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.

19,771 Comments

  1. Dear Dr. Sher,

    I’ve written to you before and I am immensely grateful for your input. I have another question for you, if you don’t mind. I had a cancelled IVF, and it still remains a mystery to me why it happened the way it did.
    A quick reminder – 43 years old, AMH 2,00 ng.ml (as of few weeks ago), FSH around 6-7, LH also. All the other relevant hormones are within normal range, including, E2, Testosterone, Progesterone, T3, T4 and TSH, with Prolactin a bit higher than next year – it’s around 431 or so. I usually have 10-ish antral follicles on my left ovary and around 2-3 on the right one. My husband is ok.
    I have an endometrioma on my right ovary, which was around 4 cm at the time of stimulation (now it is 4, 9 cm) , and two uterine fibroids which do not deform cavity. I am now preparing for another shot at IVF, but what I would first like to understand is my response to stimulation.

    It went like this: on day 22 of my normally 27-29 day long cycle I started the o,1 mg diphereline shots. On day 31 I was bleeding, and the next day I did the baseline US. I had 3 big follicles on my left ovary of size 10,5 mm and the rest were much smaller. We started with stimulation and continued with diphereline. As I predicted on that very day, this wasn’t a good start – the 3 leading follicles ran away with the starting advantage and the rest never caught up. In fact, it took mere 4 days of stimulation for the leading three to reach the “collecting” sizes of – 15, 5 mm, 18 mm and 21 mm. The rest were all much smaller, with the next one being 13 mm on the right ovary. I contend that the main reason for this lightning quick stimulation with the runaway and then scattered lead three follicles is the very beginning of it, that is the fact that they were too big already on day 2 of the cycle! So my question to you is: why do you think that happened? Why did I react with already such big follicles after only 10 days of diphereline? Has the downregulation/suppresion been achieved at all (my E2 was 91 pg/ml and LH 2, 66 on day 2 according to their lab, but I did my own and it was 103 pg/ml). One doctor suggested that it hasn’t been achieved at all and that I should have simply continued with diphereline for another few days.
    I have done a bit of research on the net afterwards, and I have found that some women have this problem of dominant follicle or two (in my case three) running way ahead of the rest and even an article about one way to handle this problem – by sacrificing the lead follicle (I forget how they do it – by aspiration, I suppose). What worries me, though, and hence my question is – that apparently the women to whom this had happened have a propensity for that, that is – it tends to happen again to the same women. Are you familiar with this problem and its cause?

    And question no. 2 if I may. I saw that you wrote about taking aspirin as a way to enhance circulation to the uterus in the first half of the cycle – up until the ovulation. What confuses me is that whenever I had IUI, I was asked to take aspirine in the luteal phase. Was that wrong?

    Thank you so very much in advance.

    • Forgot to mention that the stimulation was in February.

    • Oh, and one more thing: Is it possible that I started with the diphereline too late (CD 22)? Should I have started earlier as in some protocols – day 18,s say? Would the result have been any different?
      I should mention I wasn’t on BCP beforehand.

    • Some women have the propensity to develop early dominant follicles. In my opinion, when this happens it can be handled by early premature follicle reduction (aspiration) but it can sometimes be prevented by using a BCP to lead into the stimulation. Aspirin has little value in IVF

      Geoff Sher

  2. Hi Dr. Sher- if a patient will be taking prednisone daily as part of an immune protocol, how far in advance of the transfer do you recommend beginning the prednisone? at the very start of cycle?

    • At least 10m days prior to ET.

      Good luck!

      Geoff Sher

  3. Hi dr sher. My good friend just failed two FET in a row with PGS tested embryos. She did the ERA biopsy, which showed her uterus was pre receptive by 1 day. She added 1 extra day of progesterone, so did 6 days of shots before her transfer rather than 5, and her next FET was successful. I am curious about this era biopsy for myself. I have 2 children from prior FET, but my last 3 PGS normal embryos haven’t taken. Can receptivity change? Could my uterus be previously receptive on day 5 for my first two pregnancies and not now? Is it worth testing? What do you make of my friend’s results? Thanks.

    • Hi Allie,

      Very respectfully, I do not believe in the value of ERA. Seperately…

      Whenever a patient fails to achieve a viable pregnancy following embryo transfer (ET), the first question asked is why! Was it simply due to, bad luck?, How likely is the failure to recur in future attempts and what can be done differently, to avoid it happening next time?.
      It is an indisputable fact that any IVF procedure is at least as likely to fail as it is to succeed. Thus when it comes to outcome, luck is an undeniable factor. Notwithstanding, it is incumbent upon the treating physician to carefully consider and address the causes of IVF failure before proceeding to another attempt:
      1.Age: The chance of a woman under 35Y of age having a baby per embryo transfer is about 35-40%. From there it declines progressively to under 5% by the time she reaches her mid-forties. This is largely due to declining chromosomal integrity of the eggs with advancing age…”a wear and tear effect” on eggs that are in the ovaries from birth.
      2.Embryo Quality/”competency (capable of propagating a viable pregnancy)”. As stated, the woman’s age plays a big role in determining egg/embryo quality/”competency”. This having been said, aside from age the protocol used for controlled ovarian stimulation (COS) is the next most important factor. It is especially important when it comes to older women, and women with diminished ovarian reserve (DOR) where it becomes essential to be aggressive, and to customize and individualize the ovarian stimulation protocol.
      We used to believe that the uterine environment is more beneficial to embryo development than is the incubator/petri dish and that accordingly, the earlier on in development that embryos are transferred to the uterus, the better. To achieve this goal, we used to select embryos for transfer based upon their day two or microscopic appearance (“grade”). But we have since learned that the further an embryo has advanced in its development, the more likely it is to be “competent” and that embryos failing to reach the expanded blastocyst stage within 5-6 days of being fertilized are almost invariably “incompetent” and are unworthy of being transferred. Moreover, the introduction into clinical practice about a decade ago, (by Levent Keskintepe PhD and myself) of Preimplantation Genetic Sampling (PGS), which assesses for the presence of all the embryos chromosomes (complete chromosomal karyotyping), provides another tool by which to select the most “competent” embryos for transfer. This methodology has selective benefit when it comes to older women, women with DOR, cases of unexplained repeated IVF failure and women who experience recurrent pregnancy loss (RPL).
      3.The number of the embryos transferred: Most patients believe that the more embryos transferred the greater the chance of success. To some extent this might be true, but if the problem lies with the use of a suboptimal COS protocol, transferring more embryos at a time won’t improve the chance of success. Nor will the transfer of a greater number of embryos solve an underlying embryo implantation dysfunction (anatomical molecular or immunologic).Moreover, the transfer of multiple embryos, should they implant, can and all too often does result in triplets or greater (high order multiples) which increases the incidence of maternal pregnancy-induced complications and of premature delivery with its serious risks to the newborn. It is for this reason that I rarely recommend the transfer of more than 2 embryos at a time and am moving in the direction of advising single embryo transfers …especially when it comes to transferring embryos derived through the fertilization of eggs from young women.
      4.Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:
      a.A“ thin uterine lining”
      b.A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
      c.Immunologic implantation dysfunction (IID)
      d.Endocrine/molecular endometrial receptivity issues
      Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).
      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.
      •Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
      •Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
      •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 IVF
      •IVF: How Many Attempts should be considered before Stopping?
      •“Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
      •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
      •Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
      •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
      •How Many Embryos should be transferred: A Critical Decision in IVF.
      •The Role of Nutritional Supplements in Preparing for 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.

  4. Hi Doctor Sher
    My name is Rebecca 36 years old. I already had one baby 5 years old from Natural pregnancy with no difficulties to get that pregnancy.
    I was trying for a second baby about 1.5years.We could not get it and finally after the medical check-up doctor advised this is an unexplained reason why I am not getting pregnant. As we followed doctor’s advice we decided to go for IvF. I was on DHEA 25mg tablet one each day for two months from February to 13th of April just the day before the egg collection. I went for the egg collection last Friday 8am 14th of April. I was on Gonal F 300IU for 8 days from 4.4.17 to 11.4.17 in the evening 9.45pm and Orgalutran 250µ for 5 days, from 8.4.17-12.4.17 in the morning 6.45am. Then last Wednesday 12th April nurse called and asked me the consent that there are 3 follicles for the egg collection. As far as I remember each follicle sizes are 20mm, 19mm 20mm.I gave a consent .Then she asked me to take Ovidrel 250µ exactly 8.30pm on Wednesday 12th April 2017.
    After the egg collection process I was disappointed .Doctor said me could not collect any egg and doctor tried to flush it as well, even though it could not collect any of them. Then doctor got the blood test to check whether the Ovidrel worked or not. Then next day nurse called and said me from the blood test the Ovidrel was worked.it is mystery why there was no egg found and asked me to make an appointment to see your doctor. I am waiting to see the doctor at the moment to find out the mystery.
    Could you please advise me what could went wrong in this circumstances?
    Can I try for natural pregnancy in May or do I have to wait for few months?

    • In my opinion, the most likely cause of this scenario is the protocol used for ovarian stimulation stimulation, especially in women with diminished ovarian reserve (DOR), which seems to be likely in your case. There is no such thing as “empty follicles”. All follicles contain eggs and failure of such follicles to yield eggs, is because they remain attached to the inner walls of the follicles. The reason is because the eggs are complex chromosomally abnormal and unable to signal dispersion of the binding cells to allow the eggs to break loose. This can be due to the protocol of stimulation and/or the fact that the wrong type/dosage of hCG was used for the “trigger”. In my opinion, a late antagonist protocol is not ideal and 250mcg of Ovidrel is too low a “trigger dosage”. I am also against the prolonged use of DHEA prior ovarian stimulation (see below).

      In my opinion, the protocol used for ovarian stimulation, against the backdrop of age, and ovarian reserve are the drivers of egg quality and egg quality is the most important factor affecting embryo “competency”.
      Women who (regardless of age) have DOR have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production of LH biological activity which can result in excessive LH-induced ovarian male hormone (predominantly testosterone) production which in turn can have a deleterious effect on egg/embryo “competency”.

      While it is presently not possible by any means, to reverse the effect of DOR, certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can in my opinion, make matters worse. Similarly, the amount/dosage of certain fertility drugs that contain LH/hCG (e.g. Menopur) can have a negative effect on the development of the eggs of older women and those who have DOR and should be limited.I try to avoid using such protocols/regimes (especially) in women with DOR, favoring instead the use of the agonist/antagonist conversion protocol (A/ACP), a modified, long pituitary down-regulation regime, augmented by adding supplementary human growth hormone (HGH). I further recommend that such women be offered access to embryo banking of PGS (next generation gene sequencing/NGS)-selected normal blastocysts, the subsequent selective transfer of which by allowing them to capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” could significantly enhance the opportunity to achieve a viable pregnancy

      Please visit my new Blog on this very site, https://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 Approach
      • 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.
      • A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
      • Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
      • Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
      • 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 IVF
      • Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
      • 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 Testing (PGS) in IVF: It should be Used Selectively and NOT be Routine.
      • 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?
      • PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
      • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
      • 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
      • Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
      • 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.

  5. Dear Dr.Sher

    Is hysteroscopy required before IVf ?

    Are injections necessary in donor egg ivf program ?

    Regards
    Glory

    • My age is 43 and have a low AMH – 0.33 .

    • Either Hysteroscopy or hysterosonogram is needed to exclude the presence of surface lesions in the uterine cavity. An HSG is inadequate.

      In my opinion, it is better to use hormone replacement than to do egg donation embryo transfer in natural cycles.

      Geoff Sher