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.
Hi Dr Sher,
First, thank you for such an informative series (and your staff’s how-to videos on doing IM injections -my husband and everyone we know in IVF-land appreciate them so much).
We are in our 3rd try with donor egg IVF (diminished ovarian reserve, AMH .1, FSH 16, age 42). My husband’s sperm and the donor’s eggs produced 13 good blastocysts, 6 AA and 7B, but we’ve had a fail with the first (fresh) and second (frozen) transfer. Beyond being somewhat overweight, which my RE said was not a problem, I am in good health, thyroid is at good levels (I’ve been on Synthroid for years), and my lining has always built up nice and thick during the first three cycles. My RE said I do have a 2cm fibroid but that it was nowhere near the implantation site so not anything he was worried about. By the way, we are transferring one embryo at a time as we are trying to avoid twins. No PGS was done as I was not offered it and didn’t learn about it until later, and he said it couldn’t be done to frozen embryos without risking losing them in re-freezing.
Our question for you is, if the 3rd try doesn’t work, do you think the blood testing for these immunological issues would we worth looking into, and if so, does your clinic do testing on people who are not doing transfers at your clinic? Our RE doesn’t do a lot of testing here in Portland, it’s a very small practice, and I’m worried that this is something we should possibly consider but that he won’t bring up as he’s said it’s the embryo that has the issues, not me (but hasn’t tested me for anything after the first two fails).
thank you.
Yes! immune testing is indicated. Most hypothyroidism has an immunologic basis (antithyroid antibodies) and regardless of whether you have clinical hypothyroidism or not , in 50% of such cases there will be activation of natural killer cells (NKa) causing immunologic implantatoion dysfunction.
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.
Please visit my new Blog on this very site, http://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
•Why did my IVF Fail
•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
•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!
•Uterine Fibroids and Fertility
•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.
•IVF Egg Donation: A Comprehensive 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
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.
Geoff Sher
After so many years of researching and being my own doctor when all of the rest have given up on you and diagnosed you with that dreadful “unexplained infertility” when you know in your heart that something ELSE is wrong. I then came across your blog and I cried because I know I have found something! I am 35 years old. I have had one miscarriage in 2009 at 8 weeks (the only time I was ever pregnant that I know of). I have been through an entire work up of infertility tests which ended in a laparoscopy with the conclusion of endometriosis stage 1 and a thick uterine lining which both were removed in surgery. That was supposed to “fix” me. I bleed through an ultra ob tampon every 30 minutes to an hour with sometimes golf ball size clots and cramps so horendous that you almost could not imagine such pain. After my surgery the bleeding was worse. For almost a year I had to take transenemic acid to slow the bleeding. I had accidents at work to where I was bleeding through a tampon and a pad every 15 minutes. I have been through two fertility doctors one which says this is normal. I do however have regular periods and so ovulate as I have so many symptoms I can tell you almost exactly when I am ovulating! I have a regular physician now who listens to me and tests me when I say I think something is wrong instead of ridiculing me. I have had my thyroid and hormones tested and had an endoscopy as well. The interesting test was my autoimmune which came back three times positive for scleroderma or crest syndrome. Though the only symptoms I have of that are Raynaud’s phenomenon and the esophageal disfunction. I have all of the symptoms of candida overgrowth but have not been tested. When I asked about that one with my first fertility doc they did all but laugh in my face. And he certainly didn’t believe that autoimmune disfunction has anything to do with infertility! Ugh! If I had only read this then! Anyways before I came across this I came across an article that there are MORE tests other than fertility to take and I read about antibodies. That led me to this. I have a prescription for an antiphospholids antibody test on May 5th along with an iron test for I am anemic as well. I guess my question is am I on the right track?? What do you think???? Thank you so much for your time! And thank you for not hiding behind those god awful words “unexplained infertility”!!!!!!
P.S. My fiancé has been tested as well..
Hi Melinda,
I am convinced from your history alonew that you have an immunologic implantation dysysfunction (IID). Moreover, endometriosis can set you up for IID (see below), as can Scleroderma. This needs to be identified, typified and addressed.
Please visit my new Blog on this very site, http://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
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•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.
•Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
•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?
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
•IVF Failure and Implantation Dysfunction: The Role of Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
•Why did my IVF Fail
•Secondary Infertility: Addressing the Root Causes
•Recurrent Pregnancy Loss (RPL): Why do I keep losing my Pregnancies?
•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)
•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!
. Endometriosis
•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
•Measuring and Interpreting Blood hCG to Assess Pregnancy Viability Following ART Treatments.
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
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.
Geoff Sher
Dear Dr. Sher,
Thank you for offering your patients this space to share with you their IVF journeys. I would like to ask you as PCOS woman 31 years old with 2 failed IVF cycles due to EFS . Taking into account that I was suffering form OHSS 2 times one in short protocol using 75 IU FSH and second cycle long protocol with 75 IU too in both cycles I have been triggered with 5000 IU. My AMH level shows high reserved Ovaries. I am good responder to stimulations but at the end the result wasn’t good as EFS was announced by my doctors and they are stucked without answer. My question here is there any ready solution available in the current time for my case and do you have similar cases????
I read the blog here and I see that you are supporting that every follicle contains Egg and EFS is misnomer. Definitely this gives me a hope that I am still having a good chance.
I read that Long pituitary protocol could help me to avoid having EFS is this correct? Do you apply coasting in long pituitary protocol because my doctor says coasting in my case isn’t not recommended as it will have bad impact on the egg quality?
Last question, about trigger shot , I read that recombined HCG is better than triggering only with pregnyl for treating EFS. DO you agree with this?
Thank you very much and looking forward for your reply
Regards,
Helen
My approach is consistently to use a long pituitary DR protocol with an agonist, coming off 1-2 months on the BCP. The latter is intended to lower LH and thereby reduce stromal activation (hyperthecosis) in the hope of controlling ovarian androgen release. I then stimulate with low dosage FSHr to which I add a smidgeon of LH/hCG (Luveris/Menopur) from the 3rd day and watch for the # of follicles and [E2] starting on the 7th day of COS. If there are > 25 follicles, I keep stimulating (regardless of the [E2] until 50% of all follicles reach 14mm. Then, provided the [E2] is >2500pg/ml, I stop the agonist and the gonadotropin stimulation and follow the E2 (only) daily, without doing further US examinations. The [E2] will almost invariably climb and I watch it go up (regardless of how high the concentration of E2reaches) and track it coming down again. As soon as the [E2] drops below 2500pg/ml (and not before then ever), I administer 10,000U hCGu or hCGf (Ovidrel/Ovitrel-500mcg) as the “trigger” and perform an egg retrieval 36h later. ICSI is a MUST because “coasted” eggs usually have no cumulus oophoris and eggs without a cumulus will not readily fertilize on their own. All fertilized eggs are cultured to blastocyst (up to 6 days). And up to two (2) are transferred transvaginally under US guidance.
The success of this approach depends on precise timing of the initiation and conclusion of “prolonged coasting”. If you start too early, follicle growth will stop and the cycle will be lost. If you start too late, you will encounter too many post-mature/cystic follicles (>22mm) that usually harbor abnormally developed eggs.
Use of the above approach avoids unnecessary cycle cancellation, severe OHSS, and optimizes egg/embryo quality. The worst you will encounter is mild to moderate OHSS and this too is uncommon.
I do not use antagonists in high responders (e.g., PCOS) because it interferes with the assay of E2 (often causing the value to be understated), a valuable index in assessing risk for the development of severe/critical OHSS. I also do not believe in the agonist trigger to prevent OHSS. The reason is that the magnitude of the induced LH surge varies and if too little LH is released, meiosis can be compromised, thereby increasing the oocyte aneuploidy index.
Please visit my new Blog on this very site, http://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
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•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.
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
•IVF Failure and Implantation Dysfunction: The Role of Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Why did my IVF Fail
•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)
•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!
•Uterine Fibroids and Fertility
•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.
•Implications of “Empty Follicle Syndrome and “Premature Luteinization”
•Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
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
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.
Geoff Sher
I’m 39 yrs old turning 40 in June and my amh is around 5.3
So I did my first round of IVF in January and it failed in egg retrieval step. The plan was for me to take lupron injections and Hmg (6 units) for two weeks prior retrieval. After the 4 first Hmg injections, my body started to make lots of estrogen, so we stopped Hmg injections after day 4 for a couple of days but I continued with lupron 10 units. Even with no Hmg still the estrogen was doubling up. We went back to Hmg 3 units after 3 days , estrogen started to double up again. Finally when I had 9 follicles around 20-25 mm they did the retrieval. But of all 9 follicles, 8 were empty and only 1 egg retrieved. And unfortunately even that one didn’t make it to a blastocyst.
I really want to know what went wrong and what I can do to prevent that in my next try.
I really appreciate the time and energy you put in answering my question.
Best regard
Respectfully,
This approach is in my opinion not ideal for ovarian stimulation. Please read below!
Please visit my new Blog on this very site, http://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
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•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.
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Implications of “Empty Follicle Syndrome and “Premature Luteinization”
•Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
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
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.
Geoff Sher
Dear Dr,
1) Upon administration of Ganirelix, how much does LH fall? For example, would giving Ganirelix .25mg when LH is 3 to 7 bring LH level to 0?
2) what would happen if LH falls from 7 to 0? Will the follicles that are developing disappear?
250 mcg of Ganirelix should within a few days, bring LH to near zero. This needs in my opinion to be accompanied by feeding a small amount of Menopur daily.
Geoff Sher