion . I had a corpus luteum measuring 5cm when a progesterone of 1.5cm was observed
What are my options

reply
Dr. Geoffrey Sher

1. How do proceed with ivf in a scenario where a corpus luteum cyst found on day 21 of the cycle is resolving but still there on first day of new cycle (memstration) . On day 21 it as 5cm and now 4cm. Are my options wait or aspirate. Will birth control pills help . ? I am 41

A: I would personally not proceed until after aspiration the cyst had resoolved .

2. So on the same day 21 when I saw the corpus luteum cyst I run a progesterone tests. This came back low at 1.5 . My doctor seems to think I am not ovulating or having annuvulatory cycle or cycles with low progesterone observed in another cycle. Would this be a sound assertion . I had a corpus luteum measuring 5cm when a progesterone of 1.5cm was observed

A: This does not sound like a corpus luteum cyst to me….Either way it should be aspirated in advance of doing IVF.

Geoff Sher

reply
Nana Arhin

You note that you did not think it was a corpus lutium cyst. Is this because of the size . Can you Elaborate. Many thanks.

reply
Louise O'Brien

Greetings from Ireland,
I am just looking for your opinion on our case, I just literally found your very up to date forum, which is great. My husband, Gary (36yrs old) and I (35 , turning 36 in a few nonths, we have just undergone our second failed IVF. We are both carriers of the CF mutation, Gary has been found to be a carrier of 2 different mutations. He has CBAVD and had a TESE and successful removal of Sperm (10 vials). I had my first egg collection which resulted in 18 eggs, 11 fertilised and by day 5 this we had only 2 viable embryos, so along with our Fertility clinic we decided to do another egg collection to ”pool” our embryos in order to reduce cost and do 1 PGD rest on our samples. Second egg collection we retrieved 15 eggs, 10 fertilised and by Day 5 we had only 1 more embryo… All my work up bloods were completely normal,only issue being a carrier of the CF gene. Samples taken from our 3, 1 came back as a carrier but it came from Gary’s side, so if we were successful ad it was a male it could be affected in the same way as Gary. Our other 2 came back as ”no signal” so they could not tell if they were or were not affected. So, out only option was to re-biopsy these embryos again.. Which at a cost and high risk, we did, and they came back entirely normal. While these were being re-biopsied we proceeded with FET of out first embryo..My meds were Femotab 3mg BD and Gestone 50mg/ml, along Medrone OD for 4 days and antibiotics before the transfer. Unfortunately this did not work… Did not have bleeding or any unusual symptoms before the test date. Very disappointing, but at least we then had 2 more embryos to work with. We just did another transfer, same meds. I had a slight bleed on day 11 but it was only in the morning and nothing after that. I tested yesterday day 13 and it was negative.. I had my transfer on the 27th of July. I suppose I am wondering what would your next step be, is it worth investigating implantation dysfunction? The last embryo survived a thaw, re-biopsy, re freeze and another thaw and transfer..So I was hopeful as it was a good quality embryo that it would stick!. First embryo was a slight lower grade but had not been through as much. Would it be worth looking at changing my stimulation meds. They were happy with my uterine lining and both transfers went very well.

Thank you for taking the time to read this and I look forward to your opinion.

Regards

Louise

reply
Dr. Geoffrey Sher

The CF mutations and your failure to implant are separate issues. You have been dealing with the first issue and need to deal with the second, independently.

Whenever a patient fails to achieve a viable pregnancy following embryo transfer (ET), the first question asked is why! Was it simply due to, bad luck?, How likely is the failure to recur in future attempts and what can be done differently, to avoid it happening next time?.
It is an indisputable fact that any IVF procedure is at least as likely to fail as it is to succeed. Thus when it comes to outcome, luck is an undeniable factor. Notwithstanding, it is incumbent upon the treating physician to carefully consider and address the causes of IVF failure before proceeding to another attempt:
1. Age: The chance of a woman under 35Y of age having a baby per embryo transfer is about 35-40%. From there it declines progressively to under 5% by the time she reaches her mid-forties. This is largely due to declining chromosomal integrity of the eggs with advancing age…”a wear and tear effect” on eggs that are in the ovaries from birth.
2. Embryo Quality/”competency (capable of propagating a viable pregnancy)”. As stated, the woman’s age plays a big role in determining egg/embryo quality/”competency”. This having been said, aside from age the protocol used for controlled ovarian stimulation (COS) is the next most important factor. It is especially important when it comes to older women, and women with diminished ovarian reserve (DOR) where it becomes essential to be aggressive, and to customize and individualize the ovarian stimulation protocol.
We used to believe that the uterine environment is more beneficial to embryo development than is the incubator/petri dish and that accordingly, the earlier on in development that embryos are transferred to the uterus, the better. To achieve this goal, we used to select embryos for transfer based upon their day two or microscopic appearance (“grade”). But we have since learned that the further an embryo has advanced in its development, the more likely it is to be “competent” and that embryos failing to reach the expanded blastocyst stage within 5-6 days of being fertilized are almost invariably “incompetent” and are unworthy of being transferred. Moreover, the introduction into clinical practice about a decade ago, (by Levent Keskintepe PhD and myself) of Preimplantation Genetic Sampling (PGS), which assesses for the presence of all the embryos chromosomes (complete chromosomal karyotyping), provides another tool by which to select the most “competent” embryos for transfer. This methodology has selective benefit when it comes to older women, women with DOR, cases of unexplained repeated IVF failure and women who experience recurrent pregnancy loss (RPL).
3. The number of the embryos transferred: Most patients believe that the more embryos transferred the greater the chance of success. To some extent this might be true, but if the problem lies with the use of a suboptimal COS protocol, transferring more embryos at a time won’t improve the chance of success. Nor will the transfer of a greater number of embryos solve an underlying embryo implantation dysfunction (anatomical molecular or immunologic).Moreover, the transfer of multiple embryos, should they implant, can and all too often does result in triplets or greater (high order multiples) which increases the incidence of maternal pregnancy-induced complications and of premature delivery with its serious risks to the newborn. It is for this reason that I rarely recommend the transfer of more than 2 embryos at a time and am moving in the direction of advising single embryo transfers …especially when it comes to transferring embryos derived through the fertilization of eggs from young women.
4. Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:
a. A“ thin uterine lining”
b. A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
c. Immunologic implantation dysfunction (IID)
d. Endocrine/molecular endometrial receptivity issues
Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).

I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
• Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• IVF Failure and Implantation Dysfunction:
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Endometrial Thickness, Uterine Pathology and Immunologic Factors
• Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
• Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• The Role of Nutritional Supplements in Preparing for IVF

Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691
 800-780-7437

Geoff Sher

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
Upneet kaur

I had a Et on 28th July ( 5 Day Embryo) and on 8th August by Beta HCG was counting 110 but today (10 Aug) by beta HCG count dropped to 106?? What is happeneing and what i shall do??

reply
Dr. Geoffrey Sher

This could be reduction from a twin pregnancy down to one or it could be a failing implantation.

Repeat beta hCG in 2 days (from the last one) will tell. It shoulkd double.

Good luck!

Geoff Sher

reply
T Ghoshal

My wife went through 1 st round ivf today and egg pickup. Same happened to me 5 follicles and no eggs at all came out. She is 29 years old. Kindly help in knowing the reason and please let us know if we have any chances for future.

reply
Dr. Geoffrey Sher

This is what is often erroneously referred to as “Empty Follicle syndrome”.

I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
• Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
• A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
• Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
• Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
• Optimizing Response to Ovarian Stimulation in Women who Have Compromised Ovarian Response to Ovarian Stimulation in Women who Have Compromised Ovarian Reserve: A Personal Approach.
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF

Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691
 800-780-7437

Geoff Sher

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
Lily

Dear Dr. Sher

I am now 40 years old. Have a 6 and half year old kid. I had 3 miscarriages in 2014 and 2015. Tested FSH was 8.5 a year ago. this July I went back and it was 10, this month 11.5. My doctor asked me to take DHEA 50mg a day hoping to help with FSH number. but I was reading about DHEA and learned that it could increase estrogen and testosterone at the same time. As you commented, high level of testosterone is bad for the maturation of the egg. so in your opinion, should I take DHEA or not? also is fsh reflecting my egg quality(i know you said mainly is associated with age) or is more reflecting the ovarian reserve?

Thank you so much in advance.
Lily

reply
Dr. Geoffrey Sher

Hi Lily,

Dehydroepiandrosterone (DHEA), is steroid hormone produced by the adrenal glands and ovary. It is involved in producing the male hormones, androstenedione testosterone and also estrogen. DHEA blood levels tend to decline naturally with age.
Under the effect if luteinizing hormone (LH), DHEA is metabolized to testosterone in ovarian connective tissue (theca/stroma). Thereupon the testosterone is transported to the granulosa cells that form the innermost layer of the ovarian follicles where, under the influence of follicle stimulating hormone (FSH)-induced desmolase and aromatase enzymatic activity the testosterone is converted to estradiol. As this happens, granulosa cells multiply, follicle fluid volume increases along with estrogen output and egg development is promoted.
It is recognition of the essential/indispensable role that male hormones (mainly testosterone) play in follicle and egg development that prompted the belief that by giving DHEA and boosting ovarian testosterone production might benefit follicle/egg development. This belief was given some credence by an Israeli study that in 2010 reported on improved fertility when a group of infertile women were given the administration of 75mg of oral DHEA for 5 months. However, this study was seriously flawed by the fact that it did not separate out women who had diminished ovarian reserve, older women and those with PCOS, all of whom have increased LH-induced production of testosterone. In fact, we recently completed a study (currently being processed for publication) where we conclusively showed that when follicular fluid testosterone levels exceeded a certain threshold, egg quality was seriously prejudiced as evidenced by a marked increase in the incidence of egg chromosomal defects (aneuploidy).
Consider the following: Ovarian testosterone is needed for follicular development. However, the amount required is small. Too much ovarian testosterone spills over into the follicular fluid and has a deleterious effect on egg/follicle development. Some women (women with diminished ovarian reserve –DOR, older women and those with polycystic ovarian syndrome-PCOS) who tend to have increased LH biological activity, already over-produce testosterone. To such women, the administration of DHEA to such women, by “adding fuel to the fire” can be decidedly prejudicial, in my opinion. Young women with normal ovarian reserve do not over produce LH-induced ovarian testosterone, and are thus probably not at significant risk from DHEA supplementation. It is noteworthy that to date, none of the studies that suggest a benefit from DHEA therapy have differentiated between young healthy normal women with normal ovarian reserve on the one hand and older women, those with DOR and women with PCOS on the other hand.

In Some countries DHEA treatment requires a medical prescription and medical supervision. Not so in the U.S.A where it can be bought over the counter. Since DHEA is involved in sex hormone production, including testosterone and estrogen, individuals with malignant conditions that may be hormone dependent (certain types of breast cancer or testicular cancer) should not receive DHEA supplementation. Also, if overdosed with DHEA some “sensitive women” might so increase their blood concentrations of testosterone that they develop increased aggressive tendencies or male characteristics such as hirsuites (increased hair growth) and a deepening voice. DHEA can also interact other medications, such as barbiturates, corticosteroids, insulin and with other oral diabetic medications.
BUT the strongest argument against the use of routine DHEA supplementation is the potential risk of compromising egg quality in certain categories of women and since there is presently no convincing evidence of any benefit, why take the risk in using it on anyone.
Finally, for those who in spite of the above, still feel compelled to take DHEA, the best advice I can give is to consult their health care providers before starting the process.

Addendum: One potential advantage of DHEA therapy if used appropriately came from a study conducted by Washington University School of Medicine in St. Louis, MI and reported in the November 2004 issue of the “Journal of the American Medical Association” which showed that judicious (selective) administration of 50mg DHEA daily for 6 months resulted in a significant reduction of abdominal fat and blood insulin in elderly women.

Geoff Sher

reply
Danielle Mills

Hi Dr. Sher, My mom and dad (Melinda and Greg Mills) came to you years ago when you were at your clinic in San Francisco. I was conceived on October 3rd, 1991 and born on June 5th, 1992. I was wondering if you had any information on my egg donor that you could give me. I’m not interested in contacting her by any means, just wondering what her heritage was etc — if there is any information you can give me that would be great! Thanks so much! -Danielle Mills

reply
Dr. Geoffrey Sher

Hi Danielle

I am so glad that things worked out for your mom and dad and thus for you too.

Unfortunately, I have no access to records in SFO and thus sadly cannot be of help here.

G-d bless and please come and visit me if you come to LV.

Geoff Sher

reply
Amy

Hi Dr. Sher, I am 29 and started treatment a year and a half ago with 2 failed IUIs. After that failed we decided to do Ivf. We were able to get 30 eggs, and by day 5 we had 11 healthy great quality blastocyst. We went through 1 miscarriage with round 1 and a d&c; a very low beta and miscarriage/chemical pregnancy with round 2, and no luck at all round 3. We then sent the 8 blastocyst we had left to get genetically tested (my husband and I were both tested before we started and had nothing that we or the dr thought would be an issue). We had 5 come back perfect. 2 had abnormalities and 1 something went wrong on the reading or test so they had to disguard it. After that, we did a transfer with what was a perfectly healthy and graded embryo and had another chemical pregnancy. Beta was only 22. After that I had my third HSG with normal results like the previous ones. have never had any test or ultrasound they ran come back with bad results. I am told I am perfectly healthy with a think uterus lining and fantastic blood results. At this point I went for a second opinion and even that dr went through all of my charts and couldn’t seem to make sense of why I wasn’t pregnant at this point. He suggested going a endometrial function test. Since he was out of town, I went back to my dr for a follow up after the last cycle and asked him what he thought we should do at this point and I also mentioned I went to seek out a second opinion. At that meeting he suggested doing an endometrium receptive array test and a uterus biopsy with a scratch. Since it was more convenient to do that since it is in the same city I live in I decided to go his rout and try 1 more time with him. After being on a FET drug protocol but doing the ERA instead of a transfer my results showed that I am on the edge of maybe being a little late to implant. The test showed to wait 12 hours later than what we have done in the past and the biopsy and scratch results came back normal. Really? 12 hours makes that big of a difference? And my embryos have implanted, they just haven’t grown so I am not convinced that is the issue. I have always been told after my second blood (12 days post transfer day)draw my beta hasn’t doubled so stop my meds and let it pass. And they have, except for the first round. I am now on day 16 of lupron 10 units and I decrease it to 5 tomorrow (August 10th) and start estrace 2mg and 1 .1mg patch of minivelle. I will continue estrace daily and have a scedule for patch changes up until 8/23 at what point I start adding crinone am and pm and prog.in oil 1ml every other day to the estrace daily and minivelle patch schedule. I am to the point I don’t know what to do and a friend told me about your site and said I should run things by you to maybe ease my mind. It’s very frustrating to be told you are perfectly healthy to carry a baby but still after 2 IUIs, a fresh transfer, 3 frozen, and no luck it’s very discouraging. I don’t know what I am really asking, but after reading my book (sorry) do you have any suggestions on what I should be doing different or trying? Thank you for your time. I look forward to hearing from you.

Amy

reply
Dr. Geoffrey Sher

Respectfully, I have no confidence in the efficacy of ERA.

Whenever a patient fails to achieve a viable pregnancy following embryo transfer (ET), the first question asked is why! Was it simply due to, bad luck?, How likely is the failure to recur in future attempts and what can be done differently, to avoid it happening next time?.
It is an indisputable fact that any IVF procedure is at least as likely to fail as it is to succeed. Thus when it comes to outcome, luck is an undeniable factor. Notwithstanding, it is incumbent upon the treating physician to carefully consider and address the causes of IVF failure before proceeding to another attempt:
1. Age: The chance of a woman under 35Y of age having a baby per embryo transfer is about 35-40%. From there it declines progressively to under 5% by the time she reaches her mid-forties. This is largely due to declining chromosomal integrity of the eggs with advancing age…”a wear and tear effect” on eggs that are in the ovaries from birth.
2. Embryo Quality/”competency (capable of propagating a viable pregnancy)”. As stated, the woman’s age plays a big role in determining egg/embryo quality/”competency”. This having been said, aside from age the protocol used for controlled ovarian stimulation (COS) is the next most important factor. It is especially important when it comes to older women, and women with diminished ovarian reserve (DOR) where it becomes essential to be aggressive, and to customize and individualize the ovarian stimulation protocol.
We used to believe that the uterine environment is more beneficial to embryo development than is the incubator/petri dish and that accordingly, the earlier on in development that embryos are transferred to the uterus, the better. To achieve this goal, we used to select embryos for transfer based upon their day two or microscopic appearance (“grade”). But we have since learned that the further an embryo has advanced in its development, the more likely it is to be “competent” and that embryos failing to reach the expanded blastocyst stage within 5-6 days of being fertilized are almost invariably “incompetent” and are unworthy of being transferred. Moreover, the introduction into clinical practice about a decade ago, (by Levent Keskintepe PhD and myself) of Preimplantation Genetic Sampling (PGS), which assesses for the presence of all the embryos chromosomes (complete chromosomal karyotyping), provides another tool by which to select the most “competent” embryos for transfer. This methodology has selective benefit when it comes to older women, women with DOR, cases of unexplained repeated IVF failure and women who experience recurrent pregnancy loss (RPL).
3. The number of the embryos transferred: Most patients believe that the more embryos transferred the greater the chance of success. To some extent this might be true, but if the problem lies with the use of a suboptimal COS protocol, transferring more embryos at a time won’t improve the chance of success. Nor will the transfer of a greater number of embryos solve an underlying embryo implantation dysfunction (anatomical molecular or immunologic).Moreover, the transfer of multiple embryos, should they implant, can and all too often does result in triplets or greater (high order multiples) which increases the incidence of maternal pregnancy-induced complications and of premature delivery with its serious risks to the newborn. It is for this reason that I rarely recommend the transfer of more than 2 embryos at a time and am moving in the direction of advising single embryo transfers …especially when it comes to transferring embryos derived through the fertilization of eggs from young women.
4. Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:
a. A“ thin uterine lining”
b. A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
c. Immunologic implantation dysfunction (IID)
d. Endocrine/molecular endometrial receptivity issues
Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).

I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers Should be the Standard of Care in IVF
• Recurrent Pregnancy Loss (RPL): Why do I keep losing my Pregnancies
• Blastocyst Embryo Transfers Done 5-6 Days Following Fertilization are Fast Replacing Earlier day 2-3 Transfers of Cleaved Embryos.
• Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
• Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
• IVF Failure and Implantation Dysfunction:
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Endometrial Thickness, Uterine Pathology and Immunologic Factors
• Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• The Role of Nutritional Supplements in Preparing for IVF

Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691
 800-780-7437

Geoff Sher

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
Amy

Thank you for your response. I am curious about the DQ alpha and HLA matching embryos Is that something that would have been tested for in the Natual Killer blood test or autoimmune implantation dysfunction test is it a whole test on its own. I have had both of those done. Being 29, eggs retrieved at 28, I do not feel like I should have any issues with egg quality. Our embryos were/are great grades and they have had PGD/PGS. I. Wondering if I should look into the testing for DQ alpha or maybe it has already been done and I just don’t know. I have had so many test ran I can’t keep track. Thank you again, this message board is fantastic!

reply
Dr. Geoffrey Sher

It would not have been done without having been formerly requested separately.

Geoff Sher

reply
Amy

Hi, me again!

I am reading on your site about DQa I am somewhat confused. I have had the natural killer test ran and it came back negative. Am I understanding this correctly’ if the mother and father have matching DQa cells, it activates the NK cells? If after my 4 ET there was an issue with DQa, would my NK test have shown positive since it would have been activated? I am trying to find an office to do a DQa test because my fertility center does not offer it. I am wondering if it’s worth it though. I am scheduled for a FET September 29th. I was on birth control for 3 weeks, over lapped with lupron 10 units for 3 days. i continued lupron 10 units 16 days total before reducing it to 5 units and adding minivelle and estrace. I am on those 3 meds for 14 days then on my last day of lupron 5 units I start crinone morning and night. On day 15 I start prog in oil 1ml every other day then have my transfer on day 20. Does this protocol sound normal? I will be on progesterone for 6 full days before transfer. Thank you for your time and I hope this message isn’t too confusing.

Dr. Geoffrey Sher

I personally prefer not to use oral estrogen . IM or skin patches are preferable . If thta is what you are on then yes…this is OK. I also prefer to prescribe intramuscular progesterone rather than Crinone %, however twice daily Crinone is acceptable too.

I would urge that you and your husband have yourselves tested for DQ alpha genetic similarities. I use Reproductive Immunology Associated (RIA) in van Nuys for these tests. Look them up on Google.

Geoff Sher

Amy

Thank you for your info!

I am taking estrogen via patches and vaginally. When I start the crinone, a few days later I will start progesterone in oil intramuscular along with crinone. Hopefully that covers all the bases. I will google RIA now. I would really like to get the test done. Thanks again.

KH

Hi Dr Sher,

Can you explain why it is that a trilaminar-appearing lining is more receptive than a homogenous lining? My lining has thickened appropriately (12mm) but it is NOT trilaminar. I am concerned for my transfer, since I have read literature that suggests miscarriage rates are higher with non-trilaminar linings.

reply
Dr. Geoffrey Sher

I used to believe that it was necessary for there to be a trilaminar lining. Now we know that as long as the lining is >9mm thick it is likely to be fine. 8-9mm is a “gray zone”.

Good luck!

Geoff Sher

reply
Courtney k

Hello. I got pregnant from a fresh transfer but it ended in a blighted ovum. I had a trilaminar pattern with the fresh transfer. I tried estrogen pills and FET, my lining was thick but never trilaminar. This time we tried Gonal f so my body could produce estrogen on its own but I still don’t have the trilaminar appearance. I’ve been through so much this past year and a half and I don’t want to lose and embryo if the uterus isn’t perfect. My question, should i transfer? My lining was 9.7mm at the last scan but I have not triggered yet so it will likely be thicker. Thank you!

reply
Dr. Geoffrey Sher

Absolutely. The trilaminar pattern is not essential. It is the thickness of the estrogenizsed endometrium that counts most!

Good luck!

Geoff Sher

reply
Sheena

Hi Dr Sher, You asked me to repost my question …. what would happen if you take Suprefact nasal spray on day 21 but happened to be unknowingly pregnant. Would the medication have an impact on the health of the unborn baby?

reply
natasha

Dear Dr. Sher, First I would like to thank you for taking time to provide your insight on this matter to all of us that are seeking some advice. August of 2015 – we had spontaneous chemical pregnancy .I was 40 at that time and turned 41 nov 1 – I , will be 42 this Nov 1. my partner is 30years old. 1st Ivf jan 2016 resulted in 9 retrieved all fertilized eggs, 4 transferred( 1x 10 cell/2 x 8 cell and 1 x 7 cell) cell embryos) on day 3 resulting ultimately in D & C at 8 weeks ( no heartbeat)chromosome abnormal
the rest ( 5 from this cycle ) were frozen at day 3. The 2nd Ivf -5 follicles – by day 7 – 2and thus out of 5 we retrieved 2 mature eggs( which fertilized) , 3 were dark brown and did not fertilize. We tranfered the 2 at day 3 both 3 at 11 & 12 cells – implantation did not occur. I’ve just completed my 3rdIVF .. same protocol as other – Gona;F/menopur/ganarelix/ trigger shot 10,000 units HCG. I initially went for an IUI cycle but found 6 follicles so we decided that IVF maybe the best option. on the trigger day all 8 follicles were all at approx. the same size. Dr said even the smaller ones were still at a size that it could mature and be retrieved and the dr’s expected all eggs to be retrieved. It seemed like a very good cycle. last sonogram fr measurements were on sat- I was given last ganarelix and gona F that morning , 10,000 units of HCG at 10 pm sat night – retrieval scheduled for Monday morning t 10 am
..however -I was devastated to hear only 2 eggs were retrieved , I was told that the other follicles were empty but as you said all follicles contain an egg. I questioned what went wrong. Could it be that the retrieval was scehuled at the wrong time ? Perhaps too late ? is there anything you can identify in this protocal that could have affected the retrieval outcome ? I’m completely lost on what happened here- I’m so frustrated and ate endof my rope with tis .. I’m thinking its time to give up

reply
Dr. Geoffrey Sher

The older a woman becomes, the more likely it is that her eggs will be chromosomally/genetically “incompetent” (not have the potential upon being fertilized and transferred, to result in a viable pregnancy). That is why, the likelihood of failure to conceive, miscarrying and of giving birth to a chromosomally defective child (e.g. with Down Syndrome) increases with the woman’s advancing age. In addition, as women age beyond 35Y there is commonly a progressive diminution in the number of eggs left in the ovaries, i.e. diminished ovarian reserve (DOR). So it is that older women as well as those who (regardless of age) have DOR have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production of LH biological activity which can result in excessive LH-induced ovarian male hormone (predominantly testosterone) production which in turn can have a deleterious effect on egg/embryo “competency”.
While it is presently not possible by any means, to reverse the age-related effect on the woman’s “biological clock, certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can make matters worse. Similarly, the amount/dosage of certain fertility drugs that contain LH/hCG (e.g. Menopur) can have a negative effect on the development of the eggs of older women and those who have DOR and should be limited.
I try to avoid using such protocols/regimes (especially) in older women and those with DOR, favoring instead the use of the agonist/antagonist conversion protocol (A/ACP), a modified, long pituitary down-regulation regime, augmented by adding supplementary human growth hormone (HGH). I further recommend that such women be offered access to embryo banking of PGS (next generation gene sequencing/NGS)-selected normal blastocysts, the subsequent selective transfer of which by allowing them to to capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” could significantly enhance the opportunity to achieve a viable pregnancy
Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
• A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
• Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
• Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers Should be the Standard of Care in IVF
• Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
• Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
• Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
• Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
• Preimplantation Genetic Testing (PGS) in IVF: It Should be Used Selectively and NOT be Routine.
• Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
• PGS in IVF: Are Some Chromosomally Abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
• PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
• Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• The Role of Nutritional Supplements in Preparing for IVF
• Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
• IVF Egg Donation: A Comprehensive Overview
I invite you to arrange to have a Skype or an in-person consultation with me to discuss your case in detail. If you are interested, please contact Julie Dahan, at:

Email: Julied@sherivf.com

OR

Phone: 702-533-2691
800-780-7437

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
natasha

Dear Dr,
just to clarify , so you are saying that this is all probably because of my age that the follicles were ’empty” at the time of retrieval? I have contacted Julie for consultation

reply
Dr. Geoffrey Sher

No! It could be the protocol used for stimulation in an older person …especially if there is associated diminished ovarian reserve.

Geoff sher

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Biola

Dear Dr. Sher,

Thank you for providing this platform.

I am 32 years old and based in Nigeria. I have been trying to conceive since January 2014; past 32 months. I had a laparoscopic myomectomy done in December 2014 which revealed sub-serosal fibroids and moderate to severe endometriosis. The fibroids were removed and endometriosis was partly removed. Also dye test performed showed my tubes were open.

Attempted unsuccessfully to conceive naturally over the next 13 months and this led me to my first ever IVF in March 2016. Two Grade A embryos transferred led to my first ever pregnancy with twin heart beat at 6+ weeks. However, no heart beats detected at 7 weeks. A medical evacuation was done subsequently, however no testing was done on the products of conception as this isn’t available in Nigeria.

The IVF doctor in Nigeria suspects the cause of miscarriage as the presence of raised NK Cells, however testing is not available in Nigeria and advised that i travel abroad for testing. I came to America two weeks ago after speaking with a few doctors, they all told me the same thing – “they do not believe that Raised NK Cells theory as a cause of miscarriage” and refused to test me for this.

During the IVF procedure, my doctor in Nigeria treated me with IVIG and Intralipids pre-implantation and post pregnancy to maximise my chances “just in case in had elevated NK Cells”. However, this treatment is quite expensive in Nigeria and i also fear it may be unsafe. Thus, I would really love to test for the Raised NK so as to know if this treatment is required for my subsequent cycles.

I am currently in the Washington DC area till Friday 12 August, when i will be returning to Nigeria, Can you please let me how and where i can get tested for the Elevated NK Cells.

Thank you so much.

Bidemi

reply
Dr. Geoffrey Sher

Very respectfully, for you to be told that ther e is no basis for a relationship between NK cell activation and failed implantation is in my opinion wrong . I can understand someone telling you that they do not believe in this but to outright refuse to test you is arrogant. However, the tests you need are >than simply an NK activity test. You need to be tested for both autoimmune and alloimmune implantation dysfunction and this will require your blood being tested for the NK cell activation test (using the K-562 target cell assay), antiphospholipid antibodies and an immunophenotype and antithyroid antibodies and both your and your husband’s blood being assessed for DQ alpha/HLA genetic matching…see below. You need to contact Reproductive Immunology Associates (RIA) in Van Nuys, CA and have your blood sent there. Go to google and find their contact information. Call them , mention my name and have your blood drawn anywhere and then transported to them , following their directives to do so.

I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers Should be the Standard of Care in IVF
• Why did my IVF Fail
• IVF Failure and Implantation Dysfunction:
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Endometrial Thickness, Uterine Pathology and Immunologic Factors
• Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
• Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• The Role of Nutritional Supplements in Preparing for IVF
• Endometriosis and Infertily
• Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.

Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691
 800-780-7437

Geoff Sher

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
Mokanreoluwa

I am 6wks 4days and am still spotting is this normal having spotting for 2weeks now have stopped aspirin

reply
Dr. Geoffrey Sher

Vaginal bleeding occurs in about 25% of all pregnancies. When it happens, it almost invariably raises the concern of pregnancy loss (miscarriage). Bleeding can also be a sign of a tubal (ectopic) pregnancy, and in cases where the distended Fallopian tube ruptures it can precipitate a life-threatening crises. However, a small amount of painless vaginal bleeding can also be the result of normal embryo implantation (i.e. implantation bleeding) or it can result a local erosion of the vagina or cervix and/or trauma during intercourse.
Notwithstanding, in virtually all cases the occurrence of early pregnancy vaginal bleeding congers concerns or even alarm regarding the possibility of miscarriage. And when this happens to women who conceived following infertility treatment, the alarm often turns into panic. However, the truth is that in most such cases the bleeding soon stops and the pregnancy proceeds unabated to the birth of a healthy baby. However, because some do progress and end in miscarriage, and in most cases, only time will tell how things will ultimately turn out, we use the term “threatened miscarriage” to describe such early bleeding. The term “inevitable miscarriage” is used once symptoms and signs confirm a miscarriage is in progress. The term “complete miscarriage” is used if all products of conception are passed, leaving the uterus “empty”. An “incomplete miscarriage” refers to cases where some products remain retained in the uterus.
Miscarriage: Mild painless vaginal bleeding (often referred to as “spotting”) is usually due to hormonally induced eversion of the glandular cells that line the inner cervical canal, such that erosion develops on the outer part of the cervix that protrudes onto the vagina. The everted glandular tissue is fragile and susceptible to contact trauma, brought about sexual penetration or the insertion of vaginal suppositories. Since such local bleeding does not involve the developing conceptus located inside the uterus it is almost always innocuous. The diagnosis of a local cause of bleeding requires visual inspection of the vagina and cervical inlet a speculum examination. Thereupon, provided that the pregnancy has advanced beyond 5-6 weeks, a concomitant sonogram could confirm the presence of an unaffected pregnancy. Patients are advised to be more careful in inserting vaginal suppositories and to avoid sexual penetration until the bleeding has stopped for at least 1 week.
Sometimes bleeding occurs behind the conceptus inside the uterus (retrochorionic bleeding). Some blood will usually track down through the cervix and into the vagina. A speculum examination will often reveal blood tracking into the vagina through the cervical canal and a sonogram will reveal the presence of a retrochorionic blood clot. Although such retrochorionic bleeding can become an inevitable miscarriage, it often abates and over time the blood clot in the uterus absorbs, and the pregnancy continues normally. Treatment involves careful observation, avoidance of aspirin and other non-steroidal anti-inflammatory medications, bed rest and avoidance of vaginal penetration until the condition stabilizes, is essential.
While mild painless vaginal bleeding is usually innocuous, bright red bleeding that increases in amount and is accompanied by escalating pain is another matter altogether. It often suggests an impending inevitable miscarriage.
Before the 7th week of pregnancy a normally rising blood hCG (pregnancy hormone) titers is a comforting indicator that the pregnancy is more than likely progressing normally. Likewise, the detection of a normal heartbeat detected by ultrasound examination done after the 7th week of pregnancy is a very reassuring finding. However, even such findings by no means exclude the possibility of an inevitable miscarriage.
The causes of a miscarriage are multiple and diverse. However in most cases it is due to the developing conceptus being chromosomally/genetically abnormal. However, early miscarriages that reoccur more than twice in a row (Recurrent Pregnancy Loss-RPL) often suggest of an underlying implantation problem that could be due to a poorly developed uterine lining (endometrium) or immunologic dysfunction involving activated immune cells known as uterine natural killer (NK) and/or T-cells. Treatment requires an accurate diagnosis of the cause and selective therapy.
An ectopic pregnancy must be excluded: .Bleeding in the first 2-3 months of pregnancy especially if associated with the sudden onset of acute abdominal pain that is aggravated by movement and is accompanied by right shoulder tip pain, and light headedness or fainting could point to a bleeding ectopic pregnancy (one that is located in a Fallopian tube, outside the uterus) . The condition can be life endangering and warrants an immediate trip to the hospital as it often requires emergency surgery.
Molar pregnancy: Molar pregnancies are due to rapid overgrowth of the trophoblastic tissue that forms the placenta. Although infrequent they can cause early vaginal bleeding in pregnancy. Bleeding from molar pregnancies is often present with typical bleeding which resembles “red currents floating in a red jelly”. Bleeding from a molar pregnancy can either painful or painless. The condition is often associated with severe vomiting in early pregnancy, disproportionate enlargement of the uterus, and very elevated blood levels of hCG. Ultrasound evaluation, often reveals a rather characteristic snow-storm like image.
Patients with vaginal bleeding are often told to stay in bed. While this might reduce visible blood loss, there is no tangible evidence that it will prevent a miscarriage. Unfortunately, there is no definite treatment for this kind of bleeding in the early stages of pregnancy. Alas, in most cases only time will provide the answer.

Good luck!

Geoff Sher

reply
Lisa

Hi there,

I am a 32 year old woman located in Auckland New Zealand and hoping you can help me.
It should be noted that my husband has no fertility issues with great sperm count and mobility.

A few years back I decided to see a fertility doctor as I didn’t get my period after coming off the pill.
I am 163cms and weigh 132 pounds so my BMI is normal. I had recently come off the pill but had been amennorrheac for 4 months prior to seeing a fertility doctor. I had previously been given a diagnosis of Polycystic Ovarian Syndrome (when I was 18) however had been on the pill for about 10 years as that was the recommendation from my doctor. Relevant investigations with the fertility doctor early on were essentially normal apart from confirmation of underlying Polycystic Ovarian Syndrome . I then embarked on a Letrozole ovarian induction and subsequently Clomiphene ovulation induction but unfortunately did not respond to these medications, my doctor told me that some people were resistant, one of them being me. I then undertook a cycle of ovulation induction with gonadotrophins and produced one follicle but did not successfully conceive.

We then elected to move to IVF treatment and the first cycle of IVF treatment commenced in September 2015. This was an antagonist protocol with 150 units of FSH stimulation. My ovarian response was above average however at egg collection despite the presence of multiple follicles only 1 oocyte was obtained. This oocyte was shown to be immature and therefore did not fertilise. The other follicles appeared to be empty.
After reviewing my cycle it was mentioned that I previously had a normal LH and was given an antagonist protocol and appeard to respond exuberantly. It should also be noted that I was given a GnRD trigger injection but had no response to this so they then provided me with an Ovidrel trigger the next day- resulting in one egg as mentioned above, The other follicles appeard to be empty.

A second cycle of IVF treatment was undertaken in October 2015 again using antagonist with 150 units of Menopur as stimulation. Again a good follicular response was seen, however at egg collection despite the presence of multiple follicles only 2 eggs were obtained and again both these eggs were immature – a similar resonse to the previous round.

They then mentioned that my endocrinology appeared to possibly be a mixed picture both with PCOS and a degree of pituitary dysfunction and that I need to have some supplemental LH during my next cycle.

After discussion with the clinical team it was recommended that we try In Vitro Maturation treatment. The first cycle of IVM was undertaken in 2016 and 16 oocytes were obtained. Only 4 of these oocytes reached maturity and although all 4 fertilised only 1 4AB blastocyst was obtained and this was subsequently cryopreserved. The second IVM cycle was undertaken in March 2016 and 10 oocytes were obtained of which 5 fertilised and again 1 day 6 blastocyst was obtained and cryopreserved. Both of these blastocysts were subsequently replaced on manufactured embryo replacement cycles but neither led to successful pregnancies.

I have received some goverment funding for IVF again which comes up in September and hoped that you might be able to shed some light on my situation as it just doesnt feel right and I wonder if something could be changed for my next round which could produce more success.

I really appreciate your response and taking the time to review my post.

Thanks
Lisa

reply
Dr. Geoffrey Sher

Women with prolonged amenorrhea (>45 days) often do not respond to clomiphene or Letrozole.

I do not believe in IVM. Results are not good. In my opinion you need to do regular IVF. Since there is no such thing as a follicle that does not contain an egg, this happening is due to the eggs not being released at the time of ER. The reason for this is almost always that the eggs are so chromosomqlly abnormal that they cannot beak free from the cumulius cells that bind them to the inner wall of the follicles trhat house them. This in turn, is often the result of the protocol used for ovarian stimulation and the type of hCG trigger. Using an “agonist” to trigger (as you did could at least in part explain this…see below). The reason you were given an agonist to trigger egg maturation was in an attempt to avert severe ovarian hyperstimulation syndrome from occurring. While the use of this type of trigger does reduce this risk in women who over-respond to ovarian stimulation, the price you pay is that egg maturation is compromised, leading to an increased percentage being chromosomally incompetent.

In my opinion, you would be better served, using a modest long pituitary down-regulation protocol coming off a BCP, done in preparation for “prolonged coasting” and then triggered using 10,000U hCG (see below).

I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers Should be the Standard of Care in IVF
• Why did my IVF Fail
• Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• The Role of Nutritional Supplements in Preparing for IVF
• Implications of “Empty Follicle Syndrome and “Premature Luteinization”
• Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
• Preventing Severe Ovarian Hyperstimulation Syndrome (OHSS) with “Prolonged Coasting”
• Understanding Polycystic Ovarian Syndrome (PCOS) and the Need to Customize Ovarian Stimulation Protocols.
• “Triggering” Egg Maturation in IVF: Comparing urine-derived hCG, Recombinant DNA-hCG and GnRH-agonist:
• The “Lupron Trigger” to Prevent Severe OHSS: What are the Pro’s and Con’s?

Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691
 800-780-7437

Geoff Sher

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
Seek helper

Hi Doctor,

I am 32 years old, turning 33 in one months time. I have a live birth before and my son is six now. I have done a 5 day blastocyst transfer and the grade of my blastocyst is 4AB. During ER I had 12 matured egg out of which 10 fertilised and produce 7 good quality embryo on day 3. On day 5, I had 8 blastocyst, out of which only 2 were 4 AB and the rest 3 were 4BB. 3 other were low grade. I was on the long protocol and I am now on the cycologest 400 and another medication which is blue small tablet. What are my chances of pregancies given of my above situation.

reply
Dr. Geoffrey Sher

I cannot quantify your chances, since I do not know the details of your history or the quality of the IVF program you attend. However, your chances should be quite good, given your history of having had a baby on your own before.

Good luck!

Geoff Sher

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Seek Helper

Thanks Dr Geoffrey for the quick response. I had a follow up question, what are the chances that my 5 blastocyst that I have would be chromosomally normal. I had my right tube blocked due to which I am told to do an IVF. Additionally which blastocyst are considered good quality, like is mine 4BB considered good quality.

reply
Dr. Geoffrey Sher

On average for women under 35Y there should be about a 40% chance of an expanded blastocyst being chromosomally normal.

Geoff Sher

reply
Seek Helper

Based on your experience, which blastocyst is considered good quality and has high chances of implantation. Are 4 BB or 4 BA also considered good like 4 AA.

Seek Helper

Thanks Doctor for the swift response. My pregancy test is due tomorrow but I had spotting which is pinkish yesterday. Is this something a concern or this is a normal.

Dr. Geoffrey Sher

Usually not but alas, only time will tell!

Good luck!

Geoff Sher

Seek Helper

Thanks Doctor and yes you were right that this was an abnormal case. I am now told to do a FBT using my next 4BB blastocyst. I am a little skeptical on this as even the 4AB did not work well, would a 4BB work for me. According to the Doctor that the 4AB might not be chromosomally normal and this is the reason it did not implant. Given that the frozen one has a lower rating than the best one, would I still hope of implanation. Or it is only related to the chromosomal and not the rating of the blastocyst for the rating.

Dr. Geoffrey Sher

The chromosomal integrity trumps the s the microscopic appearance.

Good luck!

Geoff Sher

Nicole

I just finished with IVF#2. I 38 years old with PCOS and a unicornuate uterus. This round 43 eggs were retrieved, 39 mature eggs, 35 eggs fertilized with ICSI. 22, day 5 blasts. How many of these embryos do you think will be normal? We are doing PGS testing.
Also, I did the same medication protocal as ivf# 1, but only 20 eggs were retrieved the first time. I did lose about 12 pounds could this be the reason for the increase in egg production. I also did not get OHSS either.

reply
Dr. Geoffrey Sher

All good. Perhaps 1:5-8 blastocysts will be chromosomally normal. Good luck!

Geoff Sher

reply
Tania

I’ve had 3 failed transfers. My embryos were blast and my hcg levels were very good. What could go wrong? I started this process at 43. Now Im 44.

reply
Dr. Geoffrey Sher

Whenever a patient fails to achieve a viable pregnancy following embryo transfer (ET), the first question asked is why! Was it simply due to, bad luck?, How likely is the failure to recur in future attempts and what can be done differently, to avoid it happening next time?.
It is an indisputable fact that any IVF procedure is at least as likely to fail as it is to succeed. Thus when it comes to outcome, luck is an undeniable factor. Notwithstanding, it is incumbent upon the treating physician to carefully consider and address the causes of IVF failure before proceeding to another attempt:
1. Age: The chance of a woman under 35Y of age having a baby per embryo transfer is about 35-40%. From there it declines progressively to under 5% by the time she reaches her mid-forties. This is largely due to declining chromosomal integrity of the eggs with advancing age…”a wear and tear effect” on eggs that are in the ovaries from birth.
2. Embryo Quality/”competency (capable of propagating a viable pregnancy)”. As stated, the woman’s age plays a big role in determining egg/embryo quality/”competency”. This having been said, aside from age the protocol used for controlled ovarian stimulation (COS) is the next most important factor. It is especially important when it comes to older women, and women with diminished ovarian reserve (DOR) where it becomes essential to be aggressive, and to customize and individualize the ovarian stimulation protocol.
We used to believe that the uterine environment is more beneficial to embryo development than is the incubator/petri dish and that accordingly, the earlier on in development that embryos are transferred to the uterus, the better. To achieve this goal, we used to select embryos for transfer based upon their day two or microscopic appearance (“grade”). But we have since learned that the further an embryo has advanced in its development, the more likely it is to be “competent” and that embryos failing to reach the expanded blastocyst stage within 5-6 days of being fertilized are almost invariably “incompetent” and are unworthy of being transferred. Moreover, the introduction into clinical practice about a decade ago, (by Levent Keskintepe PhD and myself) of Preimplantation Genetic Sampling (PGS), which assesses for the presence of all the embryos chromosomes (complete chromosomal karyotyping), provides another tool by which to select the most “competent” embryos for transfer. This methodology has selective benefit when it comes to older women, women with DOR, cases of unexplained repeated IVF failure and women who experience recurrent pregnancy loss (RPL).
3. The number of the embryos transferred: Most patients believe that the more embryos transferred the greater the chance of success. To some extent this might be true, but if the problem lies with the use of a suboptimal COS protocol, transferring more embryos at a time won’t improve the chance of success. Nor will the transfer of a greater number of embryos solve an underlying embryo implantation dysfunction (anatomical molecular or immunologic).Moreover, the transfer of multiple embryos, should they implant, can and all too often does result in triplets or greater (high order multiples) which increases the incidence of maternal pregnancy-induced complications and of premature delivery with its serious risks to the newborn. It is for this reason that I rarely recommend the transfer of more than 2 embryos at a time and am moving in the direction of advising single embryo transfers …especially when it comes to transferring embryos derived through the fertilization of eggs from young women.
4. Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:
a. A“ thin uterine lining”
b. A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
c. Immunologic implantation dysfunction (IID)
d. Endocrine/molecular endometrial receptivity issues
Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).
My answer to patients who ask me when is the time to stop undergoing IVF is ….Aside from the weight of the financial burden, the time to stop is when in spite of thorough and comprehensive evaluation, there is no remediable and treatable explanation for repeated failure.

The older a woman becomes, the more likely it is that her eggs will be chromosomally/genetically “incompetent” (not have the potential upon being fertilized and transferred, to result in a viable pregnancy). That is why, the likelihood of failure to conceive, miscarrying and of giving birth to a chromosomally defective child (e.g. with Down Syndrome) increases with the woman’s advancing age. In addition, as women age beyond 35Y there is commonly a progressive diminution in the number of eggs left in the ovaries, i.e. diminished ovarian reserve (DOR). So it is that older women as well as those who (regardless of age) have DOR have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production of LH biological activity which can result in excessive LH-induced ovarian male hormone (predominantly testosterone) production which in turn can have a deleterious effect on egg/embryo “competency”.
While it is presently not possible by any means, to reverse the age-related effect on the woman’s “biological clock, certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can make matters worse. Similarly, the amount/dosage of certain fertility drugs that contain LH/hCG (e.g. Menopur) can have a negative effect on the development of the eggs of older women and those who have DOR and should be limited.
I try to avoid using such protocols/regimes (especially) in older women and those with DOR, favoring instead the use of the agonist/antagonist conversion protocol (A/ACP), a modified, long pituitary down-regulation regime, augmented by adding supplementary human growth hormone (HGH). I further recommend that such women be offered access to embryo banking of PGS (next generation gene sequencing/NGS)-selected normal blastocysts, the subsequent selective transfer of which by allowing them to to capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” could significantly enhance the opportunity to achieve a viable pregnancy

I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
• Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
• A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
• Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
• Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
• Induction of Ovulation With Clomiphene Citrate: Mode of Action, Indications, Benefits, Limitations and Contraindications for its ue
• Clomiphene Induction of Ovulation: Its Use and Misuse!
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers Should be the Standard of Care in IVF
• Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
• Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
• Preimplantation Genetic Testing (PGS) in IVF: It Should be Used Selectively and NOT be Routine.
• Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
• PGS in IVF: Are Some Chromosomally abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
• PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
• IVF Failure and Implantation Dysfunction:
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Endometrial Thickness, Uterine Pathology and Immunologic Factors
• Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
• Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
• Traveling for IVF from Out of State/Country–
• IVF Egg Donation: A Comprehensive Overview

Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691
 800-780-7437

Geoff Sher

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
AC

Hi Dr. Sher! My husband and I will be heading into our 3rd IVF cycle in September. Background: I am 38 and husband is 43. I have PCOS and mild hypthyroidism I don’t ovulate regularly (ie only once or twice/year). Husband had low motility and low count when we did IUI’s but we took some time prior to IVF and he improved his sperm significantly. *My husband has two healthy children from previous relationship). Aside from current fertility issues both myself and husband are healthy and active.

We did two IUIs on Letrozole before moving to IVF. Both IUIs failed. Our two IVF with ICSI cycles did not result in a pregnancy. First cycle we had 3 mature eggs collected and 1 embryo was transferred on day 2. Second cycle, 7 mature eggs were collected and 3 embryos were transferred on day 3 (all graded 2). They transferred on day 2 and 3 since we had poor fertilization rates and were worried that we would not have any Day 5 blasts to transfer.

First IVF cycle I was on lupron, 75IU GonalF and 75IU Menopur. Second cycle I was on Lurpon, 75IU Gonal F and 150IU Meonpur. Second cycle produced more eggs than first. Dr. believes that poor fertilization rates are most likely due to poor egg quality. I have read your articles on not using added LH for PCOS women. I did address this with my Dr. but he feels strongly that LH has no effect on the egg quality since he is downregulating first with the Lupron. For the third cycle, he is having my husband do SCSA test to ensure that there is no DNA fragmentation. If there is no fragementation then he stated he will most likely only increase the GonalF for 3rd IVF.

Do you have any idea on what could be causing such poor fertilization rates if my husband’s sperm shows no DNA fragmentation? In your opinion do you think it is entirely related to protocol?

reply
Dr. Geoffrey Sher

Therer are 2 issues.; The first is likely associated with the protocol used for ovarian stimulation…in my opinion. And the 2nd has to do with a possible implantation dysfunction secondary to autoimmune hypothyroidism (see below).

I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
• Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
• A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
• Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
• Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
• Induction of Ovulation With Clomiphene Citrate: Mode of Action, Indications, Benefits, Limitations and Contraindications for its ue
• Clomiphene Induction of Ovulation: Its Use and Misuse!
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers Should be the Standard of Care in IVF
• Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
• Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
• Preimplantation Genetic Testing (PGS) in IVF: It Should be Used Selectively and NOT be Routine.
• Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
• PGS in IVF: Are Some Chromosomally abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
• PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
• IVF Failure and Implantation Dysfunction:
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Endometrial Thickness, Uterine Pathology and Immunologic Factors
• Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
• Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
• Traveling for IVF from Out of State/Country–
• IVF Egg Donation: A Comprehensive Overview

Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691
 800-780-7437

Geoff Sher

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
AC

Hi Dr. Sher! Thanks for responding! Quick follow up .. I have tested negative for Thyroid antibodies. Would you still assume that further testing be done for implantation dysfunction?

reply
Dr. Geoffrey Sher

Provided that you tested negative for both antithyroglobulin and antimicrosomal antibodies, it is unlikely that this would be the cause for NKa+, but given your history, I would still test…just in case they are +ve for other reasons.

Geoff sher

reply
fatima

I have been diagnosed with low ovarian reserve. I’m 43 yrs old but would like to try again. I just had a failed cycle last December where only one egg matured to a good size. They retrieved the egg, it fertilized and during 5 day embryo growth at day 4, it stopped growing.. I don’t want to give up but I want to know if it’s impossible. I have been thru chemo for a molar pregnancy which led to GTD. Had my uterus removed and a lung resection. Have been chemo free for 2 years now.

reply
Dr. Geoffrey Sher

As women age beyond 35Y there is commonly a progressive diminution in the number of eggs left in the ovaries, i.e. diminished ovarian reserve (DOR). So it is that older women as well as those who (regardless of age) have DOR have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production of LH biological activity which can result in excessive LH-induced ovarian male hormone (predominantly testosterone) production which in turn can have a deleterious effect on egg/embryo “competency”.
While it is presently not possible by any means, to reverse the age-related effect on the woman’s “biological clock, certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can make matters worse. Similarly, the amount/dosage of certain fertility drugs that contain LH/hCG (e.g. Menopur) can have a negative effect on the development of the eggs of older women and those who have DOR and should be limited.
I try to avoid using such protocols/regimes (especially) in older women and those with DOR, favoring instead the use of the agonist/antagonist conversion protocol (A/ACP), a modified, long pituitary down-regulation regime, augmented by adding supplementary human growth hormone (HGH). I further recommend that such women be offered access to embryo banking of PGS (next generation gene sequencing/NGS)-selected normal blastocysts, the subsequent selective transfer of which by allowing them to to capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” could significantly enhance the opportunity to achieve a viable pregnancy
Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
• A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
• Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
• Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers Should be the Standard of Care in IVF
• Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
• Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
• Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
• Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
• Preimplantation Genetic Testing (PGS) in IVF: It Should be Used Selectively and NOT be Routine.
• Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
• PGS in IVF: Are Some Chromosomally Abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
• PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
• Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• The Role of Nutritional Supplements in Preparing for IVF
• Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
• IVF Egg Donation: A Comprehensive Overview
I invite you to arrange to have a Skype or an in-person consultation with me to discuss your case in detail. If you are interested, please contact Julie Dahan, at:

Email: Julied@sherivf.com

OR

Phone: 702-533-2691
800-780-7437

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
Sarah

Hello Dr. Sher,
My first IVF retrieval cycle yielded 19 eggs, but only 9 were mature. I had a total of 13 fertilize (7 ICSI and 6 naturally). By day 3, many were poor quality and only 4 made it to blast. My protocol was 150 Gonal F with Ganirelix added on day 6 (can’t remember dose). My RE wants to add 75 of Menopur for next retrieval cycle. I have good AMH if slightly high (just over 4) and high FSH of 10.6.
Does this new protocol sound like it will yield better quality eggs and embryos? Anything you would do differently? My infertility is unexplained, though I do have autoimmune thyroid disorder. I take synthroid and am managed by Dr. Kwak Kim for RI issues. Hysteroscopy showed some visual endometritis but culture was negative. I also have a short period (2 days of good flow bleeding) with spotting before and after, but have a regular cycle. Any thoughts you have would be appreciated! I’m banking embryos and then doing PGS before transfer. Thank you!

reply
Dr. Geoffrey Sher

Provided the ovarian stimulation was NOT preceded by the use of estrogen or a BCP, it should be OK (see the article on use of the BCP in IVF…(see below). See the articles below for input on my personal preference for stimulation and alsoi review the article below on thyroid autoimmune disease and implantation dysfunction.

I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• IVF Failure and Implantation Dysfunction:
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
• Traveling for IVF from Out of State/Country–

Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691
 800-780-7437

Geoff Sher

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
Maria

Hello Doctor, today I went for my egg retrieval (first Ivf) and only got 1 egg out of 4 follicles. I’m 29 years old, and have an AMH of 1.9. I’m really disappointed on the results of the ovarian stimulation and really worried that this might be the end of the road for me. Never saw this coming. I wanted to ask you what would be your recommendation for me. I have a minimal endometriosis and an AMH of 1.9 and I’m 29 years old. My husband sperm is fine.
My doctor used the antagonist protocol, Menogon HP, ganirelix and Ovidrelle. I live in Germany.
Thank you for your time.

reply
Dr. Geoffrey Sher

In my opinion, you possibly had premature luteinizatuion due to the protocol for stimulation and perhaps its implementation (see below) + the possibility that the dosage of hCG (in the form of 250mcg Ovidrel) was too low…thereby resulting in egg incompetence and so called “empty follicles”. In addition, endometriosis might also a negative effect on implantation via an immunologic implantation dysfunction (see below).

I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
• Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
• A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
• Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
• Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
• Optimizing Response to Ovarian Stimulation in Women who Have Compromised Ovarian Response to Ovarian Stimulation in Women who Have Compromised Ovarian Reserve: A Personal Approach.
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Why did my IVF Fail
• “Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
• Endometriosis and Infertily
• Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.
• Endometriosis and Infertility: The Influence of Age and Severity on Treatment Options
• Treating Ovarian Endometriomas with Sclerotherapy.
• Implications of “Empty Follicle Syndrome and “Premature Luteinization”
• Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.

Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691
 800-780-7437

Geoff Sher

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

reply
Maria

Thank you very much for your answer. I would like to ask you something else. Do you think this poor response in my first cycle has to do with a low ovarian reserve (AMH 1.93) or with the protocol used on me.
Does this first response predicts following cycles, meaning that I will always get a poor response?
Again, thank you for taking time to answer, I really appreciate it.

reply
Dr. Geoffrey Sher

Possibly, but with a revision of the stimulation protocol, this could change significangtgly.

Good Luck!

Geoff Sher

reply

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