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,
I have been taking levothyroxine for Hashimotos for the past 24 years. I was diagnosed with PCOS as a teen and put on birth control. I have been trying to get pregnant since the end of 2018 and finally decided to see an ER in March of 2020. I just completed my first IUI cycle and am waiting the two weeks to see if I am pregnant. I have been taking metformin for insulin resistance, levothyroxine, estradiol vaginally and progesterone suppositories. I have noticed that my hair shedding has increased significantly and am worried that this is not a good sign for the possible beginning of pregnancy. What would be causing this given that most of my hormonal issues have been addressed with medication? I’ve been under the belief that hair loss is not a good sign when it comes to overall health and this has been something that I’ve dealt with for years.
Hair loss is a feature of hypothyroidism and as you know ,m Hashimoto’s is an autoimmune cause of most female hypothyroidism. The remedy is an appropriate balancing of thyroid hormone levels with supplementation.
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.
•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) Why did my IVF Fail
•Recurrent Pregnancy Loss (RPL): Why do I keep losing my Pregnancies
•Genetically Testing Embryos for IVF
•Staggered IVF
•Staggered IVF with PGS- Selection of “Competent” Embryos Greatly Enhances the Utility & Efficiency of IVF.
•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.
•IVF: Selecting the Best Quality Embryos to Transfer
•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?
•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!
•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
•Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year
•A personalized, stepwise approach to IVF
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Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.
If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or, enroll online on then home-page of my website (www.SherIVF.com).
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Geoff Sher
Dr. Sherr,
Thank you for your prompt reply to my earlier question on ovulating on the BCP. You are stating: “If a balanced, monophasic BCP is used, it should NOT allow ovulation to occur.” It appears that Ortho-Novum 1/35 is just that. And I had taken active pills CD1 to CD27.
1. Would you NOT interpret E2 of 274 pg/ml and a 35mm x 25mm cyst on CD28 -a day after stopping active pills – as having ovulated? What could they mean?
2. If I truly had ovulated, would it be useless to take Ortho-Novum before FET?
Thank you so much again.
Nelly
1. Would you NOT interpret E2 of 274 pg/ml and a 35mm x 25mm cyst on CD28 -a day after stopping active pills – as having ovulated? What could they mean?
A: Not at all!
2. If I truly had ovulated, would it be useless to take Ortho-Novum before FET?
A: But you did not ovulate.
Geoff Sher
Hi Dr Sher,
I am 37 and have been trying to conceive for 5 years with no luck at all. I’ve never been pregnant. We have had 7 embryo transfers of “high quality” embryos however none have implanted.
I have done immune tests at my clinic and my NK, NK-T And B cells are low. My activated NK cells were low the first time and high the next time we tested.
My T regulatory and Th1 cells were also low but Th2 cells were high and T1 to T2 ratio high.
They tried a few cycles using intralipids, steroids, aspirin, clexane but still not pregnancy. I have also down a course of medicinal mushrooms but they didn’t work.
I am now moving to donor eggs.
Do you think it could my undiagnosed egg quality Or it could it be an immunological problem. Am I right to move to donor eggs now?
I have requested a consultation with you.
Thank you.
Dr. Sher,
I’m a 39 yr old who has been trying to conceive for the last 3 years. (I’m about to turn 40 later this year.) I did get pregnant through IUI 3 years ago but miscarried at 9 weeks due to Trisomy 13. After recovering emotionally we started our IVF journey and have had 4 cycles. My FSH hovers between 9 and 10 , not sure what my AMH is but was diagnosed with unexplained infertility.
Cycle 1 – was stimulated with Gonal F and Meopur, Cetrotide, triggered with Ovidrel. Resulted in 10 eggs, 9 mature and 8 fertilized naturally. 2 were good quality blasts and transferred, but did not work.
Cycle 2 – stimulated with Gonal F and a low dose HCG, Cetrotide, triggered with Ovidrel. Resulted in 12 eggs, 10 mature, 8 fertilized. 2 were good quality blasts and transferred. None worked.
After the 2nd cycle, I was have a major reaction to the progesterone supplementation and was later diagnosed with a progesterone hypersensitivity. (my reaction was hives, dizziness, fatigue, nausea, and other gestational issues) Cycle 3 was a freeze all cycle and each transfer was done through a natural cycle.
Cycle 3 – stimulated with Gonal F and a low dose HCG, Cetrotide, triggered with Ovidrel. Resulted in 24 eggs, 19 mature, 16 fertilized naturally. 4 were good quality blasts and transferred. None worked.
I went to a different RE at this point who had me go through a progesterone desensitization during Cycle 4 – stimulated with Gonal F and Menopur, Cetrotide, Leuprolide/PREGNL trigger. Resulted in 26 eggs, 19 mature, and 15 fertilized naturally. 2 were excellent quality so we transferred on day 3. We let the remaining embryos grow to day 5. 2 were up to the lab quality that were able to be frozen. None of these blasts worked.
Before I consider a cycle 5 (and final, I can’t do this anymore emotionally) is this purely a numbers game considering my age or should I consider a change in stimulation medications?
Any advice would be appreciated.
Dawn
Dear Doctor,
I would like to ask about so analysis as KIR. What do you think about it?
I am reading this article -https://www.sciencedirect.com/science/article/pii/S1472648316305028
and I am thinking, should it be done?
I have read this interesting article before. However, presently, it is premature to introduce KIR and HLA-C typing to predict pregnancy outcome. Sometime in the future selecting for certain combinations of KIR and HLA-C variants may prove useful.
Geoff Sher
My initial hcg test was 20. Two fays later it was 91. Thid was before my missed period. About 5 days before. Is this normal?