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.
Dear Dr Sher
I have had ongoing problems with my endometrium in both fresh and FET cycles: I miscarried 1 chromosomally normal conceptus, and had a recently chemical pregnancy of a PGS tested blastocyst
I have been treated for NKa (with steroids, intralipids and clexane), however my lining has been a consistent issue throughout all my natural and IVF cycles, and my Dr believes is the key underlying problem. My endometrium has been difficult to stimulate in my cycles (2 FET were cancelled due to non responsive lining). I have not menstruated properly since coming off the pill to start TTC: even when my lining has grown, I do not get a proper bleed, just black/brown clotty spotting.
Although I did reach 8.5mm (with very high doses of both endogenous and exogenous oestrogen, vaginal viagra and a G-CSF wash) in my most recent cycle, after ceasing progesterone after the chemical pregnancy was confirmed, I did not bleed at all.
A hysteroscopy this week revealed a healthy looking endometrium, but some minor filmy adhesions and a small fundal calcified area, although no formal Asherman’s. These were easily removed with saline flushing and did not require surgical resection.
Before we embark on another treatment cycle, the goal is to get me regularly menstruating, and encourage my endometrium to consistently both grow and shed normally. A copper IUD was inserted at the end of my hysteroscopy, and I have commenced cyclo-progynova + pentoxifylline + tocopherol therapy. The plan would be to do at least 2-3 such cycles before removing the IUD.
Would you recommend vaginal viagra be added to the protocol during the white (estradiol valerate) pills part of the cyclo-progynova cycle?
Kind regards
Katy
Alas, Vaginal Viagra might not work in your case because it sounds very much as if previous endometritis might have permanently damaged the innermost (basal/germinal) layer of your endometrium from which a new lining has to develop each cycle. If this has been intractably damaged, then you might not be able to respond to estrogen properly, even with hormonal supplementation, antiprostaglandins and Viagra. You might in fact need a gestational carrier. We really should talk and the sooner the better!
I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•The Fundamental Requirements For Achieving Optimal IVF Success
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•IVF Failure and Implantation Dysfunction:
•Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
•IVF-Gestational Surrogacy: An Overview
Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
•Email: Julied@sherivf.com
•Phone: 702-533-2691
?800-780-7437
Geoff Sher
I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Hello Dr. Sher,
I came here for advice, since I am so confused as to what direction to proceed. I turned 40 2 months ago. My husband and I have been trying to conceive since I was 35, with not one pregnancy. I started seeing fertility specialists several years back, but kept hoping for a natural conception. My latest AMH was .37 and FSH was 18. Back in February it was .9 and 7.8. 2 years ago AMH was less than .16. I also have antithyoid antibodies, take synthroid, have APA antibodies and tested positive for natural killer cells and embryo toxicity. I have never tried IVF with my own eggs. What would you recommend? I feel so hopeless. I take many supplements and go to acupuncture.
Hi Paula,
There are 2 issues. The 1st is your severely diminished ovarian reserve (DOR) and the second is your immunologic implantation dysfunction (IID).
The DOR:
I wish we could have communicated on this before your AMH dropped to 0.3ng/ml. Now, it is likely that IVF with egg donation might be your best option. Notwithstanding it might still be possible to try for a longer shot, with own eggs. You see…the older a woman becomes, the more likely it is that her eggs will be chromosomally/genetically “incompetent” (not have the potential upon being fertilized and transferred, to result in a viable pregnancy). That is why, the likelihood of failure to conceive, miscarrying and of giving birth to a chromosomally defective child (e.g. with Down Syndrome) increases with the woman’s advancing age. In addition, as women age beyond 35Y there is commonly a progressive diminution in the number of eggs left in the ovaries, i.e. diminished ovarian reserve (DOR). So it is that older women as well as those who (regardless of age) have DOR have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production of LH biological activity which can result in excessive LH-induced ovarian male hormone (predominantly testosterone) production which in turn can have a deleterious effect on egg/embryo “competency”.
While it is presently not possible by any means, to reverse the age-related effect on the woman’s “biological clock, certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can make matters worse. Similarly, the amount/dosage of certain fertility drugs that contain LH/hCG (e.g. Menopur) can have a negative effect on the development of the eggs of older women and those who have DOR and should be limited.
I try to avoid using such protocols/regimes (especially) in older women and those with DOR, favoring instead the use of the agonist/antagonist conversion protocol (A/ACP), a modified, long pituitary down-regulation regime, augmented by adding supplementary human growth hormone (HGH). I further recommend that such women be offered access to embryo banking of PGS (next generation gene sequencing/NGS)-selected normal blastocysts, the subsequent selective transfer of which by allowing them to to capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” could significantly enhance the opportunity to achieve a viable pregnancy (*see below)
Your IID:
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
•Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
• A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
•Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
•Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
•Optimizing Response to Ovarian Stimulation in Women who Have Compromised Ovarian Response to Ovarian Stimulation in Women who Have Compromised Ovarian Reserve: A Personal Approach.
•Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Blastocyst Embryo Transfers Should be the Standard of Care in IVF
•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.
•Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
•Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
•Preimplantation Genetic Testing (PGS) in IVF: It Should be Used Selectively and NOT be Routine.
•Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
•PGS in IVF: Are Some Chromosomally abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
•PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
•IVF: The first Choice for Infertile Women 40 to 43 Years of Age!
•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
•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!
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
•IVF Egg Donation: A Comprehensive Overview
•Advancing Age of the Woman and IVF: How Old is too old?
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.
Hi Dr. Sher,
I just had a failed IVF cycle. I had 13 mature eggs, 9 fertilized & 4 blastocysts made it to day 6. We sent them off for genetic testing & all came back as abnormal. I want to try IVF again but wanted your opinion on the best protocol for me. I’m almost 39 years old & did the antagonist protocol w no estrogen priming for my 1st one. My RE recommended the estrogen priming protocol for next IVF. Is that what you would recommend? She didn’t put that on me originally since had good follicle count for my age & respond well to the medications. Also I just started taking DHEA too to help egg quality. Please let me
Hi Dr. Sher. I just had twins with our first ever IVF + PGS cycle! 🙂 We have 4 frozen embryos remaining and I have two questions, I’ll make it short. 1.) Two of our blastocysts are 3BB graded. We only want 1 more baby, but are hesitant to put back only 1. What are the chances blastocysts of that grade both implanting? 2.) We have 2 day 6 embryos one is graded 4BA. Since it’s a day 6, is our 3BB a better option to transfer? Thank you kindly for your time.
I would not suggedst >1 blastocyst be transferred in light of your not wanting >1 baby, and especially if your remaining blastocysts are all PGS-normal. And yes, I would use the 3BB blastocyst.
Geoff Sher
Hi Dr. Sher! I am writing to you regarding a blighted ovum diagnosis I received this week. While I am certainly able to accept the diagnosis if it is inevitable, my husband and I have strong feelings that it’s too early to make a call. I had mirena removed early May, and my cycles were fairly abnormal for a few months. I had my last cycle on 8/8, and got a positive lh surge on an ovulation test the late afternoon of 8/23. I was also testing my BBT, which spiked substantially on 8/26. Based on my charting, I feel quite confident we conceived 8/24 or 8/25. We tested positive for pregnancy on 9/5, and had an appointment with the doctor on 10/3. Gestational dating would then put me at 8 weeks, although dating from conception would put me about 5w4d. Two ultrasounds were completed, and they observed nothing but an empty gestational sac measuring normal for a 6 week pregnancy. Hope seemed glim, and I was sent to test HCG. 10/3 HCG was 39,772. 10/5 HCG was 46,964 at about 45 hours. I was called into the office on Thursday, and was diagnosed blighted ovum. We were told the levels should have doubled, and even if my levels were unique or slow rising, the ultrasound on 10/3 would have seen more for a viable pregnancy. My husband is a nurse, and we have found so much conflicting information about when a BO should be diagnosed, as well as misinterpretation of such high HCG levels. I’m your experience, have you found it possible to date incorrectly and see only a sac with such high HCG levels? I have had no spotting or bleeding, and am struggling greatly with the idea of a D&C in the event it could have just been to early to know for certain. Any guidance would be greatly appreciated. Thank you so much!
Sadly Hillary,
By this stage, an ultrasound diagnosis should be definitive. There would be no harm in giving it another week, but there is in my opinion also no point in waiting. Whatever you decide, please be certain to have the products of conception collected and karyotyped for chromosomal configuration.
So sorry!
G-d bless!
Geoff Sher