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.
Hello Dr. Sher:
I recently had a FET. They transferred 2. I got a positive HCG on Monday of 1118 and on Tuesday I started cramping and bled light red/pinkish for then it stopped and turned into brown spotting Wedneday I had another HCG and it went up to 2209 but bled a little darker red then turned again into brown spotting. Could I have miscarried? It wasn’t alot of bleeding like to soak a pad. Right now I still have the brown spotting only
I think you need an ultrasound early next week to determine what is happening.
Good luck!
Geoff Sher
So if I have an antithyroid Antibody blood draw will it tell if I have an autoimmune disorder/disease?
No! If it is +ve then you nwill need to do a NK cell activity test (the K-562 target cell test). Only if that too is +ve will there be a potential Immunologic Implantation 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.
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 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!
•Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
•Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
•A personalized, stepwise approach to IVF
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.
Dr. Sher, I am currently on day 20 of IUI cycle and my doctor just found I did not ovulate from my left ovary. There were two follicles (20 and 18mm at the time of trigger shot-day 13 of the cycle). There were another two follicles (22 and 19mm) on the right side from which I did ovulate. Can the leftover follicles on the left side decrease my chances to get pregnant in this cycle or make any later problems?
Thank you very much
I doubt it Hannah!
Goo0d luck!
Geoff Sher
Hi Dr.Sher,
I started taking gonapeptyl 0.1mg starting on day 2 of my cycle ( estrogen was at 200 pmol/l). After 7 days, I went for ultrasound and there was one follicle (15mm), no cysts anywhere and endometrial lining was 5mm. But estrogen was at 580 pmol/l. So I couldn’t start stimulation today.
Is this normal to see a follicle after 1 week of supression? I am more concerned about me taking additional drugs and not achieving any improvement.
Regards.
Hi Madhu,
I would need much more information to respond authoritatively here.
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,
My wife and I have just gone through our first IVF cycle in Australia with poor results, 2 follicles on the left and only 1 small immature follicle on the right, unfortunately no eggs were collected which was quite a shock. My wife’s AMH levels came back as a 3 when we were initially tested at the start of our journey 6 months ago. The the IVF clinic informed us that their testing is not able to read AMH levels below 3 so we are unsure of her exact AMH reading. My wife & I turned 36 earlier this year (Aug) and are concerned with her DOR. Is this common in your experience that there was follicles present but no eggs were found..?
Another thing I would like clarified is regarding her ovarian stimulation FSH hormone Gonal F & Ganarelix (Orgalutran) that we were taking. After what I feel was not being properly informed by our clinic she continued to take both stimulants after having the trigger injection 36hrs prior to egg collection which I believe was the 25omg not the 10000 one you spoke of in another article. The instructions from our clinic were not clear whether or not to continue taking the gonal & orgalutran so she had it on both days prior to egg collection. Could this also have been an influencing factor as to why there were 2 mature size follicales but no eggs present..? Our Dr today advised that her Estrogen levels seemed to respond well to the FSH and were in the normal range and the follicle sizes were 18.9 & 15.7 or something along thise lines and that having continued the 2 hormones in the day of the trigger and the following day would not have played a role in the zero egg count.
I would appreciate a second opinion as we are going to try another cycle in 2 months time to see if we get a similar result and if again no eggs are collected are we then destined to only go down the path of an egg donor, something my wife is hesitant of for obvious reasons.
Any help and feedback would be much appreciated.
Thankyou Kindly
Peter Basis