Ask Our Doctors – Archive
Our Medical Directors are outstanding physicians that you will find to be very personable and compassionate, who take care to ensure that you have the most cutting-edge fertility treatments at your disposal. This is your outlet to ask your questions to the doctors.
Hello Dr. Sher,
I am 31 yrs old, today is CD 11 and this is my second month on Clomephene. Unlike last month, my doctor gave me Gonal-f 75 iu on D3 and another 75 iu on D4 along with Clomephene. However, there were only 2 follicles that were 9mm each on CD8 (EL was 4). So he gave FSH 150 iu injection on D8. But follicle did not grow on CD10, so he gave me HMG 150 iu on CD10 and another 150 iu on CD11. I think the total has been 600 units till CD11. In my last cycle (first time use of Clomephene), I had a fully mature follicle (22mm) on CD40 and got my periods on day 49. Do you think that my follicles would grow to be mature this month? At this rate of growth, on which cycle day do you think I might ovulate?
I am not optimistic about this cycle.
Also, in my opinion, it would be preferable to use only gonadotropins (and not combine this with clomiphene).
Good luck!
Geoff Sher
Hi Dr. Sher,
We are a healthy couple in early 30’s that already passed 2 IVF’s (fresh) and 3 FET’s (frozen) procedures in a clinic considered of high quality in Brazil. All these transfers were made with day-3 embryos graded 8A or 8B, except for one FET, that we sucessfully transfered from day-5 blastocysts. My wife has hashimoto’s (controlled with Synthroid) and I have Varicocele (but with normal sperm tests).
Unfortunately, in all these 5 attempts, we’ve transfered a total of 10 embryos and we’ve got 0 (zero) hcg blood results.
Our doctor did several blood tests (including kariotype testing, prolactin testing and thrombophilia testing) and exams (like a hysteroscopy and a testicular ultrasound) with both of us and everything seems normal . During our late IVFs and FETs, we also did some scratching and acupuncture treatments.
Our doctor always point us that the cause of the recurring failures is because of unexplained or genetic issues. Reading your blog, we came to assume that we may be experiencing Immunologic Implantation Dysfunction (IID). Unfortunately IID investigation is not common in Brazil so we may have to travel abroad.
We remain with 5 frozen embryos, but with lower quality. After these previous attempts, we are also kind of Psycologically broken.
Finally, we would appreciate your opinion about what to do next:
1 – transfer these 5 remaining embryos in 2-3 FETs?
2 – genetically test (PGS) these 5 remaining embryos? (note: PGS them will cost the same as 2-3 FETs (first option))
3 – Start a new IVF treatment?
4 – Investigate IID abroad?
We want to thank you in advance for your patience and knowledge. We really want to discover what’s going wrong and achieve our dream of being parents.
Thank you for creating this blog. It is awesome!
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.
I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•The Fundamental Requirements For Achieving Optimal IVF Success
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•Blastocyst Embryo Transfers Should be the Standard of Care in IVF
•Why did my IVF Fail
•Blastocyst Embryo Transfers Done 5-6 Days Following Fertilization are Fast Replacing Earlier day 2-3 Transfers of Cleaved Embryos.
•Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
•The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
•Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
•Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
•Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
•Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
•Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
•Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
•How Many Embryos should be transferred: A Critical Decision in IVF.
•The Role of Nutritional Supplements in Preparing for IVF
Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
•Email: Julied@sherivf.com
•Phone: 702-533-2691
?800-780-7437
Geoff Sher
I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
PS:
Finally, we would appreciate your opinion about what to do next:
1 – transfer these 5 remaining embryos in 2-3 FETs?
A: Perhaps so but only after you have tested for and/or addressed an IID
2 – genetically test (PGS) these 5 remaining embryos? (note: PGS them will cost the same as 2-3 FETs (first option)
A: I think it would be too traumatic on these embryos to thaw tem for biopsy only to refreeze them again while awaiting results nd then have to re-thaw for FET
3 – Start a new IVF treatment?
Only if/after the FET fails
4 – Investigate IID abroad?
A:olutely think this would be prudent and to do so we should talk (see above)!
Dr. Sher,
Is there a difference between a Lupron flare protocol and a microdose Lupron flare protocol? I just failed my third IVC cycle using what was called a Lupron flare protocol (20 units of Lupron that was not diluted, 300 follistim, 2 vials menopur starting day 3). Stimulation was very slow this time and took 11 days. Triggered because E2 starting to decrease (maxed at 1500) but lead follicle only 17mm. 15 eggs retrieved but none where mature and several were atretic. Wondering if too much Lupron caused this. I’m thinking this wasn’t the best protocol for me. I’m 38, no PCOS, good AMH, normal BMI. First cycle was long Lupron and got 15 eggs with most mature, 5 embryos, but none normal by PGS. Second cycle was antagonist and got 13 eggs, 3 mature, 1 normal by PGS was transferred but miscarried at 8 weeks. Trying to decide if I should keep trying after the last cycle was so poor.
Women who (regardless of age) have diminished ovarian reserve (DOR) tend to produce fewer and less “competent” eggs, the main reason for reduced IVF success in such cases. The compromised outcome is largely due to the fact that such women tend to have increased LH biological activity which often results in excessive LH-induced ovarian testosterone production which in turn can have a deleterious effect on egg/embryo “competency”.
Certain ovarian stimulation regimes either promote excessive LH production (e.g. short agonist/Lupron- “flare or microflare” protocols, clomiphene and Letrozole), augment LH/hCG delivered through additional administration (e.g. high dosage menotropins such as Menopur), or fail to protect against body’s own/self-produced LH (e.g. late antagonist protocols where drugs such as Ganirelix/Cetrotide/Orgalutron that are first administered 6-7 days after ovarian stimulation has commenced).
I try to avoid using such protocols/regimes (especially) in those with DOR, favoring instead the use of a modified, long pituitary down-regulation protocol (the agonist/antagonist conversion protocol-A/ACP) augmented by adding supplementary human growth hormone (HGH). I further recommend Staggered IVF with embryo banking of PGS (next generation gene sequencing/NGS)-normal blastocysts in such cases. This type of approach will in my opinion, optimize the chance of a viable pregnancy per embryo transfer procedure and provide an opportunity to capitalize on whatever residual ovarian reserve and egg quality still exists, allowing the chance to “make hay while the sun still shines”.
Older women as well as those who (regardless of age) have diminished ovarian reserve (DOR) tend to produce fewer and less “competent” eggs, the main reason for reduced IVF success in such cases. The compromised outcome is largely due to the fact that such women tend to have increased LH biological activity which often results in excessive LH-induced ovarian testosterone production which in turn can have a deleterious effect on egg/embryo “competency”.
Certain ovarian stimulation regimes either promote excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), augment LH/hCG delivered through additional administration (e.g. high dosage menotropins such as Menopur), or fail to protect against body’s own/self-produced LH (e.g. late antagonist protocols where drugs such as Ganirelix/Cetrotide/Orgalutron that are first administered 6-7 days after ovarian stimulation has commenced).
I try to avoid using such protocols/regimes (especially) in older women and those with DOR, favoring instead the use of a modified, long pituitary down-regulation protocol (the agonist/antagonist conversion protocol-A/ACP) augmented by adding supplementary human growth hormone (HGH). I further recommend Staggered IVF with embryo banking of PGS (next generation gene sequencing/NGS)-normal blastocysts in such cases. This type of approach will in my opinion, optimize the chance of a viable pregnancy per embryo transfer procedure and provide an opportunity to capitalize on whatever residual ovarian reserve and egg quality still exists, allowing the chance to “make hay while the sun still shines”.
Hi Dr. Sher:
I recently found out that my FET worked, and at only 7 days post transfer a home pregnancy test came out positive. On Friday my hcg was 93 and today it was 842. I had two embryos transferred, and was wondering if this could be any indication that it is multiples? Or could the hcg be too high, should I be worried?
It could be…but only time and an ultrasouynd done 2 weeks from now can tell.
Good luck!
Geoff Sher
Hi Dr Sher,
I’m 43 and have had 3 miscarriages and one ectopic pregnancy. I’ve just had an overseas donor egg procedure after 2 assisted (ovulation trigger) and two stim IVF cycles were unsuccessful. We had one high quality blast transferred. This also doesn’t seem to have worked as I got my period today, however I have some questions for my treatment going forward as we have 4 frozen day 6 blasts. I have high NK cells and heterozygous MTHFR A1298C variant mutation. For this donor cycle I was prescribed intralipid transfusion therapy (I had two transfusions, one 10 days prior to transfer and one 5 days before) as well as prednisolone on tapering increase to 20mg day of transfer. I took Lupron as a down regulator day 1. I am on progynova oral 8mg daily (tapering increase from day 3) and gestone IM 100mg daily (from 5 days before transfer). I am also on clexane SC 40mg daily (from day 3 – to counteract the progynova???) and 100mg aspirin – I had one blood test showing slightly elevated anticardiolipin levels (follow up tests were normal). My lining has always been very good. I have three small uterine fibroids that hysterscopy and scans show are not a concern with normal endometrial cavity. After exhaustive testing of myself and my partner (karyotyping, APS, etc) there appear to be no other identified issues.
Do I need this much pred if I am having the intralipids? Do I need the aspirin and clexane daily? My immunologist recommended I do not have clexane the day of the transfer, why might this be? What are your thoughts on the other medications? What are your thoughts on number of embryos to transfer? Any other thoughts going forward?
The first thing needed is to identify the cause of your immunologic implantation dysfunction (i.e. Is it autoimmune or Alloimmune –see below). The treatment differs when the NK cell activation is due to autoimmune versus alloimmune causation. If you do not do so , you might keep spinning your wheels. I suggest we talk.
I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
•Why did my IVF Fail
•Recurrent Pregnancy Loss (RPL): Why do I keep losing my Pregnancies
•IVF Failure and Implantation Dysfunction:
•The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
•Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
•Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
•Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
•Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
•Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
•Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
•Email: Julied@sherivf.com
•Phone: 702-533-2691
?800-780-7437
Geoff Sher
I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.