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Frozen Embryo Transfer (FET): What Does it Involve?

by Dr. Geoffrey Sher on November 4, 2015

Frozen Embryo Transfer (FET) A frozen embryo transfer cycle is initiated by administering an oral contraceptive (OC) to the recipient. This is later overlapped with Lupron daily for 5-6 days. The OC is then withdrawn, but the daily Lupron injections are continued until the onset of menstruation. Next, the Lupron dosage is reduced and intramuscular (IM) estradiol valerate (Delestrogen) is administered every 3 days. The objective of the estradiol is to achieve and sustain an optimal plasma E2 concentration of 500pg/ml-1000pg/ml and a 9mm endometrial lining as assessed by ultrasound examination. Intramuscular and/or intravaginal progesterone is administered daily starting about 6 days prior to the FET and continued along with twice weekly IM Delestrogen until the 10th week of pregnancy or until it has been confirmed that the patient is not pregnant.

Daily oral dexamethasone commences with the Lupron start and continues until a negative pregnancy test or until the completion of the 8th week of pregnancy. Then it is tapered down and discontinued. The recipient also receives prophylactic oral antibiotics starting with the initiation of Progesterone therapy, until the day after ET. Usually we would thaw vitrified blastocysts with the objective of having 1, 2 or 3 for transfer; depending on a couple’s stated preference. Commencing on the day following the ET, the patient inserts a vaginal progesterone suppository daily and this is continued until the completion of the 8th week of pregnancy or until a negative pregnancy test.

As an alternative regimen for women who cannot tolerate intramuscular Progesterone (PIO), we prescribe either Crinone vaginal gel or Endometrin vaginal inserts according to protocol. If you would like to explore one of these options, talk to your physician. For blastocyst FET’s, the blood pregnancy tests are performed 13 days and 15 days after the first progesterone administration is commenced.

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  • Alexandra - September 22, 2018 reply

    Hi Dr. Sher,
    Thank you for reading my email. Well, I have lean PCOS and have had 2 failed NC-FET with top quality day 5 embryos. I’ve decided to do another NC-FET but with supplemental progesterone (Urtogestan 100mg). I used Letrozole 5mg this cycle to help induce my ovulation, which worked great. I ended up with 2 large follicles about the same size 23-24mm on each ovary.
    1) is it possible to have 2 corpus Luteums and if so, would the output of progesterone be even higher in that case?
    2) I’ve heard several opinions about Urtogestan dosage. One Dr. says 100mg at bedtime and the other x2 100mg a day. Would 100mg be sufficient?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - September 22, 2018 reply

    I do not believe in NC FET’s. In my opinion, it is much more difficult to pinpoint the exact window of implantation and success rates are lower.

    Geoff Sher

  • Eva - September 17, 2018 reply

    Hi Dr Sher,
    Do you always prescribe dexamethosone for IVF, and if so, when do you start for fresh cycles?
    I’m 38, doing IVF for MFI.

    My first clinic started me on dexa during stimulation and had me on if for about 8 weeks when I had a fresh transfer success on my second IVF. Unfortunately that ended in MC at 12 weeks. I switched clinics because that one didn’t offer PGS.

    I’ve since had 3 FETs with pgs normal embryos fail, though we only discovered some uterine adhesions before the most recent FET. (Removed during hysteroscopy)
    Since we’ve had a high rate of normals (avg 70%) we are going to try a fresh transfer again as that worked before. My current clinic prescribes 5 days of a corticosteroid up to transfer. I’m wondering if I should replicate my successful cycle and ask for dexamethosone in case of some autoimmune issue. I do have hashimotos thyroid but it’s been controlled for many year.
    Thanks!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - September 17, 2018 reply

    I always prescribe a steroid such as dexamethasone , starting with the stimulation and ending by the 10th week of pregnancy (tailing it off between the 8th and the 10th week). But that is not the most important aspect of your case. If you have Hashimoto’s autoimmune hypothyroidism, you have a 50:50 chance of having NK cell activation which causes an immunologic implantation dysfunction and this needs thorough assessment.

    Between 2% and 5% of women of the childbearing age have reduced thyroid hormone activity (hypothyroidism). Women with hypothyroidism often manifest with reproductive failure i.e. infertility, unexplained (often repeated) IVF failure, or recurrent pregnancy loss (RPL). The condition is 5-10 times more common in women than in men. In most cases hypothyroidism is caused by damage to the thyroid gland resulting from of thyroid autoimmunity (Hashimoto’s disease) caused by damage done to the thyroid gland by antithyroglobulin and antimicrosomal auto-antibodies.
    The increased prevalence of hypothyroidism and thyroid autoimmunity (TAI) in women is likely the result of a combination of genetic factors, estrogen-related effects and chromosome X abnormalities. This having been said, there is significantly increased incidence of thyroid antibodies in non-pregnant women with a history of infertility and recurrent pregnancy loss and thyroid antibodies can be present asymptomatically in women without them manifesting with overt clinical or endocrinologic evidence of thyroid disease. In addition, these antibodies may persist in women who have suffered from hyper- or hypothyroidism even after normalization of their thyroid function by appropriate pharmacological treatment. The manifestations of reproductive dysfunction thus seem to be linked more to the presence of thyroid autoimmunity (TAI) than to clinical existence of hypothyroidism and treatment of the latter does not routinely result in a subsequent improvement in reproductive performance.
    It follows, that if antithyroid autoantibodies are associated with reproductive dysfunction they may serve as useful markers for predicting poor outcome in patients undergoing assisted reproductive technologies.
    Some years back, I reported on the fact that 47% of women who harbor thyroid autoantibodies, regardless of the absence or presence of clinical hypothyroidism, have activated uterine natural killer cells (NKa) cells and cytotoxic lymphocytes (CTL) and that such women often present with reproductive dysfunction. We demonstrated that appropriate immunotherapy with IVIG or intralipid (IL) and steroids, subsequently often results in a significant improvement in reproductive performance in such cases.
    The fact that almost 50% of women who harbor antithyroid antibodies do not have activated CTL/NK cells suggests that it is NOT the antithyroid antibodies themselves that cause reproductive dysfunction. The activation of CTL and NK cells that occurs in half of the cases with TAI is probably an epiphenomenon with the associated reproductive dysfunction being due to CTL/NK cell activation that damages the early “root system” (trophoblast) of the implanting embryo. We have shown that treatment of those women who have thyroid antibodies + NKa/CTL using IL/steroids, improves subsequent reproductive performance while women with thyroid antibodies who do not harbor NKa/CTL do not require or benefit from such treatment.

    Unless tests for immunologic implantation dysfunction (IID) are performed correctly and conducted by a one of the few reliable reproductive immunology reference laboratory in the United States, treatment will likely be unsuccessful. . In this regard it is most important that the right tests be ordered and that these be performed by a competent laboratory. There are in my opinion only a handful of reliable Reproductive Immunology Laboratories in the world and most are in the U.S.A. Also, it is my opinion that far too often, testing is inappropriate with the many redundant and incorrect tests being requested from and conducted by suboptimal laboratories. Finally for treatment to have the best chance of being successful, it is vital that the underlying type of IID (autoimmune IID versus alloimmune) be identified correctly and that the type, dosage, concentration and timing of treatments be carefully devised and implemented.
    Who Should Undergo IID testing?
    When it comes to who should be evaluated, the following conditions should in always raise a suspicion of an underlying IID, and trigger prompt testing:
    • A diagnosis of endometriosis or the existence of symptoms suggestive of endometriosis (heavy/painful menstruation and pain with ovulation or with deep penetration during intercourse) I would however emphasize that a definitive diagnosis of endometriosis requires visualization of the lesions at laparoscopy or laparotomy)
    • A personal or family history of autoimmune disease such as hyper/hypothyroidism (as those with elevated or depressed TSH blood levels, regardless of thyroid hormonal dysfunction), Lupus erythematosus, Rheumatoid arthritis, dermatomyositis, scleroderma etc.)
    • “Unexplained” infertility
    • Recurrent pregnancy loss (RPL)
    • A history of having miscarried a conceptus that, upon testing of products of conception, was found to have a normal numerical chromosomal configuration (euploid).
    • Unexplained IVF failure
    • “Unexplained” intrauterine growth retardation due to placental insufficiency or late pregnancy loss of a chromosomally normal baby
    What Parameters should be tested?
    In my opinion, too many Reproductive Immunologists unnecessarily unload a barrage of costly IID tests on unsuspecting patients. In most cases the initial test should be for NK cell activation, and only if this is positive, is it necessary to expand the testing.
    The parameters that require measurement include:
    o For Autoimmune Implantation Dysfunction: Autoimmune implantation dysfunction, most commonly presents with presumed “infertility” due to such early pregnancy losses that the woman did not even know she was pregnant in the first place. Sometimes there as an early miscarriage. Tests required are: a) blood levels of all IgA, IgG and IgM-related antiphospholipid antibodies (APA’s) directed against six or seven specific phospholipids, b) both antithyroid antibodies (antithyroid and antimicrosomal antibodies), c) a comprehensive reproductive immunophenotype (RIP) and, c) most importantly, assessment of Natural Killer (NK) cell activity (rather than concentration) by measuring by their killing, using the K-562 target cell test and/or uterine cytokine measurement. As far as the ideal environment for performing such tests, it is important to recognize that currently there are only about 5 or 6, Reproductive Immunology Reference Laboratories in the U.S capable of reliably analyzing the required elements with a sufficient degree of sensitivity and specificity (in my opinion).
    o For Alloimmune implantation Dysfunction: While alloimmune Implantation usually presents with a history of unexplained (usually repeated) miscarriages or secondary infertility (where the woman conceived initially and thereupon was either unable to conceive started having repeated miscarriages it can also present as “presumed” primary infertility. Alloimmune dysfunction is diagnosed by testing the blood of both the male and female partners for matching DQ alpha genes and NK/CTL activation. It is important to note that any DQ alpha match (partial or complete) will only result in IID when there is concomitant NK/CTL activation (see elsewhere on this blog).
    How should results be interpreted?
    Central to making a diagnosis of an immunologic implantation dysfunction is the appropriate interpretation of natural killer cell activity (NKa) .In this regard, one of the commonest and most serious errors, is to regard the blood concentration of natural killer cells as being significant. Rather it is the activity (toxicity) of NK cells that matters as mentioned. Then there is the interpretation of reported results. The most important consideration is the percentage of target cells “killed” in the “native state”. In most cases a level of >10% killing should be regarded with suspicion and >12% overtly abnormal. In my opinion, trying to interpret the effect of adding IVIG or Intralipid to the sample in order assess whether and to what degree the use of these products would have a therapeutic benefit is seriously flawed and of little benefit. Clinically relevant NK cell deactivation can only be significantly effected in vivo and takes more than a week following infusion to occur. Thus what happens in the laboratory by adding these products to the sample prior to K-562 target cell testing is in my opinion likely irrelevant.
    There exists a pervasive but blatant misconception on the part of many, that the addition of Intralipid (IL) /immunoglobulin-G IVIG) can have an immediate down-regulatory effect on NK cell activity. This has established a demand that Reproductive Immunology Reference Laboratories report on NK cell activity before and following exposure to IVIG and/or IL. However, the fact is that activated “functional” NK cells (NKa) cannot be deactivated in the laboratory. Effective down-regulation of activated NK cells can only be adequately accomplished if their activated “progenitor/parental” NK cells are first down-regulated. Thereupon once these down-regulated “precursor” NK cells are exposed to progesterone, they will begin spawning normal and functional NK cells, which takes about 10-14 days. It follows that to assess for a therapeutic response to IVIG/IL therapy would require that the patient first be treated (10-14 days prior to embryo transfer) and thereupon, about 2 weeks later, be retested. While at 1st glance this might seem to be a reasonable approach, in reality it would be of little clinical benefit because even if blood were to be drawn 10 -14 days after IL/IVIG treatment it would require an additional 10 days to receive results from the laboratory, by which time it would be far too late to be of practical advantage.
    Neither IVIG nor IL is capable of significantly suppressing already activated “functional NK cells”. For this to happen, the IL/IVIG would have to down-regulate progenitor (parent) NK cell” activity. Thus, it should be infused 10-14 several prior to ovulation or progesterone administration so that the down-regulated “progenitor/precursor” NK cells” can propagate a sufficient number of normally regulated “functional NK cell” to be present at the implantation site 7 days later. In addition, to be effective, IL/IVIG therapy needs to be combined with steroid (dexamethasone/prednisone/prednisolone) therapy to down-regulates (often) concomitantly activated T-cells.
    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.
    • 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!

    If you are interested in my advice or medical services, I urge you to contact my patient concierge, ASAP to set up a Skype or an in-person consultation with me. You can also set this up by emailing concierge@sherivf.com or by calling 702-533-2691 and/or 800-780-743. You can also enroll for a consultation with me, online at http://www.SherIVF.com.
    Also, my book, “In Vitro Fertilization, the ART of Making Babies” is available as a down-load through http://www.Amazon.com .

    Geoffrey Sher MD

  • Kristin - April 26, 2018 reply

    Hi Dr. Sher- I’m curious as to your input… My first FET with a day 6 euploid blast failed and I’m looking back before proceeding again and wondering if my PIO timing was miscalculated. I started my first PIO injection (.5ml) the evening of 3/13 and continued (1.0 ml) each evening till 3/17 (5 days PIO total). We transferred mid-day on 3/18 (6th day) but, prior to my PIO injection that evening. Without the benefit of an ERA, did we miss the mark in terms of standard days/hours of PIO injections prior to transfer? I’m just wondering if I should have transferred after having 6 complete doses of PIO beforehand with a transfer on 3/19 (day 7).

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - April 26, 2018 reply

    WE also do the FET on day-6 of progeste3rone shots.

    I am NOT a believer in the value of ERA.

    Geoff Sher

    Kristin - April 26, 2018 reply

    Thank you!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - April 27, 2018 reply

    You are welcome!

    Geoff Sher

  • Jessica - March 20, 2018 reply

    Hi Dr. Sher,
    I am preparing for my first FET this month. I have 6 frozen embryos. At my lining check yesterday, 1 week before the planned transfer I measured 7mm and they said they saw the triple layers. However, they have delayed by transfer and added 2 mg estrace taken vaginally to the 6 mg I was already taking spaced out over the day. They are giving me 4 days then a repeat ultrasound to see if it is above 8 in order to proceed. Do you see it increasing by 1 mm over 4 days? I am confused as to why it is not thicker anyways. I have always had a thick enough lining, even on clomid and at egg retrieval it was 8.5mm ( we did freeze all for stage 4 endo) is the lupron keeping it thin? I was on bc pills for a little over 3 weeks and did lupron overlap, starting at 20 units, npw down to 10. I asked about why my estrace doses were lower than some that I have seen and they mentioned it was because of my endometriosis. What would you do differently and why do you thick my lining is slow to grow all of a sudden?

    Thanks,
    Jessica

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - March 20, 2018 reply

    Respect6fully,

    I am not a fan of oral estrogen to prepare the lining. In my opinion parenteral E2 or Skin patches does much better. Ideal thickness is >9mm. Less than <8mm is sub-optimaL in my opinion.

    Geoff Sher

    Geoff Sher

  • Rhonda - February 20, 2018 reply

    Dr. Sher, I am 38, and had 1 IVF cycle (October 2017) which resulted into 6 PGS normal embryos; but I have had 2 failed FET’s (December 2017 and January 2018). My lining was 8.7 and 10 respectively, and good E2 levels in both; but my doctor believes I have endometriosis; and has advised this time to do two months Loestrin continuously (hormone therapy); then proceed with Delestrogen and PIO. Question, Is this a good plan or your opinion on the plan would be great? Thank you for your time and insight.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - February 21, 2018 reply

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

    • 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?
    • The Role of Nutritional Supplements in Preparing for IVF
    If you are interested in seeking my advice or services, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com You can also apply online at http://www.SherIVF.com .

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

    Geoffrey Sher MD

  • Kathleen - February 7, 2018 reply

    Hello, I’m preparing for a frozen embryo transfer and was given the option to start lupron on day 21 of this current cycle for an end of March transfer or start birth control pills and then do the lurpon with my march cycle for a mid April transfer. Do you recommend one over another? I obviously would like the one that has the higher chance of success in pregnancy a d live birth but I’m not sure if there have been studies on which protocol of suppression works best.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - February 7, 2018 reply

    I would recommend option 2.

    Geoff Sher

    Kathleen - February 7, 2018 reply

    Thank you sir!

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - February 8, 2018 reply

    You are welcome!

  • Tonya B - November 14, 2017 reply

    My daughter was due to take her trigger shot tonight and begin intramuscular prednisone tomorrow. After labs and ultrasound this morning with a 6.5 lining, they’ve put her on patches and told her to come back in two days. Can the patch increase lining in two days?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 14, 2017 reply

    Hi Tonya,

    I hope I turn out to be totally wrong but I really doubt whether estrogen patches for 2 days will change much.

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

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

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

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

    “The Viagra Connection”

    Eighteen years ago years ago, after reporting on the benefit of vaginal Sildenafil (Viagra) for to women who had implantation dysfunction due to thin endometrial linings I was proud to announce the birth of the world’s first “Viagra baby.” Since the introduction of this form of treatment, thousands of women with thin uterine linings have been reported treated and many have gone on to have babies after repeated prior IVF failure.

    For those of you who aren’t familiar with the use of Viagra in IVF, allow me to provide some context. It was in the 90’s that Sildenafil (brand named Viagra) started gaining popularity as a treatment for erectile dysfunction. The mechanism by which it acted was through increasing penile blood flow through increasing nitric oxide activity. This prompted me to investigate whether Viagra administered vaginally, might similarly improve uterine blood flow and in the process cause more estrogen to be delivered to the basal endometrium and thereby increase endometrial thickening. We found that when Viagra was administered vaginally it did just that! However oral administration was without any significant benefit in this regard. We enlisted the services of a compound pharmacy to produce vaginal Viagra suppositories. Initially, four (4) women with chronic histories of poor endometrial development and failure to conceive following several advanced fertility treatments were evaluated for a period of 4-6 weeks and then underwent IVF with concomitant Viagra therapy. Viagra suppositories were administered four times daily for 8-11 days and were discontinued 5-7 days prior to embryo transfer in all cases.

    Our findings clearly demonstrated that vaginal Viagra produced a rapid and profound improvement in uterine blood flow and that was followed by enhanced endometrial development in all four cases. Three (3) of the four women subsequently conceived. I expanded the trial in 2002 and became the first to report on the administration of vaginal Viagra to 105 women with repeated IVF failure due to persistently thin endometrial linings. All of the women had experienced at least two (2) prior IVF failures attributed to intractably thin uterine linings. About 70% of these women responded to treatment with Viagra suppositories with a marked improvement in endometrial thickness. Forty five percent (45%) achieved live births following a single cycle of IVF treatment with Viagra The miscarriage rate was 9%. None of the women who had failed to show an improvement in endometrial thickness following Viagra treatment achieved viable pregnancies.

    Following vaginal administration, Viagra is rapidly absorbed and quickly reaches the uterine blood system in high concentrations. Thereupon it dilutes out as it is absorbed into the systemic circulation. This probably explains why treatment is virtually devoid of systemic side effects

    It is important to recognize that Viagra will NOT be effective in improving endometrial thickness in all cases. In fact, about 30%-40% of women treated fail to show any improvement. This is because in certain cases of thin uterine linings, the basal endometrium will have been permanently damaged and left unresponsive to estrogen. This happens in cases of severe endometrial damage due mainly to post-pregnancy endometritis (inflammation), chronic granulomatous inflammation due to uterine tuberculosis (hardly ever seen in the United States) and following extensive surgical injury to the basal endometrium (as sometimes occurs following over-zealous D&C’s).

    Combining vaginal Viagra Therapy with oral Terbutaline;
    In my practice I sometimes recommend combining Viagra administration with 5mg of oral terbutaline. The Viagra relaxes the muscle walls of uterine spiral arteries that feed the basal (germinal) layer of the endometrium while Terbutaline, relaxes the uterine muscle through which these spiral arteries pass. The combination of these two medications interacts synergistically to maximally enhance blood flow through the uterus, thereby improving estrogen delivery to the endometrial lining. The only drawback in using Terbutaline is that some women experience agitation, tremors and palpitations. In such cases the terbutaline should be discontinued. Terbutaline should also not be used women who have cardiac disease or in those who have an irregular heartbeat.
    About 75% of women with thin uterine linings see a positive response to treatment within 2-3 days. The ones that do not respond well to this treatment are those who have severely damaged inner (basal/germinal) endometrial linings, such that no improvement in uterine blood flow can coax an improved response. Such cases are most commonly the result of prior pregnancy-related endometrial inflammation (endometritis) that sometimes occurs post abortally or following infected vaginal and/or cesarean delivery.
    Viagra therapy has proven to be a god send to thousands of woman who because of a thin uterine lining would otherwise never have been able to successfully complete the journey “from infertility to family”.

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

    If you are interested in my advice please contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com You can also apply online at http://www.SherIVF.com .
    *FYI
    The 4th edition of my newest book ,”In Vitro Fertilization, the ART of Making Babies” is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

    Geoff Sher

  • Oly - November 2, 2017 reply

    Hi I was on 4mg Progynova 3times a day to thicken my endometrium before the FET and was asked to continue plus 400mg Cyclogest bd and 100mg progestan inj daily. I’m 6days after the FET. My question is :isn’t the Progynova dosage supposed to be reduced by now

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - November 2, 2017 reply

    No! It should not be reduced at this point!

    Geoff Sher

  • Abby - August 22, 2017 reply

    Hey dr sher, I was just on my fifth day of progesterone for a transfer tomorrow but unfortunately my utuerus is contracting and lining has thinned from my last check on Friday in which it was perfect and ready to go. My doctor wants to continue my estrace 3x a day and start Lupron Thursday. The Lupron and estrace will overlap in until I stop estrace on Tuesday. When would a Lupron period begin?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - August 23, 2017 reply

    Abby,

    I am not sure I understand, but regardless, I can tell you that at this time you need to follow the advice of your treating RE implicitly.

    Good luck!

    Geoff Sher

  • Angela - July 9, 2017 reply

    Thank you so much for replying Dr Sher. I am almost 43 and have now done 7 fresh cycles and 2 frozen cycles, 1 natural and 1 medicated. A lot is riding on this last medicated frozen cycle due to my age. 2 top grade embryos were transferred, one day 5 and one day 6 and my pregnancy test is tomorrow. I was just worried that my estrogen may have been too high and my progesterone too low for implantation to occur due to the high estrogen dosage. I have suffered 3 miscarriages, 1 chemical and 1 blighted ovum and are still praying to have a miracle baby Thank you again Angela 🙂

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 9, 2017 reply

    I understand and responded accordingly!

    Geoff Sher

  • Angela - July 9, 2017 reply

    Dear Dr Sher, my question is regarding a frozen medicated cycle. My concern is if you think that the cycle may of been comprised due to high estrogen and not enough progesterone ie 2 x crinone per day ? I was instructed to continued on the same estrogen dosage after transfer as well ie 6 x 2mg tablets and a 100 patch.
    Your opinion would be greatly appreciated thank you

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 9, 2017 reply

    No! I do not believe it likely was compromised.

    Geoff Sher

  • Angela - July 9, 2017 reply

    Would you increase the progesterone dose if you were on a high estrogen dose ie 6 progynova tablets plus one estrogen patch? Do you think 2 x crinone a day is adequate?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 9, 2017 reply

    2 Crinone per day should suffice.

    Geoff Sher

  • Macy - September 25, 2016 reply

    Dear Dr Sher, My question is about FET and Progynova. Usually i am very punctual with my medicines but yesterday I missed two doses of progynova. i was prescribed progynova for FET cycle and I was supposed to be taking 2 tablets of Progynova ( 2 mg ) three times in a day i.e about 12 mg progynova per day. I took morning dose at 10 AM and then I forgot doses at lunch and dinner time. ie just 4 mg instead of 12. I realized that at 4 AM ( after 18 hours of first dose) in morning and immediately took one dose. did I screw my FET cycle? Pls advice. I will be very grateful if you answer my question.
    macy

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - September 25, 2016 reply

    I doubt this alone would compromise the cycle significantly.

    Good luck!

    Geoff Sher

  • Maria - July 20, 2016 reply

    Dr. Sher, Why is Lupron used in FETs? My understanding is that it induces an LH surge, which is not required for ovulation during FET, and it also reduces estrogen, which will need to be increased for implantation through injections or patches. Thank you.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 20, 2016 reply

    It is not absolutely esse3ntial but in my opinion it helps negate ovarian hormone contribution and thus enhance endometrial response. Bear in mind that the negative effect of LH is on the ovarian follicles and eggs, not on the endometrium.

    The Lupron starts about 5-7 days prior to stimulation and by the time the estrogen therapy begins the increased LH has dissipated and the ovaries are quiescent…the desired effect.

    Geoff Sher

    Maria - July 20, 2016 reply

    For someone with good endometrial response, would you still recommend Lupron for FET? Also, what do you mean by “stimulation” in a FET scenario?

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - July 20, 2016 reply

    Hormonal (estrogen/progesterone ) replacement therapy. I do not think it is absolutely essential, but I do believe it is the optimal approach and one that I favor for my patients.

    Geoff Sher

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