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 been looking at your webpage for several years now, but never had the courage to write to you – thought it would be too complicated, because we are from too far away (Denmark). But now we are about to loose hope, which is why I finally decided to contact you…
I am 35, my husband is 34. Both healthy, normal weight and normal bloodtests. I even had a culdoscopy, which was normal.
We have been together for 11 years – never pregnant before (any of us).
We have been trying to conceive since january 2014. In 2015 we found out, that my husbands spermquality was decreased (normal concentration 30 mio/ml but motility grade 2 (no progressive sperm)) – Since then the quality has been varying, both in concentration (sometimes low, sometimes normal) and quality.
We went straight to ICSI (and we have tried 3 different clinics).
1. ICSI: long protocol with menopur 112 IE. 8 eggs aspirated, 3 fertilized, none made it to day 5.
2. ICSI: long protocol, menopur 187 IE. 15 eggs aspirated, 4 fertilized, 1 blastocyst. Neg. pregnancy test.
3. ICSI: short protocol with Elonva and Bemfola. 17 eggs aspirated, 4 fertilized, no blastocyst (a 7-cell was put up on day three – neg. pregnancy test).
4. ICSI: short protocol, menopur 300 IE. 17 eggs aspirated, (6 to IVF, 11 to ICSI), a 9-cell was put back on day three, a grade 3AB blastocyst was frozen (didn’t make it to FET).
5. ICSI: short, pergoveris 225 IE, nothing on day 3.
6. ICSI: short, menopur262,5 IE, 10 eggs out, 8 fertilized, 1 blastocyst grade 3 (fragmented), neg. pregnancytest.
7. ICSI: short protocol, pergoveris 300 IE + prednisolone 10 mg, same picture, no eggs on day 3.
8. ICSI: short protocol, menopur 300 IE, 9 eggs aspirated, 7 mature and 6 fertilized with SPERMDONOR, 3 blastocysts (grade 4AB)!!
9. ICSI: same procedure with spermdonor, 11 eggs out, NO blastocysts!!
10. ICSI: with husbands sperm, one fragmented blastocyst which was frozen.
Two times we have calcium-activation of the eggs and one time we tried assisted hatching of the blastocyst.
Acupuncture and dietary supplementation, doing more or less exercise etc. no effect.
We have also tried 2 x IUI with my husbands sperm and 1xIUI with donorsperm without success.
We have tried FET with two of the donor-blastocysts, but neg. pregnancy test.
The endometrium is another problem – the first two ICSI’s the endometrium was around 8 mm., but since then it has decreased and usually it is around 4,5-6 mm, rarely 7-8 mm.
I have tried a mock-estrogen cycle with 2 mg estradiol x 3 + estradiol patch + viagra, but the endometrium reached only 4,6 mm after 3-4 weeks.
3 times (4th ICSI, mock-estrogen cycle and this last natural cycle) I have had fluid in the endometrial cavity (not in the salpinges) and clear, watery discharge. I believe this is because of medical stimulation (except this last cycle?).
I have a sparce period, bleeding only 1-2 days and almost nothing! (when I was young I had normal periods, bleeding heavily for 1-3 days and light for the rest, total 5-7 days). I used NuvaRing as prevention for 7 years, and I am afraid, that this has affected my endometrium…
Sometimes I think it is my immunesystem (I have never called in sick from work (except in case of fertility treatment).
We are so frustrated and scared that we will never be able to conceive. We have read a lot about this and we always try to pin out the problem and look for a solution – but it seems like we have problems in all aspects: decreased sperm quality, bad eggs (bad development) and thin endometrium.
And we have never had a positiv pregnancy test!
How can one couple be so unlucky?
Spermdonor has only been a partly success so far. We are thinking about eggdonor, but with that endometrium, it is probably also unlikely. Surrogacy is illegal in Denmark, but we have thought about it…but hopefully we won’t have to go there!
We are both doctors, I am actually specializing in pediatrics – but it kills me to think, that I might never have my own children.
Our fertility doctors are confused and don’t really have answers – and the same goes for us despite intensive studying…Next step is endometrial biopsy, but I they don’t do it at our clinic – and ofcourse another ICSI with donorsperm to see if that one ICSI with 3 good blastocysts was only luck.
They don’t really use intralipids or immuneglobulines anywhere near us (except in the public hospital 4 hours away, and we can’t be admitted there…)
Can you please help us Dr. Sher??
Is there any investigation or treatment you can recommend??
Kind regards TH
Hi Tanja,
My heart goes out to you. I am wondering whether the emphasis on the sperm issue might not be misplaced and that in fact both your poor lining, and poor egg/embryo quality are possibly linked to the protocol used for ovarian stimulation and/or its implementation. Yopu mainly used short (“flare”) protocols aare often associated with increased pituitary LH which in turn increases the ovarian testosterone production. The latter, if produced in excess can compromise egg competency as well as adversely affect endometrial response to estrogen and thus lead to a thin endometrium. This having been said, one thing that flies against this is the fact that even duringhormone replacement cycles (e.g. as with embryo adoption ), you apparently still had a poor lining (am I correct in this assumption?). Regardless, in my opinion it is ill-advised to transfer embryos to an endometrium which at the time of the trigger or administration of progesterone is <8mm. I simply never do this.
In my opinion, the protocol used for ovarian stimulation, against the backdrop of age, and ovarian reserve are the drivers of egg quality and egg quality is the most important factor affecting embryo “competency”. Certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can in my opinion, 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 women 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 capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” could significantly enhance the opportunity to achieve a viable pregnancy
Please visit my new Blog on this very site, https://www.drgeoffreysherivf.com, find the “search bar” and type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
• A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
• Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
• Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers should be the Standard of Care in IVF
• Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
• Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
• Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
• Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
• Preimplantation Genetic Testing (PGS) in IVF: It should be Used Selectively and NOT be Routine.
• Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
• PGS in IVF: Are Some Chromosomally Abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
• PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
• Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• The Role of Nutritional Supplements in Preparing for IVF
• Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
• IVF Egg Donation: A Comprehensive Overview
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 .
*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.
Geoffrey Sher MD
Hi Dr. Sher,
We are trying to conceive for many years, now. First we tried a few iui’s then 3x ivf in the last 1,5 years, without success. I’m 37 with Hashimotos -not taking meds, tsh 1,4, my husband has a lower sperm count. Can there be an immunological problem for the implantation failure? Or was it simply not the right embryo(we’ve had transfers always on day 2 or 3) I’m Kir AA, and my epitop c1 is pos, c2 neg.(my husband has the same epitop). Does this matter in getting pregnant? Do we still have a chance?
Thank you very much
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.
Geoff Sher
Thank you Dr. for your quick answer.
the thyroid disfunction may cause the infertility as well. So it is important to take thyroid meds or just try IL/steroids? And what about the immunology? Could our composition cause problems, too? I’m more afraid of that, I guess.
Thank you.
Hi, is there an alternative to steroids for nk cells and dq alpha match? I had a successful cycle on steroids and intralipids. I had an unsuccessful cycle on just intralipids. I don’t want to take steroids again as they affected my vision. Is there anything else that produces a similar effect?
To my knowledge not!
Sorry!
Geoff Sher
Hi my wife has DOR and she had a cancelled cycle at Cornell. She was on estrogen patch, clomid , Gonal F and menopur. She had the cycle cancelled due to low estrogen on day 11 and no follicular activity.
So we are going to try another cycle with estrogen priming, day 2 start with menopur and then cetrotide later on.
What do u think
Thanks in Adavance
In my opinion, the protocol used for ovarian stimulation, against the backdrop of age, and ovarian reserve are the drivers of egg quality and egg quality is the most important factor affecting embryo “competency”.
Women who (regardless of age) have DOR have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production of LH biological activity which can result in excessive LH-induced ovarian male hormone (predominantly testosterone) production which in turn can have a deleterious effect on egg/embryo “competency”.
While it is presently not possible by any means, to reverse the effect of DOR, certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can in my opinion, 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 women 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 capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” could significantly enhance the opportunity to achieve a viable pregnancy
Please visit my new Blog on this very site, https://www.drgeoffreysherivf.com, find the “search bar” and type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• The Fundamental Requirements For Achieving Optimal IVF Success
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
• A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
• Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
• Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• Blastocyst Embryo Transfers should be the Standard of Care in IVF
• Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
• Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
• Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
• Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
• Preimplantation Genetic Testing (PGS) in IVF: It should be Used Selectively and NOT be Routine.
• Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
• PGS in IVF: Are Some Chromosomally Abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
• PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
• Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• The Role of Nutritional Supplements in Preparing for IVF
• Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
• IVF Egg Donation: A Comprehensive Overview
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 .
*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.
Geoffrey Sher MD
Hello Dr. Sher,
I am 29 with DOR, AMH of 0.2. FSH 4-10, AFC 6. I have open tubes b/l but “indirect” evidence of scar tissue on my left tube, he thinks from my ureter coursing differently? I started my first IVF last month with 300 gonal f and 150 menopur along with femara +antagonist. My E2 was <20 after 8 days of stims and took a break for a week and then restarted stims. Unfortunately only one follicle developed but we decided to go through with retrieval. Not surprisingly no egg was retrieved and we did a rescue IUI which was silly in my opinion.
Thoughts on decreasing dose of menopur next cycle? Any other tweaks you would suggest? Desperately in need of some hope.
THANK YOU,
-LG
Forgot to mention, one thing I read below is that 250mcg ovidrel was not enough for a trigger, this is what I used.