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
38 yrs, AMH less than 0.2, FSH 66 LH 54!!
I wanted to freeze my eggs as I don’t have a partner to have kids with but I was told I have become premature menopause!
I have still periods much less in length and bleeding compared to before but has not stopped yet.
Some months it’s only 2,3 days of light bleeding
My FSH and LH were less than 10 only 4 months back ( did not check AMH ) back then
Doctors told me egg freez chances r very low but I have no other option now and want to try before my period stops. Do u think it is a sensible decision or most likely nothing will come out of it?
I have started CoQ10, DHEA 25mg*3. I get headaches but do u think it’s good to take DHEA until the procedure starts or it is harmful and I better not take it?
Regards
Shishi
With that level of DOR, I honestly do not believe egg freezing is a wise decision.
Geoff Sher
Should I ask my RE for the endometrial receptivity test? I am trying to have a second baby but I only have two frozen embryos (day 5 blastocyts) and will not be doing any more IVFs due to my age (43). Below is my medical history:
May 2013 Fresh IVF (2 embryos transferred) resulted in ectopic pregnancy confirmed by ultrasound
November 2014 Frozen embryo transfer (1 embryo transferred) resulted in suspected ectopic or a biochemical
March 2014 Fresh IVF (1 embryo transferred) resulted in biochemical
May 2014 Fresh IVF (2 embryos transferred) resulted in successful pregnancy (1 baby).
My question essentially is that since IVF or FET (except for my last fresh IVF which was successful) always resulted in either ectopic or biochemical pregnancies for me, does that mean that the endometrial receptivity test would be helpful in choosing the timing of my transfer for my upcoming FETs. Are biochemical/ectopic pregnancies indicative of a receptive or nonreceptive uterus?
Very respectfully, I do not believe in a benefit for the ERA. That is my opinion. You must decide based upon advice from your personal RE.
Geoff Sher
Hi Dr Sher
What is the normal range of Beta HCG for 7dp5dt? This is my 3rd FET (transfered 2 blastocysts) and the result is HCG=44, could it be a chemical pregnancy? Progesterone = 50 (based on 3x duphaston a day, + 100units of PIO injection every 2 days, + 6 utrogestuan inserts per day)
For the same woman , is it possible that HCG levels vary significantly across different healthy pregnancies.
Thanks
That is a clear +ve and while it could be a chemical pregnancy, I doubt it…unless the level fails to double in the ensuing 2 days.
Geoff Sher
Age: 42…. no kids…. miscarriage at 5 weeks in 2016 (IUI)
AMH: 0.14 ng/ml
E2: 440 pmol/L
FSH: 4.2 U/L
Dr. I started my IVF on 18/6. Took Lucrin Depot and was on Gonal F 225IU and Fostimon 75 IU. Also took Cetrotide 0.25. Also did endo scratching. Ultrasound picked up 5 follicles but only 3 retrieved. 2 fertilised and 3 day embryos transferred on 5 July. Been on cyclogest 200mg thrice daily and Estropause twice daily. Day 10 beta test came back as negative. My Dr has asked me to continue with Cyclogest and re-test on Day 14.
My question: Do you think this protocol was the best? Do you have any other suggestions that I could use in the next IVF?
Dr. Geoffrey Sher ..
Sir,
I am Eshita Newaz. I am 29 years old. I have hypo thyroid problem
And PCOS issues. I am married. My husband have high blood pressure and he take high cholesterol medicine.My husband and me .. we trying for 4 years to get pregnant. But no positive results! We also tried IUI twice.. both time I had bad urine infection. And had bad allergic reaction with penicillin type antibiotics!! That’s why both time there was no possibilities for pregnancy!
After 2.5 years we decided to go India for Ivf ! In this case can you suggest anything for me please.
We both are staying in United States. We need someone who can suggest us best .
We will be very glad if u have any suggestions for us . Please!
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.
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•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 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!
•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
•How Many Embryos should be transferred: A Critical Decision in IVF.
•Avoiding High Order Multiple Pregnancies (Triplets or Greater) with IVF
•The Role of Nutritional Supplements in Preparing for IVF
If you are interested in my advice or medical 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.
Also, my 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