Measuring and interpreting Blood hCG to Assess Pregnancy Viability Following ART Treatments

I know of no medical announcement associated with the degree of emotional anticipation and anguish as that associated with a pending diagnosis/confirmation of pregnancy following infertility treatment. In fact, hardly a day goes by where I am not confronted by a patient anxiously seeking interpretation of a pregnancy test result.

Testing urine or blood for the presence of human chorionic gonadotropin (hCG) is the most effective and reliable way to confirm conception. The former, is far less expensive than the latter and is the most common method used. It is also more convenient because it can be performed in the convenience of the home setting. However, urine hCG testing for pregnancy is not nearly as reliable or as sensitive e as is blood hCG testing. Blood testing can detect implantation several days earlier than can a urine test. Modern pregnancy urine test kits can detect hCG about 16-18 days following ovulation (or 2-3 days after having missed a menstrual period), while blood tests can detect hCG, 12-13 days post-ovulation (i.e. even prior to menstruation).

The ability to detect hCG in the blood as early as possible and thereupon to track its increase, is particularly valuable in women undergoing controlled ovarian stimulation (COS) with or without intrauterine insemination (IUI) or after IVF. The earlier hCG can be detected in the blood and its concentration measured, the sooner levels can be tracked serially over time and so provide valuable information about the effectiveness of implantation, and the potential viability of the developing conceptus.

There are a few important points that should be considered when it comes to measuring interpreting blood hCG levels. These include the following:

  • All modern day blood (and urine) hCG tests are highly specific in that they measure exclusively for hCG. There is in fact no cross-reactivity with other hormones such as estrogen, progesterone or LH.
  • Post conception hCG levels, measured 10 days post ovulation or egg retrieval can vary widely (ranging from 5mIU/ml to above 400mIU/ml. The level will double every 48–72 hours up to the 6th week of gestation whereupon the doubling rate starts to slow down to about 96 hours. An hCG level of 13,000-290, 0000 mIU/ml is reached by the end of the 1st trimester (12 weeks) whereupon it slowly declines to approximately 26,000– 300,000 mIU/ml by full term. Below are the average hCG levels during the first trimester:
    • 3 weeks LMP: 5 – 50 mIU/ml
    • 4 weeks LMP: 5 – 426 mIU/ml
    • 5 weeks LMP: 18 – 7,340 mIU/ml
    • 6 weeks LMP: 1,080 – 56,500 mIU/ml
    • 7 – 8 weeks LMP: 7, 650 – 229,000 mIU/ml
    • 9 – 12 weeks LMP: 25,700 – 288,000 mIU/ml
    • A single hCG blood level is not sufficient to assess the viability of an implanting embryo. Caution should be used in making too much of an initial hCG level. This is because a normal pregnancy can start with relatively low hCG blood levels. It is the rate of the rise of the blood hCG level that is relevant.
    • In some cases the initially hCG level is within the normal range, but then fails to double in the ensuing 48-72hours. In some cases it might even plateau or decline, only to start doubling appropriately thereafter. When this happens, it could be due to:
      • A recovering implantation, destined to develop into a clinical gestation
      • A failing implantation (a chemical pregnancy)
      • A multiple pregnancy which is spontaneously reducing (i.e., one or more of the concepti is being lost) or,
      • An ectopic pregnancy which will either absorb spontaneously (a chemical-tubal gestation), or evolve into a full blown tubal pregnancy continue and declare itself through characteristic symptoms and signs of an intraperitoneal bleed.
  •  The blood hCG test needs to be repeated at least once after 48h and in some cases it  will need to be repeated one or more times (at 48h intervals) thereafter, to confirm that implantation is progressing normally.
  • Ultimately the diagnosis of a viable pregnancy requires confirmation of the presence of an intrauterine gestational sac by ultrasound examination. The earliest that this can be achieved is when the beta hCG level exceeds 1,000mIU/ml (i.e., around 5-6 weeks).
  • Most physicians prefer to defer the performance of a routine US diagnosis of pregnancy until closer to the 7th week. This is because by that time, cardiac activity should be clearly detectable, allowing for more reliable assessment of pregnancy viability.
  • There are cases where the blood beta hCG level is extraordinarily high or the rate of rise is well above the normal doubling rate. The commonest explanation is that more than one pregnancy has implanted. However in some cases it can point to a molar pregnancy  
  • Finally, there on rare occasions, conditions unrelated to pregnancy can result in detectable hCG levels in blood and urine. They include ovarian tumors that produce hCG, such as certain types of cystic teratomas (dermoid cysts) and some ovarian cancers such as dysgerminomas.

984 Comments

Kari

Good evening! I havent been able to see/find my last post so posting again.
Monday 1/20 U/S with yolk sac present. HCG levels were 10897. 48hr retest was only 15267. 40% increase. My drs office prepared me for a miscarriage. Do you believe this could be a viable pregnancy with those levels still? Beyond worried and wont go in for another U/S for 2 weeks. 2/7.

Thank you for your insight.

reply
Dr. Geoffrey Sher

Yes! It is possible because the rate of rise in hCG slows down after the level goes above 3-5,000.

Good luck!

Geoff Sher

reply
Khushi

Hello Dr Geoffrey,
I had sequential frozen embryo (day3) followed by Blastocyst day5 (4BC) on 8th and 10th January 2020:
My Beta (on 22nd January): 135.9 iu/ml
My second Beta (24th Jan) : 32 iu/ml
I got call by nurse to discontinue all medications and repeat hcg on 28th Jan, please advise what it means? And if failed then why repeated hcg? Thank you so much

reply
Dr. Geoffrey Sher

This clearly is a failing implantation. However, it is always safest to follow thye hCG level down zero.

So sorry!

Geoff Sher

reply
Khushi

Thank you Sir,
Second post
I want suggestion: (after hcg got reduced from 135.9 to 32)
1. Should I wait for another FET (I have 14 months girl via IVF and I’m 35 years old)
2. What could be the reason for failure of implantation as my lining was 9.2 mm with triple line, Blast was 4BC (my concern , I was breastfeeding during night to my LO).

reply
Hanna

Hi Dr. Sher,
I had blood test done for HCG and Progesterone on 13 DPO.
HCG was 100 and Progesterone 26 nmol/l which is roughly 8 ng/ml.
2 days later at 15 DPO HCG was 230.
I am concerned about the low progesterone. Is it possible I have implanted late and the progesterone will still raise? How fast should progesterone raise?
I am worried I am going to lose this pregnancy.
I had one miscarriage 4 months ago.
Thank you

reply
Hanna

Just to add the pregnancy test came back positive on 11 DPO with Clearblue test.
9 and 10 DPO were negative

reply
Dr. Geoffrey Sher

I personally do not think there is a peroblem..but discuss with your RE to see if he/she wishes to supplement hormoner.

Geoff Sher

reply
Kate

Hi, I am 7weeks2days and my hcg is on the low end and very slow to rise.
6w2d – 5074
6w5d – 6040
7w2d – 6470
Is this a sure sign of an impending miscarriage?
Thank you

reply
Dr. Geoffrey Sher

At this stage an ultrasound would be confirmatory …one way or the other!

Geoff Sher

reply
Dr. Geoffrey Sher

I personally do not think there is a peroblem..but discuss with your RE to see if he/she wishes to supplement hormones.

Geoff Sher

reply
Megan

Hello Dr. Sher,

Firstly, thank you for taking the time to answer so many questions. I’ve read through the majority of them to get a better understanding of my own HCG levels. I’m hoping you can help give me insight.
My first HCG beta came out at 97. Second test three days later my HCG was 608.
The jump seems high?

reply
Dr. Geoffrey Sher

It is a very significant rise. Wait for 2 weeks and do an US to see if this is a single or multiple pregnancy!

Geoff Sher

reply
Vicky

Hello dr – I am 7+1 week and just received my HCG results from last week and am very concerned as they did not double. Nurse said they are not where they like them to be but scheduled a ultrasound for end of week. Could there be any chance that this pregnancy is still viable? Concerned after history of missed miscarriage!
@ 6 weeks – 19,449
@ 6 weeks 2 days – 27,952

reply
Dr. Geoffrey Sher

The hCG levels do not continue to double. As your hCG level rises above 4,000 to 5,000 the rate of increase slows down. In my opinion your r5ate of rise is impressive and reason for some confidence that all is going well at this time.

Good luck!

Geoff Sher

reply
Lauren S

Hi Dr.
I am 6 weeks and 6 days today and received my hCG results back today from last week.

At 6 weeks and 1 day, my hCG level was 36,000.
At 6 weeks and 3 days, my hCG level was 48,000.

The office called today to say that they’re concerned my levels didn’t double and called me in for an ultrasound tomorrow. Should I be concerned for a miscarriage or even ectopic pregnancy?

reply
Dr. Geoffrey Sher

I urge you to do an US for a definitive answer. Note that after hCG levels rise above 5,000U, it wont double every 2 days any more.

Geoff Sher

reply
Shelby

Hello! I found out I was pregnant January 13th, I was estimated at 7 weeks by my last period. I started having spotting on the 19th, I went to the emergency room and they did all the tests they have to do to rule out miscarriage. The ER doctor said that everything is ok. My hcg levels was 745 and he said that’s the 5 weeks range. I went for my ultrasound that was originally scheduled that afternoon so that I could see that everything was ok. She showed me two small sacs that measured that of 5 weeks. They were equal in size too.
I am irregular so I’m not surprised about the due date being off.
My friend who is pregnant with twins said she bled more when she had implantation bleeding. Could I be having twins?
The ultrasound tech said there was definitely two little sacs.

reply
JJ

Hi Dr. Sher,
Hoping to get your insight having had several miscarriages and chemicals in the past….At 16 dpo I had an hcg of 56. At 18 dpo it was 196. At 25 dpo it jumped to 3594. These seem like more than normal increases….should I be worried about a molar? multiples? Or am I just paranoid? Thanks!

reply
Jordan

Hi Dr. Sher,

I had an embryo transfer on 1/9/2020 with 2 PGS normal, good quality embryos (5AA & 4AA). On 1/18/2020, my HCG levels were 74. On 1/20/2020, my levels were 86. I’m wondering what your thoughts are on these results. And what your course of action would be from here. Thank you for your time!

reply
Dr. Geoffrey Sher

This looks precarious to me. Repeat the hCG in 2 days to see if it doubles!

Sorry!

Geoff Sher

reply
Prachi A

Hello dr,
My beta hcg was 43 on my 23rd day.. 83.35 on my 27th day.. is the rate growth normal?

reply
Dr. Geoffrey Sher

That is a low hCG for that far along. I am not optimistic but please recheck the levels every few days and be in touch with your personal treating physician.

Geoff Sher

reply
Jordan

I had my tubes tied in 2013 ive had 3 micarriages since i had a hsg done saying one tube was partially open. I found out i was pregnant 2 weeks ago my first visit they saw a sac and my levels were 134 second visit they were 250 i started spotting today and the said my levels were 64. Is this a certain loss? Whys this keep happening? What can i do

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.SherIVF.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 IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
• 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
• 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: How Many Attempts should be considered before Stopping?
• “Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
• 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:
• 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

______________________________________________________
ADDENDUM: PLEASE READ!!
INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.

Patients are encouraged to share the information I provide, with their treating Physicians and/or to avail themselves of my personal hands-on services, provided through batched IVF cycles that I conduct every 3 months at Los Angeles IVF (LAIVF) Clinic, Century City, Los Angeles, CA.

If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or, enroll online on then home-page of my website (www.SherIVF.com).

PLEASE SPREAD THE WORD ABOUT SFS!

Geoff Sher

reply
Shannon Fults

Hi Dr. Sher,
On 12/22/19 I ovulated, at 9dpo on 12/31/19 I got my first positive hcg. My first beta was at 12dpo and it was 182. My 2nd beta was at 17 dpo and it was 2,889. My 3rd beta was at 24 dpo and was 29,609 exactly 5weeks+3. Is it possible I’m going to see twins at my first ultrasound based on these levels?

reply
Nadine

Hi Dr Sher.

I have very irregular cycles so I don’t know when I ovulated or exactly how far along I am.

Did HCG test and levels were 48 and 72 hours later my levels were 308.

I suspect I am around 4- 5 weeks? My Dr is concerned about early pregnancy loss.

Should I be worried?

reply
Misty Holt

Hello.
I had a tubal ligation almost 13 years ago about five days ago I received a positive pregnancy test my hCG levels went on Friday at 140, Saturday to 235 and Monday to 363 the doctor is concerned about the numbers are rising too slowly. Do you think this pregnancy has a chance or am I looking more towards an ectopic pregnancy

reply
Dr. Geoffrey Sher

I am not optimistic about this pregnancy. Only time/follow-up will tell!

Sorry!

Geoff Sher

reply
Kristyn

Hi Dr. Sher!
My OB put me on Letrozole and I got a positive test on 12/13.
HCG levels were checked on 1/7 and they were 5500.
Checked again 1/9 and were only 5700.
Checked a third time on 1/12 and were 6800.
Ultrasound was performed on 1/7 and saw a sac attached to uterus. Ultrasound performed again on 1/12 and saw sac, yolk and fetal pole. Measuring 5weeks 6days.
OB wants to repeat ultrasound in 1 week. Any way this would be a viable pregnancy?

reply
V

Hi, Dr. Sher,

OPK and basal temperature confirmed the ovulation date and I had my first blood work checked on DPO 14 (Jan 14th), My HCG level was 768 and my progesterone was 22.3 , I won’t have my second one until my first appointment on Feb 4th. Is my HCG level look high to you? Will it be multiple? I get pregnant naturally and based on the info that I read online, 768 for DPO 14 seems high.

reply
Dr. Geoffrey Sher

Hard to say whether it is a singleton or a multiple. BUT I am relatively optimistic all will turn out OK!

Good luck!

Geoff Sher

Geoff Sher

reply
Liana

The uterus measures 9.7 x 3.1 x 3.9 cm ultrasound they say there is a abnormal shaped gestational sac but my HGC levels have doubled since Jan 4 and is now 31446 . should I be worried ? I thought I was six weeks could I have ovulated late?

Dr. Geoffrey Sher

I am still hopeful for you. Repeat the US in 1 week and lets reassess

Geoff Sher

Mackenzie Sanchez

Hi Dr. Sher,
Had a miscarriage in November.
LMP 12/15/19
+OPK 12/25/19
+urine test 1/4/20
Beta HCG on 1/6/20 was 59
Beta HCG on 1/8/19 was 204

I thought they were looking for it to double in 48 hours, but the nurse told me they were looking for it to double in 24 hours. Does this seem high/fast doubling? Should I raise concern again with the doctor? Thank you!

reply
Anna

Hello

I am 9+5 weeks. I did a blood test at 8+0 weeks for bioactive testosterone (0,1nmol/l) and DHEAS 1,7 umol/l. They seem to be extremely low.

I took DHEA (50 mg per day) before IVF cycle and stopped at 5+0 weeks. Now I take prednisolone 10 mg.

Do you think I should take DHEA again?

Thank you very much for your time!

reply
Ava Francis

Hi Dr. Sher,

I had a FET on 12/17. My hcg level on 12/24 was 33, 35 on 12/26 and 214 on 12/30. After my second beta the RE asked to stop estrogen/progesterone supplements, since they think this is most likely
a chemical pregnancy. What do you think? Do I have hope or should I discontinue medication?

Thanks a lot for your time and response.

reply
Dr. Geoffrey Sher

I personally would not stop meds until there is complete evidence of a loss!

Happy New Year!

Geoff Sher

reply
Samantha

Hi there!

I did a medicated IUI and got a positive pregnancy test. My bloodwork hcg 17 DPO was 354 and then 735 at 19 DPO – exactly 48 hours. But my next one 4 days later was 1450. My RE said they were looking for a number over 1000 and not to worry. But since it didn’t double of course I worry! I just hit six weeks and have lots of symptoms and was also told that over 1000 it may not double as quickly but I was within normal range. Going for an US in four days. Should I be concerned? Thanks!

reply
SIMONE REA

Hello!

I am not sure when I ovulated but I KNOW the night we had sex was 20/12/19. On the 07/01/2020 (18days after we had sex) my hcg levels were 145. Does that number seem ok? (I took a pregnancy test the day before that and it was a clear positive)

reply
Erica Chapman

Good Morning Dr. Sher,

I transferred a fresh day 3 embryo on 12/4. My first beta was 12/14 HCG 89. Beta two was 12/16 HCG 210. Beta three was 12/19 HCG 984. Is my HCG rising too quickly? Is it ok if HCG more than doubles?

Thank you in advance for your insight!
ERica

reply
Kaitlyn Hucker

Multiple chemical pregnancies (7) and still no successful pregnancies. No endometritis. No endometriosis. Tried LMWH, Intralipids via IV, and still nothing. What should I do next? .

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.SherIVF.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 IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
• 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
• 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: How Many Attempts should be considered before Stopping?
• “Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
• 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:
• 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

______________________________________________________
ADDENDUM: PLEASE READ!!
INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.

Patients are encouraged to share the information I provide, with their treating Physicians and/or to avail themselves of my personal hands-on services, provided through batched IVF cycles that I conduct every 3 months at Los Angeles IVF (LAIVF) Clinic, Century City, Los Angeles, CA.

If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or, enroll online on then home-page of my website (www.SherIVF.com).

PLEASE SPREAD THE WORD ABOUT SFS!

Geoff Sher

reply
Earlisha Mosley

I transferred 2 embryos 12/5 and got Beta results back today at 12dp5dt and it was 930. Do you think that’s for one or two? Next Beta is Thursday

reply
Joanna Duarte

Hi Dr. Sher

Had a 5 day blast transferred 11/29. 10dp5dt HCG was 221.4
45 hours later HCG was 382.3.
Then i was cleared until the 7 week ultrasound, but i stupidly asked for one more Beta, even tho my clinic was closing early for xmas party. Third beta was 39 hours after the last draw and only came back at 535. Going for scan tomorrow and I AM TERRIFIED. I want this baby more than anything. What are your thoughts?

reply
Dr. Geoffrey Sher

39 hours is too short a period for the beta to double. You need 48h. Separately, it is probably too early to detect ultrasound evidence of a pregnancy. You would need to wait about 7 days.

Good luck!

Geoff Sherr

reply
Anna

Hello

Thank you for taking time to answer the questions!

Could you please tell me your opinion on my values. According to my doctor, my HCG is way too high for a singleton.

I did a fresh 3 day transfer (one 8 cell embryo)
HCG (15 dp3dt, week 4+4) 1.458

HCG (20 dp3dt, week 5+2) 6.720 (doubling time 54 hours), done in a different lab and after IL drop 2 days prior, don´t know if it affected the value

Estradiol (20 dp3dt, week 5+2) 4.119pmol/L (1.122pg/ml)

Progesteron (20 dp3dt, week 5+2) >190 nmol/l (59 ng/ml) (I take Lutinus vagitories 300 mg per day)

I also take prednisolone 10 mg and have done 2 intralipid drops

reply
Anna

Hello again. So does it mean that these values above are no good? Can it be a molar pregnancy?

reply
Dr. Geoffrey Sher

No! I do not think it is molar. And yes, as I recall…. the values are OK!

Geoff Sher

reply
Lizelle

Hi Doc

My first HCG beta was 79 then in 46hours it was 131 and then after 96 hours it was 290. We used timed intercourse.

6 months ago I had an ectopic. Do you think these levels mean another one?

Thanks

reply
Jamie

Hey,

The first day of My last period was December 9, 2019! I got my my positive test on January 13,2020. My hcg levels on January 13 was 921. I did another hcg test on January 16 and it was 1156. Is this good or bad news? I did another one today but haven’t got the results yet.

Dr. Geoffrey Sher

It is a slow rise. You should repeat it again tomorrow. It needs to be around 3500 +..by then.

Good luck!

Geoff Sher

victoria

Hello
I had a frozen embryo transfer with PGS testing of a perfectly normal hatching embryo. I went for my 9dpt and my level was 29. I have had 4 losses and this is my first attempt at IVF. I go back Saturday to see if they double. That doctor said it’s not bad news yet and yes there could be another miscarriage but he had women with lower numbers go on to have normal pregnancies. I’m a wreck. Thanks for your insight.

reply
Katie

Hi Dr. Sher,

I transferred a day 6 PGS normal embryo on 11/21. On 11 dpt hcg was 460, but hcg went up to 1630 after 56 hours. My dr said no need to repeat the test again and just to see him on 12/16 for an ultrasound. I thought HCG doubles every 48-72 hours, but mine more than tripled in 56 hours. Should I be concerned for molar pregnancy? Your comment is highly appreciated.

reply
Dr. Geoffrey Sher

I agree with your RE’s opinion….No need to repeat the test. Just wait for an US in about 2-3 weeks time.

Geoff Sher

reply
Michelle

Hi Dr. Sher,

We had our first beta today 9dpt5d and got 18. The 2nd beta will be in 48hrs and they’re looking for mom 60% increase every 48hrs.

First question: what are chances beta starting this low turns into a viable pregnancy?

Second: even if the beta doubles every 48hrs, I feel like that’s not enough to get into “normal” range. Wouldn’t it be correct to assume beta needs to almost triple or quadruple eventually to ?catch up”

reply
Dr. Geoffrey Sher

This is a normal day-9 beta.

I know of no medical announcement associated with the degree of emotional anticipation and anguish as that associated with a pending diagnosis/confirmation of pregnancy following infertility treatment. In fact, hardly a day goes by where I am not confronted by a patient anxiously seeking interpretation of a pregnancy test result.
Testing urine or blood for the presence of human chorionic gonadotropin (hCG) is the most effective and reliable way to confirm conception. The former, is far less expensive than the latter and is the most common method used. It is also more convenient because it can be performed in the convenience of the home setting. However, urine hCG testing for pregnancy is not nearly as reliable or as sensitive e as is blood hCG testing. Blood testing can detect implantation several days earlier than can a urine test. Modern pregnancy urine test kits can detect hCG about 16-18 days following ovulation (or 2-3 days after having missed a menstrual period), while blood tests can detect hCG, 12-13 days post-ovulation (i.e. even prior to menstruation).
The ability to detect hCG in the blood as early as possible and thereupon to track its increase, is particularly valuable in women undergoing controlled ovarian stimulation (COS) with or without intrauterine insemination (IUI) or after IVF. The earlier hCG can be detected in the blood and its concentration measured, the sooner levels can be tracked serially over time and so provide valuable information about the effectiveness of implantation, and the potential viability of the developing conceptus.
There are a few important points that should be considered when it comes to measuring interpreting blood hCG levels. These include the following:
• All modern day blood (and urine) hCG tests are highly specific in that they measure exclusively for hCG. There is in fact no cross-reactivity with other hormones such as estrogen, progesterone or LH.
• Post conception hCG levels, measured 10 days post ovulation or egg retrieval can vary widely (ranging from 5mIU/ml to above 400mIU/ml. The level will double every 48–72 hours up to the 6th week of gestation whereupon the doubling rate starts to slow down to about 96 hours. An hCG level of 13,000-290, 0000 mIU/ml is reached by the end of the 1st trimester (12 weeks) whereupon it slowly declines to approximately 26,000– 300,000 mIU/ml by full term. Below are the average hCG levels during the first trimester:
o 3 weeks LMP: 5 – 50 mIU/ml
o 4 weeks LMP: 5 – 426 mIU/ml
o 5 weeks LMP: 18 – 7,340 mIU/ml
o 6 weeks LMP: 1,080 – 56,500 mIU/ml
o 7 – 8 weeks LMP: 7, 650 – 229,000 mIU/ml
o 9 – 12 weeks LMP: 25,700 – 288,000 mIU/ml
• A single hCG blood level is not sufficient to assess the viability of an implanting embryo. Caution should be used in making too much of an initial hCG level. This is because a normal pregnancy can start with relatively low hCG blood levels. It is the rate of the rise of the blood hCG level that is relevant.
• In some cases the initially hCG level is within the normal range, but then fails to double in the ensuing 48-72hours. In some cases it might even plateau or decline, only to start doubling appropriately thereafter. When this happens, it could be due to:
o A recovering implantation, destined to develop into a clinical gestation
o A failing implantation (a chemical pregnancy)
o A multiple pregnancy which is spontaneously reducing (i.e., one or more of the concepti is being lost) or,
o An ectopic pregnancy which will either absorb spontaneously (a chemical-tubal gestation), or evolve into a full blown tubal pregnancy continue and declare itself through characteristic symptoms and signs of an intraperitoneal bleed.
• The blood hCG test needs to be repeated at least once after 48h and in some cases it will need to be repeated one or more times (at 48h intervals) thereafter, to confirm that implantation is progressing normally.
• Ultimately the diagnosis of a viable pregnancy requires confirmation of the presence of an intrauterine gestational sac by ultrasound examination. The earliest that this can be achieved is when the beta hCG level exceeds 1,000mIU/ml (i.e., around 5-6 weeks).
• Most physicians prefer to defer the performance of a routine US diagnosis of pregnancy until closer to the 7th week. This is because by that time, cardiac activity should be clearly detectable, allowing for more reliable assessment of pregnancy viability.
• There are cases where the blood beta hCG level is extraordinarily high or the rate of rise is well above the normal doubling rate. The commonest explanation is that more than one pregnancy has implanted. However in some cases it can point to a molar pregnancy
• Finally, there on rare occasions, conditions unrelated to pregnancy can result in detectable hCG levels in blood and urine. They include ovarian tumors that produce hCG, such as certain types of cystic teratomas (dermoid cysts) and some ovarian cancers such as dysgerminomas.
I strongly recommend that you visit http://www.SherIVF.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.

• A Fresh Look at the Indications for IVF
• The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
• 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
• Genetically Testing Embryos for IVF
• IVF Failure and Implantation Dysfunction:
• Management of Immunologic Implantation Dysfunction (IID).
• The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• Avoiding High Order Multiple Pregnancies (Triplets or Greater) with IVF
• The Role of Nutritional Supplements in Preparing for IVF
• Ectopic Pregnancy
• Molar pregnancies

_______________________________________________________
ADDENDUM: PLEASE READ!!
INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
Hitherto I have personally performed IVF- treatment and related procedures on patients who, elected to travel to Las Vegas to be managed by me. However, with the launching of Sher-Fertility Solutions (SFS) in April 2019, I have taken on a new and expanded role. Now, rather than having hands-on involvement I confine my services to providing hour-long online Skype consultations to an ever-growing number of patients (emanating from >40 countries), with complex Reproductive problems, who seek access to my input, advice and guidance. All Skype consultations are followed by a detailed written report that meticulously describes and explains my recommendations for treatment. All patients are encouraged to share this report with their personal treating doctor(s), with whom [subject to consent and a request from their doctor] I will, gladly discuss their case with the “treating Physician”.
Through SFS I am now able to conveniently provide those who because of geography, convenience and cost, prefer to be treated at home or elsewhere by their chosen Infertility Physician.
“I wish to emphasize to all patients with whom I consult, that in the final analyses, when it comes to management, strategy, protocol and implementation of treatment, my advice and recommendations are always superseded by that of the hands-on treating Physician”.

Anyone wishing to schedule a Skype consultation with me, can do so by: Calling my concierge (Patti Converse) at 1-800-780-7437 (in the U.S.A or Canada) or 702-533-2691, for an appointment. Patients can also enroll online on my website, http://www.SherIVF.com, or email Patti at concierge@SherIVF.com .
I was very recently greatly honored in receiving an award by the prestigious; International Association of Top Professionals (IAOTP). For more information, go to the press release on my website, http://www.sherIVF.com .

PLEASE HELP SPREAD THE WORD ABOUT SFS!

Geoff Sher

reply
Erin

My level is a 39.77 also 9dpt5dt. My doctor made me nervous this is too low and I have to go back Sunday. Should I be concerned?

reply
Dr. Geoffrey Sher

I , in turn am cautiously optimistic for you. BUT time will tell!

Good luck!

Geoff Sher

reply
Rhian

I’m currently 12dp3dt – I regrettably started taking home tests at 8dpt, 9dpt and had faint positives.

Yesterday (11dpt) my positive lines have vanished.

Is it possible that my HCG levels at 8 & 9dpt where from my trigger injection?

My test date is Saturday the 14th (In 3 days) and I wishful thinking that a positive might appear and my HCG levels are rising super slow?

reply
Dr. Geoffrey Sher

You could do a beta hCG blood test today b(day 12, post D3-ETR) and get a meaningful result. Otherwise, I would just wait patiently until Saturday!

Good Luck!

Geoff Sher

reply
Monica

LMP=11/5/19
HCG @ 51 on 12/6/19 and @ 107 on 12/9/19
mild cramping and spotting on and off since 12/6/19

GP not entirely convinced this is a viable pregnancy and sending me for serial blood work, every 48 hours. What do you think, doc?

reply
Dr. Geoffrey Sher

It is high but it depends on how long after transfer you did the test.

Geoff Sher

reply
Willi

I have done IVF on 11/22 and done hcg on 12/6 which is 52. Is there any chances of pregnancy?

reply
Dr. Geoffrey Sher

Repeat the test 2 days later. If it doubles, there could be reasonable hope.

Good Luck!

Geoff Sher

reply
Willi

On 12/8 again hcg done and it is 79, earlier done on 12/6 and hcg was 52. Now what is your opinion about chances of pregnancy.

reply
Dr. Geoffrey Sher

That is a disappointing slow rise.We will have to wait and see how it continues. However it now does not look encouraging.

Geoff Sher

reply
Willi

Again HCG done on 12/10 and it is 89. Should we continue the medicines or stop them. Kindly advice what we do now. Is there any medicines to remove this or it will remove automatically. Thank you in anticipation

Willi

Medicines stopped on 12/10. And periods started on 12/15 but these are much more painful than ever before. Bleeding is also very heavy. Is the pain due to failed IVF or something wrong. Kindly advice.

Dr. Geoffrey Sher

I doubt that there is anything wrong. Periods often start earlier and are heavier, after a failed IVF.

Geoff Sher

Carmen

Hi, I had a 3 fresh 5-day blastocysts transferred.
My hcg numbers were:
Day 12 after transfer – 165
Day 14 after transfer – 244
Day 16 after transfer – 421
Are these numbers normal? I am very concerned. Thanks!

reply
Dr. Geoffrey Sher

Give it a few days and repeat the hCG test. Then in 2 weeks do an US.

Geoff sher

reply
Carmen

Hello Doctor,
3 days later (day 19 after transfer) the result was 991.
We also saw one sac in the uterus in a vaginal ultrasound.
The clinic asked me to come again 2.5 weeks from now for a heartbeat detection ultrasound.
Do you think the numbers are OK or should I continue with the hCG tests?

and one last question – which week am I? The transfer of fresh blastocysts (day 5) was on 11/19.

Thank you very much. This website is so helpful!

reply
Dr. Geoffrey Sher

You are at 5-6 weeks. A repeat ultrasound done in 10 days from now, should, in mky opinion be completely revealing.

Geoff Sher

reply
Marie

I have a question regarding whats better to do. I have 2, 5 day blastocyst left. I am turning 40 in January, I just did one transfer with one blastocyst, I got pregnant but unfortunately it ended at 7-1/2 weeks with a miscarriage. I have two children already and this is my first miscarriage ever. My question is do i transfer both or one at a time. I would love twins but I have also heard that if one egg is bad it could affect the good egg. Your thoughts are greatly appreciated.

reply
Eva

Was on agonist protocol in July 2019.ER -8/5.I had my FET on 12/5 after zoladex injection administered on 9/5.bhcg less than 5 on 12/16.Am so confused.what is your advice?Try again on antagonist?Am in early 40s…

reply
Dr. Geoffrey Sher

I invite you to set up an online consultation with me to discuss (see below).

The importance of the IVF stimulation protocol on egg/embryo quality cannot be overstated. This factor seems often to be overlooked or discounted by t IVF practitioners who use a “one-size-fits-all” approach to ovarian stimulation. My experience is that the use of individualized/customized COS protocols can greatly improve IVF outcome. While no one can influence underlying genetics or turn back the clock on a woman’s age, any competent IVF specialist should be able to tailor the protocol for COS to meet the individual needs of the patient.
Gonadotropins (LH and FSH), whether produced by the pituitary gland or administered by way of fertility drugs, have different “targeted” sites of action in the ovary. FSH targets cells that line the inner wall of the follicle (granulosa cells) and also form the cumulus cells that bind the egg to the inner surface of the follicle. Granulosa cells are responsible for estrogen production.
LH, on the other hand, targets the ovarian connective tissue (stroma/theca) that surrounds ovarian follicles resulting in the production of male hormones such as testosterone (predominantly), androstenedione and DHEA. These androgens are then transported to the granulosa cells of the adjacent follicles in a “bucket brigade fashion”. There FSH converts testosterone to estradiol, causing granulosa cells to multiply (proliferate) and produce estradiol, follicles to grows and eggs to develop (ovogenesis) It follows that ovarian androgens (mainly testosterone) is absolutely indispensable to follicle/ egg growth and development.
However, the emphasis is on a “small” amount of testosterone. Over-exposure of the follicle to testosterone can compromise egg development and lead to an increased likelihood of chromosomal irregularities (aneuploid) following LH/hCG-induced egg maturational division (meiosis) and compromise embryo “competency/quality.
Ovarian androgens can also reach the uterine lining where they sometimes will compromise estrogen receptor -induced endometrial growth and development.
Many older women and those who have diminished ovarian reserve (DOR) have increased LH activity is increased. Such women either over-produce LH and/or the LH produced is far more biologically active. Chronically increased LH activity leads to overgrowth of ovarian connective tissue (stroma/theca). This condition, which is often referred to as Stromal Hyperplasia or hyperthecosis can result in excessive ovarian androgen/testosterone production and poorer egg-embryo quality/competency, Similarly, women with polycystic ovarian syndrome (PCOS), also characteristically have Stromal hyperplasia/hyperthecosis due to chronically increased LH activity. Thus they too often manifest with increased ovarian androgen production. It is therefore not surprising that “poor egg/embryo quality” is often also a feature of PCOS.
In my opinion, the over-administration of LH-containing menotropins such as Menopur, [which is comprised of roughly equal amount of FSH and hCG ,which acts similar to LH)], to older women, women with DOR and those who have PCOS can also lead to reduced egg/embryo competency . Similarly, drugs such as clomiphene or Letrozole that cause the pituitary gland to release excessive amounts of LH, are also potentially harmful to egg development and in my opinion, are best omitted from IVF COS protocols. This is especially the case when it comes to older women and those with DOR, who in my opinion should preferably be stimulated using FSH-dominant products such as Follistim, Puregon, Fostimon and Gonal-F.
Gonadotropin releasing hormone agonists (GnRHa): GnRHa such as Lupron, Buserelin, Superfact, Gonopeptyl etc. are often used to launch ovarian stimulation cycles. They act by causing an initial outpouring followed by a depletion of pituitary gonadotropins. This results in LH levels falling to low concentrations, within 4-7 days, thereby establishing a relatively “LH-free environment”. When GnRHa are administered for about 7 days prior to initiating gonadotropin stimulation (“long” pituitary down-regulation”), the LH depletion that will exist when COS is initiated, will usually be protective of subsequent egg development. In contrast, when the GnRHa administration commences along with the initiation of gonadotropin therapy, there will be a resultant immediate surge in the release of pituitary LH with the potential to increase ovarian testosterone to egg-compromising levels , from the outset of COS. This, in my opinion could be particularly harmful when undertaken in older women and those who have DOR.
GnRH-antagonists such as Ganirelix, Cetrotide and Orgalutron, on the other hand, act very rapidly (within hours) to block pituitary LH release. The purpose in using GnRH antagonists is to prevent the release of LH during COS. In contrast, the LH-lowering effect of GnRH agonists develops over a number of days.
GnRH antagonists are traditionally given, starting after 5th -7th day of gonadotropin stimulation. However, when this is done in older women and those (regardless of age) who have DOR, LH-suppression might be reached too late to prevent the deleterious effect of excessive ovarian androgen production on egg development in the early stage of ovarian stimulation. This is why, it is my preference to administer GnRH-antagonists, starting at the initiation of gonadotropin administration.
My preferred Protocols for Controlled Ovarian Stimulation (COS):
1. “Long” GnRHa (Lupron/Buserelin/Superfact/Gonopeptyl) Pituitary Down-regulation Protocol: The most commonly prescribed protocol for GnRHa/gonadotropin administration is the so-called “long protocol”. Here, GnRHa is given, starting a week or so prior to menstruation. This results in an initial rise in FSH and LH , which is rapidly followed by a precipitous fall to near zero. It is followed by a withdrawal bleed (menstruation), whereupon gonadotropin treatment should commence, while daily Lupron injections continue, to ensure a “low LH” environment. A modification to the “long protocol” which I prefer prescribing for older women and in cases of DOR, is the Agonist/Antagonist Conversion Protocol (A/ACP) where, upon the onset of a GnRHa-induced bleed, the agonist is supplanted by an antagonist (Ganirelix/Cetrotide/Orgalutron) and this is continued until the hCG trigger. In many such cases I often supplement with human growth hormone (HGH) in such cases in an attempt to enhance egg mitochondrial activity and so enhance egg development. This approach is often augmented with preimplantation genetic screening (PGS) of all embryos that reach the expanded blastocyst stage of development by day 5-6 post-fertilization. I also commonly recommend blastocyst banking to many such patients.
2.
3. Short (“Flare”) GnRHa Protocol: Another GnRHa usage for COS is the so called “(micro) flare protocol”. This involves initiating gonadotropin therapy commensurate with initiation of gonadotropin administration. The supposed objective is to deliberately allow Lupron to elicit an initial surge (“flare”) in pituitary FSH release in order to augment FSH administration by increased FSH production. Unfortunately, this “spring board effect” constitutes “a double-edged sword”. While it indeed increases the release of FSH, it at the same time causes a surge in LH release. The latter can evoke excessive ovarian stromal/thecal androgen production which could potentially compromise egg quality, especially when it comes to older women and women with DOR. I am of the opinion that by evoking an exaggerated ovarian androgen response, such “(micro) flare protocols” can harm egg/embryo quality and reduce IVF success rates, especially when it comes to COS in older women, and in women with diminished ovarian reserve. Accordingly, I do not prescribe such protocols to my IVF patients.
4. Estrogen Priming – This is the approach I sometimes prescribe for my patients who have virtually depleted ovarian reserve , as determined by very low blood anti-Mullerian hormone AMH levels (<0.2ng/ml or 2 pmol/L) and are thus likely to be very “poor responders”. It involves a modified A/ACP. We start with the birth control pill (BCP) for 10 days or longer, overlap it for 3 days with a GnRHa whereupon the BCP is stopped. Th GnRHa is continued until the onset of menstruation (usually 5-7 days later) to cause pituitary LH, down-regulation. Upon menstruation and confirmation by ultrasound and measurement of blood estradiol levels that adequate ovarian suppression has been achieved, the dosage of GnRHa is stopped and is immediately supplanted by daily administration of GnRH antagonist. The patient is given twice-weekly injections of estradiol valerate (Delestrogen) for a period of 8 days whereupon COS is initiated using a relatively high dosage FSH-(Follistim, Fostimon, Puregon or Gonal F), which is continued along with daily administration of GnRH antagonist until the “hCG “trigger.” This approach is often augmented with HGH administration throughout the process of COS and by preimplantation genetic screening (PGS) of all embryos that reach the expanded blastocyst stage of development by day 5-6 post-fertilization. I also commonly recommend blastocyst banking to many such patients.
Estrogen Priming has succeeded in significantly enhancing ovarian response to gonadotropins in many of otherwise very poor responders.
Triggering egg Maturation prior to egg Retrieval: hCG versus GnRHa
With ovulation induction using fertility drugs, the administration of 10,000U hCGu (Pregnyl; Profasi, Novarel) or 500mcg hCGr (Ovidrel/Ovitrel) “trigger”) sends the eggs (into maturational division (meiosis). This process is designed to halve the chromosome number, resulting in mature eggs (M2) that will have 23 chromosomes rather that the 46 chromosomes they had prior to the “trigger”. Such a chromosomally numerically normal (euploid), mature (MII) eggs, upon being fertilized will (hopefully) propagate euploid embryos that have 46 chromosomes and will be “: competent” to propagate viable pregnancies. In my opinion, the key is to always “trigger” with no less than 10,000U of hCGu or 500mcg hCGr (Ovidrel/Ovitrel). Any lesser dosage often will reduce the efficiency of meiosis and increase the risk of the eggs being aneuploid. I personally do not use the agonist (Lupron) “trigger”, unless it is combined with (low dosage) hCG. The supposed reason for using the agonist, (Lupron) “trigger” is that by inducing meiosis through compelling a surge in the release of LH by the pituitary gland, the risk it reduces the risk of OHSS. This may be true, but it comes at the expense of egg quality because the extent of the induced LH surge varies and if too little LH is released, meiosis can be compromised, thereby increasing the likelihood of aneuploid and immature (MI) eggs. And there are other better approaches to preventing OHSS (e.g. “prolonged coasting”), in my opinion.
Use of the Birth Control Pill (BCP) to launch IVF-COS.
In natural (unstimulated) as well as in cycles stimulated with fertility drugs, the ability of follicles to properly respond to FSH stimulation is dependent on their having developed FSH-responsive receptors. Pre-antral follicles (PAF) do not have such primed FSH receptors and thus cannot respond properly to FSH stimulation with gonadotropins. The acquisition of FSH receptor responsivity requires that the pre-antral follicles be exposed to FSH, for a number of days (5-7) during which time they attain “FSH-responsivity” and are now known as antral follicles (AF). These AF’s are now able to respond properly to stimulation with administered FSH-gonadotropins. In regular menstrual cycles, the rising FSH output from the pituitary gland insures that PAFs convert tor AF’s. The BCP (as well as prolonged administration of estrogen/progesterone) suppresses FSH. This suppression needs to be countered by artificially causing blood FSH levels to rise in order to cause PAF to AF conversion prior to COS commencing, otherwise pre-antral-to –antral follicle conversion will not take place in an orderly fashion, the duration of ovarian stimulation will be prolonged and both follicle and egg development may be compromised. GnRH agonists cause an immediate surge in release of FSH by the pituitary gland thus causing conversion from PAF to SAF. This is why women who take a BCP to launch a cycle of COS need to have an overlap of the BCP with an agonist. By overlapping the BCP with an agonist for a few days prior to menstruation the early recruited follicles are able to complete their developmental drive to the AF stage and as such, be ready to respond appropriately to optimal ovarian stimulation. Using this approach, the timing of the initiation of the IVF treatment cycle can readily and safely be regulated and controlled by varying the length of time that the woman is on the BCP.
Since optimizing follicular response to COS requires that prior to stimulation with gonadotropins, FSH-induced conversion from PAF to AF’s first be completed and the BCP suppresses FSH, it follows when it comes to women launching COS coming off a BCP something needs to be done to cause a rise in FSH for 5-7 days prior to menstruation heralding the cycle of CO S. This is where overlapping the BCP with a GnRHa comes in. The agonist causes FSH to be released by the pituitary gland and if overlapped with the BCP for several days and this will (within 2-5 days) facilitate PAF to AF conversion…. in time to start COS with the onset of menstruation. Initiating ovarian stimulation in women taking a BCP, without doing this is suboptimal.
I strongly recommend that you visit www.SherIVF.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 IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• The Fundamental Requirements For Achieving Optimal IVF Success
• Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
• 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)
• Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
• 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 with Compromised Ovarian Response to Ovarian Stimulation: A Personal Approach.
• Egg Maturation in IVF: How Egg “Immaturity”, “Post-maturity” and “Dysmaturity” Influence IVF Outcome:
• Commonly Asked Question in IVF: “Why Did so Few of my Eggs Fertilize and, so Many Fail to Reach Blastocyst?”
• 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?
• Staggered IVF
• Staggered IVF with PGS- Selection of “Competent” Embryos Greatly Enhances the Utility & Efficiency of 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.
• IVF: Selecting the Best Quality Embryos to Transfer
• 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 outcome: How Does Advancing Age and Diminished Ovarian Reserve (DOR) Affect Egg/Embryo “Competency” and How Should the Problem be addressed.

___________________________________________________________
ADDENDUM: PLEASE READ!!
INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
Hitherto I have personally performed IVF- treatment and related procedures on patients who, elected to travel to Las Vegas to be managed by me. However, with the launching of Sher-Fertility Solutions (SFS) in April 2019, I have taken on a new and expanded role. Now, rather than having hands-on involvement I confine my services to providing hour-long online Skype consultations to an ever-growing number of patients (emanating from >40 countries), with complex Reproductive problems, who seek access to my input, advice and guidance. All Skype consultations are followed by a detailed written report that meticulously describes and explains my recommendations for treatment. All patients are encouraged to share this report with their personal treating doctor(s), with whom [subject to consent and a request from their doctor] I will, gladly discuss their case with the “treating Physician”.
Through SFS I am now able to conveniently provide those who because of geography, convenience and cost, prefer to be treated at home or elsewhere by their chosen Infertility Physician.
“I wish to emphasize to all patients with whom I consult, that in the final analyses, when it comes to management, strategy, protocol and implementation of treatment, my advice and recommendations are always superseded by that of the hands-on treating Physician”.

Anyone wishing to schedule a Skype consultation with me, can do so by: Calling my concierge (Patti Converse) at 1-800-780-7437 (in the U.S.A or Canada) or 702-533-2691, for an appointment. Patients can also enroll online on my website, http://www.SherIVF.com, or email Patti at concierge@SherIVF.com .
I was very recently greatly honored in receiving an award by the prestigious; International Association of Top Professionals (IAOTP). For more information, go to the press release on my website, http://www.sherIVF.com .

PLEASE HELP SPREAD THE WORD ABOUT SFS!

Geoff Sher

reply
Amanda

Transferred one non pgs tested embryo
7dp6dt- 108
10dpt- 469
13dpt- 2,720
Does this sound normal? I’m Witt yes the high numbers mean somethings wrong. First ultrasound next week.

reply
Jane

Hi Dr. Sher

I just had my blood test today for hCG and progesterone today.
My result is 118 for hCG
and 60 ng/mL

I’m worried sick that it will be a miscarriage, I have slight cramps in the stomach as well.

How do you think it looks?

reply
Dr. Geoffrey Sher

Impossible to say without follow-up blood testing and ultimately an US at 7 weeks.

Good luck!

Geoff Sher

reply
Jane

Thank you for your nasser.

I forgot to say that the last test was taken at 16dpo.

I’m going for another test tomorrow. Im hoping to see a number above 230.

Does the progesterone level say anything, I can read that it’s a bit on the high side.

reply
Jane

Thank you for your answer.

I just got news from my blood test today 18dpo, that the hCG levels are now at 302.

Which means that my data looks like this:

16dpo: hCG 118 – Progesterone 60ng/mL
18dpo: hCG 302

I had stomach cramps, but they have stopped now.

Does this seem normal, and is the pregnancy viable?

Best regards, Jane

Dr. Geoffrey Sher

I am cautiously optimistic and encouraged!

Good luck!

Geoff Sher

Melissa Gomez

Hello Dr, just looking for some feedback. 5 day embryo transferred on 12/9.
HCG levels at 8 days past= 92
Hcg at 10 days past= 148

I’m worried that it didn’t double. Should I be worried this isn’t viable? The blood work was taken at two different labs at around 47.5 hours difference (not full 48 hours)
Thank you!

reply
Dr. Geoffrey Sher

I would not be over-concerned, unless the hCG level fails to increase by doubling every 48h or so, from here on out!

Good luck!

Geoff Sher

Sophie

Hi Dr Sher,
I got a hcg of 14 12dp5dt, then 16dpt got a result of 131 and then 23dpt got a result of 2311. I have a scan booked for when I’ll be 6.5 weeks for viability but the nurses are very confident that this will likely be a blighted ovum or potentially an ectopic. They don’t seem to think viable pregnancy is a possibility at all. What do you think my odds are?

reply
Dr. Geoffrey Sher

I would not write this off yet. I have seen much stranger things happen.

Good luck and G-d bless!

Geoff Sher

reply
Allie

Hi Dr Sher,

I’m 8 weeks FET and I have a hematoma. I had heavy bleeding with clots twice so far. I was told to stop the baby aspirin I was because of the bleeding I am having . I also have Compound Heterogeneous MTHFR but my homocysteine were not elevated, it was a 5.5. Should I be concerned to stop the baby aspirin?

Thank you

reply
Dr. Geoffrey Sher

In my opinion, aspirin has no merit and I do not prescribe it in IVF cycles or during ensuing pregnancies.

Geoff Sher

reply
Allie

Thank you Dr Sher.

What are your thoughts on MTHFR and pregnancy risks? I have read a lot of scary possible outcomes.

Dr. Geoffrey Sher

The single mutation (heterozygous) is not that serious and requires folic acid supplementation. A double mutation (homozygous) is more serious and usually requites heparin (Lovenox therapy).

Geoff Sher

Allie

I have Compound Heterozygous MTHFR C677T & A1298C. Is that once of the severe ones?

Dr. Geoffrey Sher

It will probably require Lovenox therapy:

Thrombophilia (Hereditary Clotting Defect) is defined as the genetic predisposition to developing intravascular thrombosis. It is due to hypercoagulability of blood leading to impairment of initial vascularization that takes place during implantation.
Thrombophilia affects as many as one in five people in the United States and is responsible for pregnancy loss (most particularly after the 1st trimester) and “unexplained” infertility, as well as being a factor in some cases of “unexplained” IVF failure. Whether (and/or the extent to which) thrombophilia causes 1st trimester recurrent pregnancy loss (RPL) is the subject of debate and is controversial. In fact, first-trimester RPL is far more likely to be due to immunologic implantation dysfunction (IID) and/or irregularities in the contour of the uterine cavity or insufficient thickness of its lining (a thin endometrium). Thrombophilia has also been associated with late pregnancy-induced complications such as preeclampsia, premature separation of the placenta (abruptio placenta), placental insufficiency with intrauterine growth retardation, and in “unexplained” intrauterine death.
This having been said, it is a fact that most women with a thrombophilia go on to experience healthy pregnancies.
Diagnosis of Throbophilia
Thrombophilia is diagnosed when one or more of the following is detected:
• Mutational defect involving methylenetetrahydrofolate reductase (MTHFR), which occurs in at least 20% of affected cases. Homozygosity for a common C677T mutation in the MTHFR gene that is associated with hyperhomocysteinemia is the most common form of hereditary thrombophilia leading to a 3-fold increase in risk of complications.
• Mutation of factor V Leiden (FVL),
• A mutation of prothrombin G20210A,
• Deficiency of antithrombin III
• Deficiency of protein C
• Deficiency of protein S
Risk Factors
• Pregnant women with predisposing factors such as:
• A personal or family history of thromboembolism (deep vein thrombosis), pulmonary embolism (blood clot in the lung), cerebrovascular accidents (i.e. strokes)
• A personal history of pregnancy complications such as unexplained intrauterine death, preeclampsia, abruptio placenta, intrauterine growth retardation, placental insufficiency, should be tested for the condition.
Treatment
Treatment should be initiated as soon as possible after pregnancy is diagnosed biochemically (blood or urine hCG test) and be continued throughout gestation.
Severe thrombophilias (e.g. homozygous MTHFR mutations, protein C deficiency, prothrombin G20210A mutation) as well as cases of mild thrombophilias associated with one or more of the pregnancy complications mentioned above, are best treated with low-molecular weight heparin (LMWH).
For other (milder) thrombophilias and no history of prior pregnancy complications: Low-dose aspirin with the B vitamins folic acid, B6 and B12.

Geoff Sher

Renea

As of today I am 4 weeks, 1 day pregnant. I went in for my beta hcg test on Monday when I was 3 weeks plus 6. My hcg level was 90. This morning I went for a second test. I got a call that my level was 153 and tat was at the minimum so I have to go back again in 48 hours. Should I be worried?

reply
Dr. Geoffrey Sher

I am not at all pessimistic at this stage. Do another beta hCG in 2 days Hopefully it will double (or better)
Good luck!

Geoff Sher

reply
T

I got my first positive test at 11dpo, but at 15dpo my hcg was only at 20. Do you think this is a chemical pregnancy?

reply
Dr. Geoffrey Sher

I test result is not sufficient. You will need to repeat the test 2 days later . If it doubles, then there is a chance all will be fine. If not, perhaps repeat it 2 days later again and so forth.

Good luck!

Geoff Sher

reply
Tina Ebron

Hello Dr. Geoff Sher
I have suffered 2 miscarriages. First one 3/9/19 second one 9/19/19. I was suppose to get muy period again 11/17/19 but missed it. Checked my hcg levels on Tuesday 11/19/19 and hcg level was at 296 is this a good number to begin with

reply
Lindsey

Hello – This is my 6th round of infertility treatment. IUI in 2017, and I miscarried at 12 weeks; 4 unsuccessful IUIs after that. IVF Chemical pregnancy in May 2019. Just finished second round of IVF; I am 14dp5dt. Beta # 1 was 104, Beta #2 160. Feeling pretty low (numerically and emotionally). This doesn’t sound like a viable pregnancy, does it?

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
e. Ureaplasma Urealyticum (UU) Infection of cervical mucous and the endometrial lining of the uterus, can sometimes present as unexplained early pregnancy loss or unexplained failure following intrauterine insemination or IVF. The infection can also occur in the man, (prostatitis) and thus can go back and forth between partners, with sexual intercourse. This is the reason why both partners must be tested and if positive, should be treated contemporaneously.
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.

• The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
• 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
• Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
• 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: How Many Attempts should be considered before Stopping?
• “Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
• 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:
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF?

_______________________________________________________
ADDENDUM: PLEASE READ!!
INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
Hitherto I have personally performed IVF- treatment and related procedures on patients who, elected to travel to Las Vegas to be managed by me. However, with the launching of Sher-Fertility Solutions (SFS) in April 2019, I have taken on a new and expanded role. Now, rather than having hands-on involvement I confine my services to providing hour-long online Skype consultations to an ever-growing number of patients (emanating from >40 countries), with complex Reproductive problems, who seek access to my input, advice and guidance. All Skype consultations are followed by a detailed written report that meticulously describes and explains my recommendations for treatment. All patients are encouraged to share this report with their personal treating doctor(s), with whom [subject to consent and a request from their doctor] I will, gladly discuss their case with the “treating Physician”.
Through SFS I am now able to conveniently provide those who because of geography, convenience and cost, prefer to be treated at home or elsewhere by their chosen Infertility Physician.
“I wish to emphasize to all patients with whom I consult, that in the final analyses, when it comes to management, strategy, protocol and implementation of treatment, my advice and recommendations are always superseded by that of the hands-on treating Physician”.

Anyone wishing to schedule a Skype consultation with me, can do so by: Calling my concierge (Patti Converse) at 1-800-780-7437 (in the U.S.A or Canada) or 702-533-2691, for an appointment. Patients can also enroll online on my website, http://www.SherIVF.com, or email Patti at concierge@SherIVF.com .
I was very recently greatly honored in receiving an award by the prestigious; International Association of Top Professionals (IAOTP). For more information, go to the press release on my website, http://www.sherIVF.com .

PLEASE HELP SPREAD THE WORD ABOUT SFS!

Geoff Sher

reply
Lindsey Fuquen

Hi Dr. Sher – Thank you that was very helpful. Beta #3 went up to 514; so it’s going up! This still seems viable! So that would put me at 5 weeks with a beta of 514, so we’ll see!! I’ll definitely look into doing a Skype consultation.

reply
Layla Rehany

Hi Dr. Sher,

I took 2 pregnancy tests with positive results. Went for blood work 2 days past expected period with HcG of 474. Receptionist at my doctor office says this is low and wants me to repeat blood work in 10 days. Is there any reason for concern? Should I do repeat prior to the 10 days?

Thank you!

reply
Dr. Geoffrey Sher

I would repeat the blood test 2 days later to make sure it has at least doubled.

Geoff Sher

reply
Bellangele@gmail.com

Hello Dr, my Hcg at 11dp5dt was 2600 mUI/ml and went to 5900 at 13dp5dt. We transferred two untested embryos. I haven’t seen numbers this high in my research even with multiple pregnancies. I’m currently 5 weeks and will go in at 6weeks +4 for my first ultrasound. Have you seen numbers this high in your experience?

Thanks

reply
Cathleen

Hi Doctor Sher!

I had the following HCG values. Wondering if the huge jump btwn 19 and 21 is concerning because it’s doubling every 25 hours or so. Heard it could be molar?

15 DPO: 118
19 DPO: 773
21 DPO: 2813

I had an ectopic once, and despite some side cramping w/ this one, ultrasound showed what they thought was likely a teeny tiny gestational sac in uterus on 20 DPO. As such, I was feeling cautiously optimistic except the huge jump in HCG made me worry the other way!

Thanks in advance for calming my (likely paranoid) concerns!

reply
Kelly

Hi, I had a 5 day low grade mosaic embryo transferred on November 3. My HCG numbers are 8 at 7dpt, 46.5 at 14dpt and 84.33 at 16dpt. I feel like my numbers are on the low side, but trying to stay optimistic. I believe they are still in the normal range, but maybe it was a late implanter? Thoughts?

reply
Nikki

Do you have a follow up on how this played out? My numbers are similar
9dp 29
11dp 38
13dp 67
15dp 125

reply
Dr. Geoffrey Sher

This is an erratically slow rise, but I would not discount the possibility of a recovering implantation.

Only time will tell! I would wait 10-14 days and then do an ultrasound.

Geoff Sher

reply
Nicolina

Hi there! So I am 5 days passed my expected period, and my test lines are getting darker but they are not dark yet like I feel they should be at this point (with my other kids the lines were very strong at this point). I got blood work done yesterday and my hcg levels were only 64, but progesterone and estradiol looked fine. Any idea what could be going on? If this is not going to stick (which I’m totally fine with actually) how quickly will I know? This limbo stuff is so hard! Thank you for taking the time to respond to everyone!!

reply
Dr. Geoffrey Sher

Interpretation of the urine test can be subjective. I would repeat the quantitative hCG test in 2 days and if need be again 2 days later to determine if the levels are rising appropriately.

Geoff Sher

reply
Nicolina

Hey again Dr Sher, as you recommended I had two additional labs done, my results are as follows.
11/14: 64
11/16: 170
11/18: 440
First day of last period was 10/13, so these results, while doubling at an appropriate clip, are still “delayed” as in I should have seen these numbers days ago. What are your thoughts on why this might be happening? Should I be overly cautious about this pregnancy or once those numbers start growing I should just assume it’s a viable pregnancy? What kind of risks are associated with delayed hcg numbers? I have no history of miscarriages or issues getting pregnant if that is relevant information for your POV! Thanks in advance!!!!

reply
Dr. Geoffrey Sher

To the contrary, I am quite optimistic about this “pregnancy” being viable.

Please keep me in the loop.

Geoff Sher

reply
sarah

my HCG 10dp5dt was 347 , the 14dp5dt 2450, 18dp 7500
progesterone hovering around 90 atm
i hope I am tracking okay?

reply
Michelle

Thank you for the hope
Today’s results were 267 so climbing about the same. They did an ultra sound and nothing was showing. They have booked me in next Thursday for another ultra sound

reply
Dr. Geoffrey Sher

I concur with that decision, A repeat hCG level should also be measured in a few days time.

Geoff Sher

reply
Michelle

Just an update and to get your opinion. So I went for the 6 week ultrasound and they saw a sac that measured 4.5Weeks. The fertility doctor wants me to stop the progesterone and thinks I will miscarry naturally in a few days. What are your thoughts? Should i wait two more weeks? Is there a chance.
My HCG levels are below

Nov 8th – 50.7
Nov 12th – 187
Thursday Nov 14th -267
Tuesday Nov 18 – 600.36 – 5 weeks 1 day
Thursday Nov 21 – 1137.20 – 6 weeks 1 day

reply
Michelle

I am so glad we took your advise and waited. The doctor prescribed the medication and I said I have to be 1000 percent sure there is no baby. Guess what, there is a heart beat and the baby measures 6 weeks 3 days (I should be 7 weeks). The sac is 6mm and the baby is 4mm with a heart beat of 124. The HCG levels are still low but are still increasing 3612.7.

Tina Kumar

Hi i did a beta hcg test at 13dp3dt and it was 17.9 Doctor asked me to stop all medicines as its a non viable pregnancy. What are your thoughts? Should i stop all medicines or give it 2 more days

Michelle

Hi,
Here are my beta levels
1st beta @ 9dp6dt-16.2
11dp6dt-22.5
13dp6dt-62.5
15dp6dt-151.7
17dp6dt-357.6
22dp6dt-3,427 (5weeks6days)
It was a very slow start but my #s have been slightly more than doubling every 48 hours since my 3rd beta. Do you think this is a viable pregnancy? Or most likely blighted ovum? I’ve had no bleeding or cramping.

reply
Dr. Geoffrey Sher

It could well be a viable pregnancy. Do an US next week and you should have the answer.

Good luck!

Geoff Sher

Michelle Bronson

Today at 26dp6dt my gestational sac was measuring at 5weeks4days and my hcg was 9,928 but they could not see a yolk. Is this pregnancy most likely not viable?

Dr. Geoffrey Sher

I would do another US in 1 week before making a final determination.

Good luck!

Geoff Sher

Michelle

I did a 5 day blastocyst transfer on Oct 28th.
My HCG level on Nov 4th was 26.
But on Nov 6th it only went to 30.
Nov 8th – 50.7
Nov 12th 184
Doesn’t look great. The doctor is telling me i will miscarry

reply
Dr. Geoffrey Sher

I would not write this off quite yet!

Do an US in 10 days time and please keep me in the loop!

Geoff Sher

reply
Casey G

I had a 5 day transfer with 2 follicles

My first HCG level was 1,725 14dpo
2nd test had my HCG levels at 3715 16dpo

Does this sound like a multiple pregnancy?

reply
Sophie

I had a 5 day transfer on the 6th of nov.
Hcg taken 12 later was only 14. Had a repeat done 16 days post transfer and went up too 131. Any hope? Or likely to be non-viable?

reply
Dr. Geoffrey Sher

Yes there is hope. Do an ultrasound examination in about 2 weeks from now.

Good luck!

Geoff Sher

reply
Anxiously Waiting

Date of 1 embryo day 5 FET: 10/28 @12PM
1st beta hcg 11/6@7am- 7.09
Progesterone-21.34
E2-128
Any hope this will be promising?

reply
Jouline

Hi Dr. I did an IUI insemination on Oct 17th and did my first hcg today Nov 6. My cycle is usually 29 day. My hcg test is 131 is that normal? (Last day of past period was Oct 11)

reply
Lina

Hi,
We had a perfect blastocyst transferred oct 12. HCG 9 days later was 109, then at 12 days it was 296, and 16 days after transfer it was 1600. Is there high chance of viable pregnancy based on these numbers? I have very few symptoms, now 6+2, and very anxious.

reply
Lina

Thank you for your quick reply. You think the numbers look good?

I am so scared, the few symptoms I have (slightly tender breasts and slightly cramping, like in periode) keep coming and going.

reply
Allie

Hi Dr. Sher

I had my first HCG at 9 DPT 127.8 then second HCG at 11 DPT 388.1. PSG normal 6AA. I have a history of chemical miscarriages. All my other previous chemicals had very low HCGs. Do these numbers look promising for a good pregnancy?

Thanks!

reply
Dr. Geoffrey Sher

Not looking very promising…I am afraid! Repeat the beta in 2 days and hope for the best.

Sorry!

Geoff Sher

reply
Angela

My HCG is 25 today—9 days past 5 day transfer. An FET. The clinic said it is unlikely to be viable. Would you agree?

reply
Dr. Geoffrey Sher

I respectfully do not agree. This could be a viable pregnancy. Repeat the test in n2 days to see if it doubles.

Geoff Sher

reply
Chris P

Good afternoon Dr. Sher,

We transferred a day 5 PGS Normal embryo on 12/16. Our first beta was 12/27 HCG 470Beta two was this morning 12/29 HCG 531. Going back on Tuesday for Beta 3. Anyway we’re very concerned about that slow rise. Any insight you can give would be great.

Thank you! Chris

reply
Dr. Geoffrey Sher

It is of some concern but only time will tell. Rewpeat the test in 2 days and if thge lkevel continues to rise, do an US in 2-3 weeks .

Good luck and G-d bless!

Geoff Sher

georgia

i had my first beta at 10dp5dt and it was 170
my second was 47 hours later and it was 288.9
I had two early blastocysts transfed
is it still any hope for me?

reply
lorraine

Good morning Dr Sher
I did a beta blood test and hcg was 0.5miu/ml after4. 75 days after 5 day transfer. My clinic is saying its way to early.
Do you think i still have a chance of getting a positive result?

reply
Priscilla

Hi Dr Sher,

I had a 5-day FET on 10/16, first hcg level was 52 on 10/25, 83 on 10/28, 234 on 10/30 and 689 on 11/1

The numbers seem very low, do I still have hope for an ongoing normal pregnancy?

I am very concerned.

Thank you

reply
Dr. Geoffrey Sher

Frankly, I am not very concerned. Frankly, I am even cautiously optimistic.

Good luck!

Geoff Sher

reply
Matutina

Bonjour,

13 jours apres transfert d’un J5 mon Bhcg etait à 68. Y a-t-il encore un espoire?

reply
Claudia

Hi, I had a 2 5 day blastocysts transferred. My hcg numbers are were 32 at 5 dpt, 114 at 7dpt, 292 at 9dpt and 670 at 11dpt. I know that they are doubling and that is what is important, but do these numbers generally look ok ? The normal range is so varied that it’s hard to get a feel for what is good. Does normal doubling mean its more likely to be a singleton? thanks!

reply
Katie

Hi Dr. Sher,

I transferred one PGS tested normal day 6 embryo on 11/21. My hcg was 460 11 day post transfer and after 56 hours, my hcg was 1630. Should I be concerned for molar pregnancy as it has more than tripled? The two tests weren’t done in the same lab. I have my first ultrasound scan on 12/16. Thank you!

reply

Ask a question or post a comment

Your email address will not be published. Required fields are marked *