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.
Hi Dr. Sher! I recently completed an IVF/egg retrieval that resulted in 0 embryos which has left me very disappointed and confused. I have a lot of questions and have a follow up consult scheduled with the dr in two weeks. I don’t have any real diagnoses other than high NKC and MTHFR. I’m considered unexplained, I believe. Husband’s sperm was normal in most recent analysis. I’m 32 yo and AMH was recently 3.86. Other hormones have always been normal other than low “day 21” progesterone. This was our 2nd egg retrieval but our first with Sher St Louis. Our first 5yrs ago in Indianapolis resulted in 30 eggs retrieved and 6 blastocysts. One chemical pregnancy from that. For this cycle, I took BCP for awhile then overlapped with lupron. Then 150 gonal-f and 75 menopur. Triggered with HCG 36 hrs prior. Approx 31 follicles were observed during ultrasounds, some too big, some too small, most in the right range. Egg retrieval only yielded 16 eggs and took quite a while bc the dr was flushing and searching for the eggs. Nine eggs were M2 – mature from what I understand. The rest were immature. We used PCSI. 7 of those fertilized. 6 arrested around day 2-3. One expanded blastocyst was present on day 6 but was poor quality and unable to be frozen. We had planned to freeze all and do PGS. My biggest questions are why were nearly half of my follicles “empty” and why were the 16 eggs retrieved such poor quality? From my understanding embryo failure like mine is a result of poor egg quality. Also, can immunology affect egg development? I have ongoing food intolerances and angioedema which are suspected to be from a autoimmune disorder. Thanks in advance for taking the time to read this and provide some clarity!
Frequently, when following vigorous and often repeated flushing of follicles at egg retrieval they fail to yield eggs, it is ascribed to “Empty Follicle Syndrome.” This is a gross misnomer, because all follicles contain eggs. So why were no eggs retrieved from the follicles? Most likely it was because they would/could not yield the eggs they harbored.
This situation is most commonly seen in older women, women who have severely diminished ovarian reserve, and in women with polycystic ovarian syndrome (PCOS). In my opinion it is often preventable when an optimal, individualized and strategic protocol for controlled ovarian stimulation (COS) is employed and the correct timing and dosage is applied to the “hCG trigger shot.”
Normally, following optimal ovarian stimulation, the hCG “trigger shot” is given for the purpose of it triggering meiosis (reproductive division) that is intended to halve the number of chromosomes from 46 to 23 within 32-36 hours. The hCG trigger also enables the egg to signal the “cumulus cells” that bind it firmly to the inner wall of the follicle (through enzymatic activity), to loosen or disperse, so that the egg can detach and readily be captured at egg retrieval (ER).
Ordinarily, normal eggs (and even those with only one or two chromosomal irregularities) will readily detach and be captured with the very first attempt to empty a follicle. Eggs that have several chromosomal numerical abnormalities (i.e., are “complex aneuploid”) are often unable to facilitate this process. This explains why when the egg is complex aneuploid, its follicle will not yield an egg…and why, when it requires repeated flushing of a follicle to harvest an egg, it is highly suggestive of it being aneuploid and thus “incompetent” (i.e., incapable of subsequently propagating a normal embryo).
Older women, women with diminished ovarian reserve, and those with polycystic ovarian syndrome, tend to have more biologically active LH in circulation. LH causes production of male hormone (androgens, predominantly testosterone), by ovarian connective tissue (stroma/theca). A little testosterone is needed for optimal follicle development and for FSH-induced ovogenesis (egg development). Too much LH activity compromises the latter, and eggs so affected are far more likely to be aneuploid following meiosis.
Women with the above conditions have increased LH activity and are thus more likely to produce excessive ovarian testosterone. It follows that sustained, premature elevations in LH or premature luteinization (often referred to as a “premature LH surge”) will prejudice egg development. Such compromised eggs are much more likely to end up being complex aneuploid following the administration of the hCG trigger, leading to fruitless attempts at retrieval and the so called “empty follicle syndrome.”
The developing eggs of women who have increased LH activity (older women, women with diminished ovarian reserve, and those with PCOS) are inordinately vulnerable to the effects of protracted exposure to LH-induced ovarian testosterone. Because of this, the administration of medications that provoke further pituitary LH release (e.g., clomiphene and Letrozole), drugs that contain LH or hCG (e.g., Menopur), or protocols of ovarian stimulation that provoke increased exposure to the woman’s own pituitary LH (e.g., “flare-agonist protocols”) and the use of “late pituitary blockade” (antagonist) protocols can be prejudicial.
The importance of individualizing COS protocol selection, precision with regard to the dosage and type of hCG trigger used, and the timing of its administration in such cases cannot be overstated. The ideal dosage of urinary-derived hCG (hCG-u) such as Novarel, Pregnyl and Profasi is 10,000U. When recombinant DNA-derived hCG (hCG-r) such as Ovidrel is used, the optimal dosage is 500mcg. A lower dosage of hCG can, by compromising meiosis, increase the risk of egg aneuploidy, and thus of IVF outcome.
There is in my opinion no such condition as “Empty Follicle Syndrome.” All follicles contain eggs. Failure to access those eggs at ER can often be a result of the protocol used for controlled ovarian stimulation.
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.
•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.
•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!
•ffective Treatment to Help Thicken a Thin Uterine Lining
•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
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.
Hi Dr. Sher, I conceived naturally and had a son without issues in feb 2016. I am a 30 Years old. After our son was born, we elected to do ivf to screen for a genetic mutation I carry. I did two rounds of egg retrieval’s in April and October of 2017 without issue and have 5 frozen, healthy embryos that don’t carry the gene. When I was doing those cycles I had an iud in. We decided to do a frozen transfer in jan 2018, and I had polyps removed along with my IUD in dec 2017. I was put on a birth control pill and then started Lupron and estrogen in jan. My uterine lining did not exceed 2 mm. They then tried delesteogen injections and that got my lining to a 3mm. I took a month off and had a period which made me think my lining had thicker sufficiently. I went into ultra sounds a few weeks after my period ended and it was at a 3.3mm. I started delesteogen again without lupron and lining did not thicken. I have since Been on viagra suppositories with delesteogen, L -arg, baby aspirin, and nothing is helping. The viagra helped get my lining to a max of 4.8mm. I also take 75 of thyroid medication. My doctor is puzzled and has given me two options: nueprogen wash or full stim cycle to try and get the lining to grow. I don’t know what to do because the cycle is so expensive and painful. I don’t have any known damage to my uterus or lining, but my body is not responding to any medications. I should also mention that we don’t think my genetic mutation affects fertility, though I have had a significant medical history including a year of anti fungal medications when I was 14. I don’t think that is the issue now since I was able to conceive previously. Would love your thoughts on next steps. Thank you.
This really sounds like a damaged basal endometrium. Usually it is caused by endometritis post pregnancy. We need to discuss this along with options.
I really recommend that we talk.
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
Hello Doctor,
Me and my husband are 36 years old, I have blocked tubes problem. We got IVF cycle done last year July and were able to freeze 9 good quality embyo’s.Our first two FET’s resulted in negative beta HCG. 3rd FET which was done on May 4th 2018 . 12 days post transfer two 5 days blastocysts (May 15), I got positive beta hcg of 87.My RE asked me to repeat beta in another 2 days.Beta hcg level was 120. Third time beta hcg was repeated on May 19 which came out to be 74.I was on progesterone supplements and womenex injection. My RE asked me to stop all the medicines after 3rd low beta HCG saying that it is a early miscarriage.I have not got my periods until today.Is there still any hope that my beta level would go up
This is discouraging. Sadly, it looks as if this is a failing implantation.
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
If you are interested in seeking my advice or 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 .
*The 4th edition of 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
I am 40 nearly 41. I have low Amh. I have a naturally conceived 4 year old. I’ve been trying to conceive for about 18mths. I had 1 miscarriage in that time. I did my first ivf a month ago. Only retrieved two eggs both fertilised, both looked good. No pgd. Put one in at day 3 and froze the other. It didn’t work. It was the clinic’s standard protocol. Synarel from day 21 then 225 gonal f from day 2 for 12 days. They only do day 3 transfers. I’m doing my next round now. My fs advised the same protocol but increased gonal f to 450. I asked about other protocols (flare aacp etc) and he said there was no evidence that they were any better. Same with hgh and other supplements. He said the lower cost of the standard meant I could do more. This cycle I started the synarel 4 days late because I thought I might be pregnant. Will that have a bad effect? I feel over suppressed on this protocol. My estrogen levels were higher in my natural cycle prior to my last ivf than during the actual ivf cycle. Can synarel be used to do a flare if I didn’t start it until day 2? I am still breastfeeding my 4 year old twice a day because she’s very psychologically dependent on it. Could this be preventing pregnancy even though my prolactin is low? I have extreme anxiety and depression over not being able to conceive. None of the standard antidepressants work for me, I’m using Ativan to try and cope but still wake early and am losing weight. I feel like this must be affecting my ability to conceive. I just don’t know what to do. Should I be on a different protocol? Do I need to stop breastfeeding? I am considering donor embryos but will that even work if I can’t relax? I’m so stuck and distressed. Your advice is much appreciated.
Hi Amty,
Very respectfully, in my opinion, the protocol used for ovarian stimulation and its implementation have a profound effect on egg/embryo quality. At 41 years, I personally would not use a Lupron-flare protocol and would recommend HGH augmentation. Since your prolactin is normal, I do not believe BF would play a role in response to stimulation. However BF (probably via an oxytocin mechanism) can increase uterine contractility and this is obviously undesirable around the time of ET.
I think we should talk!
Call Julie at 800-780-7437 and set up a Skype consultation at your convenience.
Geoff Sher
Hello, I found your site today and came here for a question. My wife and I are doing IVF, we had a problem with her lining not getting to .8cm after the Lupron and estrogen patches. So we are on our second cycle. my wife asked me to give her her Lupron shots and I did so, However, last night I realized i was giving her too much lupron. I feel horrible that this past cycle of starting the process was a complete screw up by me. I was trying to figure out how much to give her and I read the Box and somehow not the instruction that the Dr. had given us. I was giving her 20units of Lupron for the first week then I started 10units after the first 7 days. We went for an ultra sound and she was not ready. So they told us to continue the Lupron for another week. Again the next week she was not ready. So they gave us one more week and again Giving her 10units of Lupron. Again nothing. the Dr. office gave her more estrogen and still did not work. The Clinic told me to continue to give her the Lupron even after the 3rd week. Then on the 4th week we were told the person handling our procedure was wrong to have us continue the Lupron. ( we had to buy a second Set of Lupron and I basically put a 1 and 1/2 bottole of Lupron in her for 5 weeks. we were off a month and now I got the correct instructions and undestood them. So my question is. how long does it take for it to get out of your system. I gave her the correct dosage of Lupron this morning of 10units. I cannot get an answer about the length of time to leave your system? I am heartbroken and scared I could have hurt my wife. its all my fault for reading the box and not understanding her paperwork.
The Lupron should in my opinion be gone within a week or so!
Geoff Sher