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 am scheduled for a FET on Feb 11 (my lining is 9mm+ and all looks good). I am on 50 mcg of levothyroxine and my TSH level unexpectedly increased from 2.086 mIU/L on Jan 14 to 4.197 mIU/L today. I started the medication when it was 5.75 mIU/L on Dec 23. Would you proceed with the transfer based on that level (4.197 mIU/L) or postpone it by one week? I’m increasing my dose to 75 mcg starting today.
Your advise is much appreciated!
My only concern is that you might have an undiagnosed immunologic implantation dysfunction associated with 5)% of women who harbor thyroid antibodies.
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 several Pre-scheduled “Batches” per Year
•A personalized, stepwise approach to IVF
______________________________________________________
ADDENDUM: PLEASE READ!!
INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
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).
PLEASE SPREAD THE WORD ABOUT SFS!
Geoff Sher
Hi there – at 10dp5dt my beta was 446. At 13dp5dt, beta was 1159. Increase of 89% in 48 hrs or double every 52 hours. Is this concerning at all or considered on the slower end? It’s slower than my first pregnancy which is why I’m concerned. I also keep reading that beta not doubling in 48 hours is abnormal
I would not be overly concerned. Get an US done at 6-7 weeks for a more definitive answer.
Good luck!
Geoff Sher
I gave birth in 1993 After IVF at your Marin County, Ca. My daughter is 27 and has very little health problem, but thru genealogy I have learned my husbands family , every female in his Family, great grandma, grandma, mother and sister all has had cancer and died before age 40. Sister only female over 40 in family. They carry the gene, my daughter is almost a identical twin to her grandma, my daughters PCP said gene usually comes through the mother, but she is a IVF baby, 7 embryos in, 3 implanted , miscarried 2 at 16 weeks, one healthy baby at 37 weeks. Should I be concerned ,?
Great hearing from you!
I suggest you seek out a genetic counselor in your area.
Please keep me in the loop!
I send you and yours my love and best wishes!
Geoff Sher
Hi Dr. I hope you are still answering questions… I’m confused about hcg numbers. We did iui on the 19th of January had 4 large folicles. There is no fertility issues as well. 11dpo tested positive. Went to Dr’s 13dpo they said hcg is at 65. How do I understand the numbers. Is 65 high? Could it mean multiple pregnancy? Thank you.
The level is raised but needs to double or better in 2 days…Repeat!
Geoff Sher
Thank you Dr. Sher.
I think my last post did not show up properly. I am 35 and husband is 30. No explained fertility issues. I went through 1st cycle of IVF at age 28 (2013) and transferred 2 frozen embryos the first time, had fraternal twin boys. I developed hypothyroidism after my first pregnancy, currently taking eltroxin (synthroid)
I just went through IVF cycle #2 in June 2020, had 1 poorly graded fresh embryo transfer – it was a negative outcome.
I just had a frozen 4bb 5day blastocyst transfer on Jan 13, 2021. On progesterone oil injection every 3rd day, Estrace twice a day and endometrin inserts 3 times per day.
Last TSH was 3.06
Jan 22 – 1st HCG = 11
Jan 24 – 2nd HCG = 21
Jan 26 – 3rd HCG = 70
SYMPTOMS: mild cramping, pulling and stretching from the lower abdomen to lower vaginal cavity, some light pink spotting today.
Early Ultrasound Feb 9.
My nurse told me to prepare for the worse as these low numbers look unlikely for a Viable pregnancy, but continue with medication until ultrasound. What are your thoughts on this?
I would not give up on this pregnancy. Repeat the blood hCG in 2 days and do a confirming US at 6-7 weeks.
Good luck!
Geoff Sher