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.
Dr Sher I’ve been reading about your conversion protocol. How long does it take for the burn control to suppress the pituitary glands output of LH? Thank you
You need at least 8-10 days on the BCP!
Geoff Sher
Hi there – I had an FET on July 31st with a PGS tested embryo. On 8/10 i had my first beta of 51, followed by a second on 8/12 which was 126. My RE is concerned that the figures are low – the third beta on 8/14 is 488. We did an initial sonogram to check tubes for an ectopic pregnancy but didn’t see anything on the early scan. Should I be concerned and are the numbers too low to indicate a viable pregnancy? Thank you!
To the contrary! It is somewhat early and in fact I am guardedly optimistic for a viable pregnancy!
Have an US done in 10-14 days. That should be definitive.
Geoff Sher
Hi there – i had a frozen transfer on July 31st (using a PGS tested embryo). Had my first beta on 8/10 which was 51. On 8/12 it rose to 125 and doctor is concerned that it is too low. Repeated it on 8/14 and result was 488. How concerned should i be? Could this turn into a viable pregnancy or are the figures just too low?
Personally, I am optimistic that this will be a viable pregnancy! Do an US 1n 10-14 days!
Please keep me in the loop!
Geoff Sher
Hi Dr. Sher,
I am 35 years old and conceived at 33 years old spontaneously on my second time of trying in August 2017 and miscarried at 6 weeks. After miscarrying my husband and I were advised to try for one year, which we did and did not conceive. After one year, we visited a fertility clinic and we had 3 IUIs which all failed and tried timed intercourse which also was not successful. In, July, 2019, at 34 years old I underwent my first cycle of IVF with the following protocol: estrace priming followed by gonal-F 150 and luveris 75 IU and orgalutran 250 mcg and suprefact as my trigger. I responded very well (in fact I almost went into OHSS because of my response) and 24 eggs were retrieved and 19 eggs were viable. Out of the 19 eggs 17 fertilized and out of the 17 eggs that fertilized 12 made it to blast and my clinic froze 9 because the additional 3 embryos apparently had too few cells – I never received a clear answer. The 9 embryos that were frozen were graded as follows: 3AB; 3BB x 2; 4BB x 4; 4BC; 3BC. None of my embryos were genetically tested; I was advised that due to my young age that PGT-A wasn’t necessarily. I had karytotype testing which came back normal. Since my egg retrieval I have had 5 failed FETS with one of my FETs being a double embryo transfer. I have tried a natural cycle; I have had an ERA which held that I was pre-receptive so my clinic added on an additional 12 hours of progesterone. I have also had progesterone in oil added to my FET protocol. I have 3 embryos left. In 2018, my AMH was 24 and my antra-follicular count was 7 on the right and 8 on the left.
In march, 2020, my husband and I increasingly became suspicious of the clinic’s reasoning that we are simply unexplained and we one of the rare cases that they had seen. We started seeking different opinions. I went to a naturopath reviewed my fertility clinic medical chart and told me that I had thyroid antibodies (TPO at 116 and TGO at 218) and was subclinical hypothyroid (TSH at 3.86). My family doctor put me on levothyroxine and it has changed my quality life – I am no longer fatigued, cold, and constipated all the time. In May, 2020, my husband decided to move ahead with a different fertility clinic. I have now been screened for thrombophilia and other immunological concerns as well as PCOS. I don’t have PCOS, protein C/S issues, or thrombophilia, etc. The only immunological issue that I have is Hashimotos, but I remain on my meds and my TPO and TGO are dropping due to me taking natural supplements to reduce the antibodies. I may also have progesterone resistance as on my ERA the tissue sample showed that it was Day 3 of progesterone when I had been on progesterone for 6 or 7 days. My husband and I have decided to move on to a new clinic with a second round of IVF w/ PGT-A and leave our 3 untested embryos frozen at my old clinic. My new protocol involves androgel 1% and estrace 4mg for my priming followed by Gonal-F 225 IUs and Menopur 150 IUs and either HCG or suprefact for my trigger and then intralipids and prednisone and baby aspirin for my FET. My question is as follows: does the dosage of menopur and gonal-f seem too high? Should I talk to my RE about lowering it due to me almost going into OHSS during my first round of IVF? Secondly, could the higher dosage of menopur and gonal-f result in poorer quality embryos? Finally, should I be asking for a HGH i.e. saizen or letrozole to be co-administered? When seeking a second opinion, one RE suggested that the embryo quality from my first round of IVF was not the greatest for someone who was 34 years of age and he suggested that I might have an egg quality issue – do you agree that the embryos were not the greatest quality for a 34 year old. I do not know my current AMH but I am now 35 years old (about to 36 in fall) and on a recent day 3 baseline scan my antra-follicular count was 10 on the left and 10 on the right. I have also been taking ubiquinol; inositol; vitamin D; vitamin E; omegas, selenium, glutathione; NAC to assist with egg quality.
There are a few issues:
1. At risk of developing OHSS which in my opinion requires a revision of your protocol for ovarian stimulation :
Severe ovarian hyperstimulation syndrome (OHSS) is a life-endangering complication that occurs in some women undergoing controlled Ovarian Stimulation (COS). OHSS is often accompanied by a profound reduction in egg “competency” and on fertilization often yield an inordinately high percentage of “incompetent” embryos which have a reduced potential to propagate viable pregnancies.
Concern that a patient will develop of OHSS often leads the treating RE to take measures aimed at reducing the risk of this life-endangering condition. One such measures is to “trigger” egg maturation prematurely in the hope of arresting further follicular growth and the other, is to initiate the “trigger” with a reduced dosage of hCG (i.ed. 5,000U rather than the usual 10,000U of of Pregnyl/Profasi/Novarel, to use or 250mcg rather than 500mcg of Ovidrel or to supplant the hCG “trigger” with a Lupron “trigger” which causes a prompt LH surge from the woman’s pituitary gland to take place. While such measures do indeed reduce the risk of OHSS to the mother, this often comes at the expense of egg quantity and “competency”. Fewer than the anticipated number of eggs are harvested and those that are retrieved are far more likely to be “immature” and chromosomally abnormal (aneuploid”), or “immature” , thereby significantly compromising IVF outcome.
Against this background, It is my considered opinion that when it comes to performing IVF in women at risk of developing OHSS, the most important consideration must be the selection and proper implementation of an individualized or customized ovarian stimulation protocol. Thereupon, rather than prematurely initiating the “trigger” to arrest further follicle growth, administering a reduced dosage of hCG or “triggering with a GnRH agonist (e.g. Lupron/Buserelin) that can compromise egg “competency”….. use of one of the following techniques will often markedly reduce the risk of OHSS while at the same time protecting egg quality:
1.PROLONGED COASTING (PC): OHSS can be a life-endangering complication of ovarian stimulation with gonadotropins. The risk of OHSS begins with the hCG “trigger”. The complication occurs in very high responders to gonadotropin stimulation. Women with PC0S, irregular cycles and AMH levels that are X3 the normal are at the greatest risk of developing OHSS. In such patients, ovarian stimulation commences with the same approach as above (using a BCP launch and an agonist (e.g Lupron/buserelin/Superfact/aminopeptidyl) overlap. Only in such patients a very low dosage regime of FSHr /menotropin isused . Then, starting on day 7 of ovarian stimulation, serial daily blood estradiol (E2) and ultrasound follicle assessments are done to track follicle development and [E2]. If there are > 25 follicles, gonadotropin stimulating continues, regardless of the [E2]. As soon as 50% of all follicles reach 14mm and the [E2] exceeds 2,500pg/ml gonadotropin stimulation id abruptly stopped, while daily agonist injections continue. Daily blood [E2 ] is tracked, (without necessarily continuing serial ultrasound follicle measurements). The [E2] will almost invariably continue to rise for a few days whereupon it will begin to, drop. As soon as the [E2] drops below 2,500pg/ml, a “trigger” shot of 10,000U hCGu or hCGr is administered and an egg retrieval is performed 36 hours later. At this point, All mature (MII) eggs are either cryobanked (vitrified) or (as is far more commonly the case), are fertilized by intracytoplasmic Sperm Injection (ICSI) and are then cultured for 5-6 days to the blastocyst stage whereupon they are either biopsied for preimplantation genetic screening and then cryopreserved (vitrified) for future use vitrified without prior biopsy for PGS or e transferred fresh, to the uterus during the same cycle of treatment. The outcome of PC depends on the precise timing of the initiation and conclusion of “prolonged coasting”. If you start PC too early, follicle growth will arrest, and the cycle will be lost. Conversely, if you start too late, you will encounter too many post-mature/cystic follicles (>22mm) that usually harbor abnormally developed eggs. Use of “Coasting” avoids severe OHSS, and minimizes the risk of poor egg/embryo quality in a group of women who otherwise would be at severe risk of life-endangering complications and prone to producing a high percentage of “incompetent” eggs/embryos.
2.EMBRYO FREEZING AND DEFERMENT OF EMBRYO TRANSFEDR (ET): OHSS is always a self-limiting condition. In the absence of continued exposure to hCG, symptoms and signs as well as the risk of severe complications will ultimately abate. Thus, in the absence of pregnancy, all symptoms, signs and risks associated with OHSS will disappear within about 10-14 days of the hCG trigger. Conversely, since early pregnancy is always accompanied by a rapid and progressive rise in hCG , the severity of OHSS will increase until about the 9th or tenth gestational week whereupon a transition from ovarian to placental hormonal dominance occurs, the severity of OHSS rapidly diminishes and the patient will be out of risk. Accordingly, in cases where in spite of best effort to prevent OHSS, the woman develops symptoms and signs of progressive overstimulation prior to planned ET, all the blastocysts should be vitrified and cryostored for FET in a subsequent hormone replacement cycle. In this way women with OHSS can be spared the risk of the condition spiraling out of control
A Likely immunologic implantation dysfunction (IID), inked to your Hashimoto’s disease (autoimmune hypothyroidsmm):
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.
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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 15y 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
e.Ureaplasma Urealyticum (UU) Infection of cervical mucous and the endometrial lining of the uterus, can sometimes present as unexplained early pregnancy loss or unexplained failure following intrauterine insemination or IVF. The infection can also occur in the man, (prostatitis) and thus can go back and forth between partners, with sexual intercourse. This is the reason why both partners must be tested and if positive, should be treated contemporaneously.
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?
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ADDENDUM: PLEASE READ!!
INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.
If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or, enroll online on then home-page of my website (www.SherIVF.com).
PLEASE SPREAD THE WORD ABOUT SFS!
Geoff Sher
Hi there
I am about to begin IVF however I have a left hydrosalpinx that cannot be removed as the tube is fused to my bowel and the surgeon would not go through with even clipping it. My right side tube is open however they cannot get eggs from the Ovary due to a cyst, they can only collect eggs from my left Ovary. I was just wondering if you knew what the possibilities were of getting pregnant with the hydrosalpinx and if you have had any patients who have done?
Ideally you need a laparoscopic proximal ligation of the affected tube: I suggest you get a second opinion. However, if this is not possible, a pregnancy could still occur but consider the following
In cases where the ends of the fallopian tubes are blocked, pus may collect and distend the tube(s). The pus is usually absorbed over time and replaced by clear straw-colored fluid. The resulting, occluded, fluid-filled, distended, and often functionless fallopian tube(s) is referred to as a hydrosalpinx.. Such distended Fallopian tubes (hydrosalpinges) can leak fluid back into the uterine cavity where the can destroy transferred embryos upon contact. This is why patients who have hydrosalpinges and are considering undergoing IVF, should first have hydrosalpinges surgically removed or at the very least have the affected tube(s) surgically clipped or tied as they emerge through the uterine wall. This will avoid subsequent back flow when IVF is performed. Understandably, it is often hard for patients to come to terms with the fact that following such surgery they no longer have any possibility of having functional Fallopian Tubes. tubes affected by hydrosalpinges are functionless and any attempt to open such tubes surgically in an attempt to restore fertility is almost invariably an exercise of futility.
Good luck!
Geoff Sher
PH: 702-533-2691