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Dear Dr Sher
I’m 5 weeks and 4 days pregnant after a fresh Donor egg cycle. I have a 5 year old naturally conceived son and then had a pregnancy that had to terminate due to abnormalities after which I failed to get pregnant. I tried ivf with my own eggs twice. First attempt ended in a missed miscarriage. Second attempt ended with nothing to transfer back as we did a PGD. So we moved on to DE. Through blood test they discovered this last time that I have factor V Laiden. So I have been injecting Clexane 20mg at night since 5 days before transfer.
I’m writing as I am experiencing light bleeding, red and brown. I have just had a scan showing me a sac and Yolk measuring right for my time of pregnancy yet there is no explanation from the scan to explain the bleeding that started this morning and hasn’t stopped yet.
Does this mean an impending miscarriage? Could this be due to the Clexane?
Thank you very much!
As long as the bleeding is and remains painless…it will hopefully turn out fine. Try to rest up. Discuss with your RE.
Geoff Sher
Hi Dr Sheer ,
I have history of microadonema for last 10 years with elevated prolactin level and thyroid. Though both are controlled now under medication. Previously I took weekly Cabergoline 0.5 mg and daily dose of Levothyroxine of 0.5 mg.
I am trying to conceive from last 3 yrs and after initial investigation it’s found that my husbands sperm motality was low and we have been suggested to proceed with IVF/ICSI.
I responded very well to stimulation , generate 11 healthy eggs , out of which 4 embies made to blastocyst stage of good qulaity . They had transferred one of the best quality back and froze 3 for future use.
However , with the best quality embryo transferred , it resulted in a fail cycle.
Can you please help me to understand why does that happened or whether my medical history of endocrine disorder has anything to do with that.
Thanks,
I do not believe that treatment of your prolactinoma is the reason for failure. It could simply be bad luc. Bear in mind that microscopic embryo grading does not in any way assure embryo “competency” (ability to propagate a viable pregnancy). The most beautiful looking blastocysts can be completely incompetent. Embryo competency is more largely (but not exclusively) linked to embryo numerical chromosomal integrity (ploidy) which can only be assessed through ull embryo karyotyping (preimplantation genetic sampling (PGS). Another factor is that your thyroid condition could be autoimmune in origin and if so there would be a 50:50 chance of uterine natural killer cell activation witha an immunologic implantation dysfunction (!!D).
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
•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
•Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
•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)
•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
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
I invite you to arrange to have a Skype or an in-person consultation with me to discuss your case in detail. If you are interested, please contact Julie Dahan, at:
Email: Julied@sherivf.com
OR
Phone: 702-533-2691
800-780-7437
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
Whats your view on continueing progesterone in oil injections and estradiol 2mg vaginal tablets until the 16th week due to bleeding caused by a decent sized subchorionic hematoma?
If there is no real benefit, is there harm to the fetus from these 2 hormones?
Thanks!
I do not think there is any harm but whether it will do any good is debatable.
Geoff Sher
Dear Dr. Sher,
My first ivf cycle was cancelled today. I only had one follicle developing on my left ovary and today there was nothing there. My estrogen level dropped to 25.2 from 31.3 on day 10 of stims. I was put on micro dose lupron (20 in am and pm), gonal f (225 first two days then 150) and menopur (75). The nurse told me that I may have been over suppressed. I’m not sure what that means. I had to take a low does progesterone pill for a month and a half to help eliminate my cysts.
My doctor won’t see me until later this week. I was told that he’s busy with retrievals and can’t schedule me in until possibly the end of the week. I’m not sure which questions to ask. I’d like to move forward with a second cycle but it’s clear that this protocol didn’t work on me.
What would cause my estrogen levels to drop? Why did my follicle disappear?
Stats: 30 yrs old, diminished ovarian reserve, amh 0.025, and fsh 33
Thank you for taking the time to read this.
That is a very low estradiol and it suggests that you probably did not respond to the protocol you were on. I suspect that you might have diminished ovarian reserve (DOR).Older women as well as those who (regardless of age) have diminished ovarian reserve (DOR) tend to produce fewer and less “competent” eggs, the main reason for reduced IVF success in such cases. The compromised outcome is largely due to the fact that such women tend to have increased LH biological activity which often results in excessive LH-induced ovarian testosterone production which in turn can have a deleterious effect on egg/embryo “competency”.
Certain ovarian stimulation regimes either promote excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), augment LH/hCG delivered through additional administration (e.g. high dosage menotropins such as Menopur), or fail to protect against body’s own/self-produced LH (e.g. late antagonist protocols where drugs such as Ganirelix/Cetrotide/Orgalutron that are first administered 6-7 days after ovarian stimulation has commenced).
I try to avoid using such protocols/regimes (especially) in older women and those with DOR, favoring instead the use of a modified, long pituitary down-regulation protocol (the agonist/antagonist conversion protocol-A/ACP) augmented by adding supplementary human growth hormone (HGH). I further recommend Staggered IVF with embryo banking of PGS (next generation gene sequencing/NGS)-normal blastocysts in such cases. This type of approach will in my opinion, optimize the chance of a viable pregnancy per embryo transfer procedure and provide an opportunity to capitalize on whatever residual ovarian reserve and egg quality still exists, allowing the chance to “make hay while the sun still shines”.
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
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•The Fundamental Requirements For Achieving Optimal IVF Success
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•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?
•Blastocyst Embryo Transfers Should be the Standard of Care in
•Why did my IVF Fail
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
•Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
•Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
•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?
•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.
•The Role of Nutritional Supplements in Preparing for IVF
•IVF Egg Donation: A Comprehensive Overview
I invite you to arrange to have a Skype or an in-person consultation with me to discuss your case in detail. If you are interested, please contact Julie Dahan, at:
Email: Julied@sherivf.com
OR
Phone: 702-533-2691
800-780-7437
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
Hello,
I am on my first cycle of Femara along with a trigger shot. What is the purpose of doing the trigger shot in a set of 3? I took 5000iu on the first day, 2500iu 3 days later, and then 2500iu 3 days after that. How is this helpful for ovulation? Thank you for your time.
Respectfully Jennifer,
I do not see the logic behind this!
Geoff Sher
800-780-7437