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,
I am 33 year old woman with unexplained fertility undergoing fertility treatments for the past year (3 failed iuis and 2 rounds of IVF, starting my third IVF round in Sept).
The first IVF protocol in November was 1 vial menopur and 150 follistim with a pregnal trigger. Resulted in 8 eggs, 7 mature, 6 fertilized, 4 made to 5 day blast.
First FET was successful however resulted in miscarriage at 7 weeks. The next FET we transferred two embryos that failed to implant (the other embryo did not make the thaw).
Started a new round of IVF in June (now protocol was 4 vials of menopur, 150 follistim, pregnal and lupron trigger mix). Retrieved 8 eggs, all mature and fertilized but then we were down to 2 blasts by day 5. Sent for testing and we have one mosaic and one abnormal.
I’m confused as to what is happening between the various protocols and their varying results, why I am not retrieving more eggs and getting more blasts (Dr says I have a good egg reserve), if I should transfer my mosaic embryo or bank it as a reserve and what changes to my protocol can be made to ensure a more successful round to result in healthy baby.
Thank you.
Dr. Sher,
I had a endo biopsy in May that showed mild endometritis (likely cause is retained placenta, from D&E, which was removed). I took 10 days of doxy 100mg but apparently the endometritis did not go away.
My biopsy in June shows “focal occasional positive cells identified, suggestive of chronic mild endometritis.”
My doctor is prescribing azythromycin (z-pack x 5 days) this time.
My doctor says that the significance of asymptomatic endometritis is unclear in Fertility literature and she feels okay for me to proceed even with this condition, but I have read it is bad for implantation / pregnancy. I don’t know why the doxy did not get rid of it but would feel better with it gone.
Which antibiotics have you used to successfully get rid of chronic mild endometritis?
If the endometritis does not go away, would you proceed with FET as long as the lining is thick and trilaminar?
Thank you for your help!
I am not a believer of chronic endometritis with the exception of tuberculosis which is extremely rare in 1st world countries. It is more commonly found in Asia. Furthermore, such a diagnosis requires the detection of plasma cells in the biopsy specimen. In my opinion, with the exception of tuberculous endometrititis, treatment is rarely needed.
Geoff Sher
Hi , me and my husband have just had PGD For gender selection , we have conceived 2 perfectly healthy boys naturally and wanted to complete our family with a daughter . So it started with a follicle scan in the uk , which showed I had 14 follicles , my stimulation protocol and meds got sent over , I was on Menogon 225 & orgalutran 0.25 . I got to clinic and I was told I had 11 mature eggs and my womb lining was 12mm . So all seemed so perfect . My eggs were fertilised, only 8 fertilised out of 11 , and only 6 made it to PGD testing . Only 1 of my embryos were normal , all of my other embryos had Monosomy x , Monosomy 18 , Trisomy x , Trisomy 13 , chaotic , & nuclear blastomer . I was so shocked , I am 26 & my husband is 28 we are both healthy and fertile . And we had no good news . Our one healthy embryo grade aa got put back and has yesterday resulted in a chemical pregnancy . Could there be any other reason for this ? I can’t see me and my husband carrying these genetic or chromosome abnormalities . I want our daughter so bad and I don’t know what our next steps could be ?
Your autosomally monosomic and trisomic embryos might not ne “incompetent”. They could ne “mosaic”…
Human embryo development occurs through a process that encompasses reprogramming, sequential cleavage divisions and mitotic chromosome segregation and embryonic genome activation. Chromosomal abnormalities may arise during germ cell and/or preimplantation embryo development, and represents a major cause of early pregnancy loss. About a decade ago, I and an associate, Levent Keskintepe PhD were the first to introduce full embryo karyotyping (identification of all 46 chromosomes) through preimplantation genetic sampling (PGS) as a method by which to selectively transfer only euploid embryos (i.e. those that have a full component of chromosomes) to the uterus. We subsequently reported on a 2-3 fold improvement in implantation and birth rates as well as a significant reduction in early pregnancy loss, following IVF. Since then PGS has grown dramatically in popularity such that it is now widely used throughout the world.
Most IVF programs that offer PGS services, require that all participating patients consent to all their aneuploid embryos (i.e. those with an irregular quota of chromosomes) be disposed of. However, there is now growing evidence to suggest that following embryo transfer, some aneuploid embryos will in the process of ongoing development, convert to the euploid state (i.e. “autocorrection”) and then go on to develop into chromosomally normal offspring. In fact, I am personally aware of several such cases occurring within our IVF network. So clearly , summarily discarding all aneuploid embryos as a matter of routine we are sometimes destroying some embryos that might otherwise have “autocorrected” and gone on to develop into normal offspring.
Thus by discarding aneuploid embryos the possibility exists that we could be denying some women the opportunity of having a baby. This creates a major ethical and moral dilemma for those of us that provide the option of PGS to our patients. On the one hand, we strive “to avoid knowingly doing harm” (the Hippocratic Oath) and as such would prefer to avoid or minimize the risk of miscarriage and/or chromosomal birth defects and on the other hand we would not wish to deny patients with aneuploid embryos, the opportunity to have a baby.
The basis for such embryo “autocorrection” lies in the fact that some embryos found through PGS-karyotyping to harbor one or more aneuploid cells (blastomeres) will often also harbor chromosomally normal (euploid) cells (blastomeres). The coexistence of both aneuploid and euploid cells coexisting in the same embryo is referred to as “mosaicism.” As stated, some mosaic embryos will In the process of subsequent cell replication convert to the normal euploid state (i.e. autocorrect)
It is against this background, that an ever increasing number of IVF practitioners, rather than summarily discard PGS-identified aneuploid embryos are now choosing to cryobanking (freeze-store) certain of them, to leave open the possibility of ultimately transferring them to the uterus. In order to best understand the complexity of the factors involved in such decision making, it is essential to understand the causes of embryo aneuploidy of which there are two varieties:
1.Meiotic aneuploidy” results from aberrations in chromosomal numerical configuration that originate in either the egg (most commonly) and/or in sperm, during preconceptual maturational division (meiosis). Since meiosis occurs in the pre-fertilized egg or in and sperm, it follows that when aneuploidy occurs due to defective meiosis, all subsequent cells in the developing embryo/blastocyst/conceptus inevitably will be aneuploid, precluding subsequent “autocorrection”. Meiotic aneuploidy will thus invariably be perpetuated in all the cells of the embryo as they replicate. It is a permanent phenomenon and is irreversible. All embryos so affected are thus fatally damaged. Most will fail to implant and those that do implant will either be lost in early pregnancy or develop into chromosomally defective offspring (e.g. Down syndrome, Edward syndrome, Turner syndrome).
2.“Mitotic aneuploidy” occurs when following fertilization and subsequent cell replication (cleavage), some cells (blastomeres) of a meiotically euploid early embryo mutate and become aneuploid. This is referred to as mosaicism. Thereupon, with continued subsequent cell replication (mitosis) the chromosomal make-up (karyotype) of the embryo might either comprise of predominantly aneuploid cells or euploid cells. The subsequent viability or competency of the conceptus will thereupon depend on whether euploid or aneuploid cells predominate. If in such mosaic embryos aneuploid cells predominate, the embryo will be “incompetent”). If (as is frequently the case) euploid cells prevail, the mosaic embryo will be “competent” and capable of propagating a normal conceptus.
Since some mitotically aneuploid (“mosaic”) embryos can, and indeed do “autocorrect’ while meiotically aneuploid embryos cannot, it follows that an ability to differentiate between these two varieties of aneuploidy would be of considerable clinical value. And would provide a strong argument in favor of preserving certain aneuploid embryos for future dispensation.
Aneuploidy, involves the addition (trisomy) or subtraction (monosomy) of one chromosome in a given pair. As previously stated, some aneuploidies are meiotic in origin while others are mitotic “mosaics”. Certain aneuploidies involve only a single, chromosome pair (simple aneuploidy) while others involve more than a single pair (i.e. complex aneuploidy). Aside from monosomy involving absence of the y-sex chromosome (i.e. XO) which can resulting in a live birth (Turner syndrome) all monosomies involving autosomes (non-sex chromosomes) are lethal and will not result in viable offspring). Some autosomal meiotic aneuploidies, especially trisomies 13, 18, 21, can progress to viable, but severely chromosomally defective babies. All other meiotic autosomal trisomies will almost invariably, either not attach to the uterine lining or upon attachment, will soon be rejected. All forms of meiotic aneuploidy are irreversible while mitotic aneuploidy (“mosaicism) often autocorrects in the uterus. Most complex aneuploidies are meiotic in origin and will almost invariably fail to propagate viable pregnancies.
There is presently no practical test that can reliable differentiate between meiotic and mitotic aneuploidy. Notwithstanding this, the fact that some “mosaic” embryos can autocorrect in the uterus, makes a strong argument in favor of transferring aneuploid of embryos in the hope that the one(s) transferred might be “mosaic” and might propagate viable healthy pregnancies. On the other hand, it is the fear that embryo aneuploidy might result in a chromosomally abnormal baby that has led many IVF physicians to strongly oppose the transfer of aneuploid embryos to the uterus.
Certain meiotic aneuploid trisomy embryos (e.g. trisomies 13, 18, & 21) can and sometimes do, result in aneuploid concepti. Thus, in my opinion, unless the woman/couple receiving such embryos is willing to commit to terminating a resulting pregnancy found through amniocentesis or chorionic villus sampling (CVS) to be so affected, she/they are probably best advised not to transfer such embryos. Other autosomal trisomy embryos will hardly ever produce viable euploid concepti and can thus, in my opinion be transferred in the hope that auto correction will occur in-utero. However, in all cases, and amniocentesis or CVS should be performed to make certain that the baby is euploid. Conversely, no autosomal monosomy embryos are believed to be capable of resulting in viable pregnancies, thereby making the transfer of autosomal monosomy embryos, in the hope that they are “mosaic”, a far less risky proposition. Needless to say, if such action is being contemplated in any such cases, it is absolutely essential to make full disclosure to the patient (s) , and to insure the completion of a detailed informed consent agreement which would include a commitment by the patient (s) to undergo prenatal genetic testing (amniocentesis/CVS) aimed at excluding a chromosomal defect in the developing baby and/or a willingness to terminate the pregnancy should a serious birth defect be diagnosed.
Good luck!
Geoff Sher
Dr. Sher,
I was your patient back in 1997 and conceived twins. I know that I had implantation dysfunction. At that time you placed me on Heparin 5,000 U bid, a baby ASA, glucocorticoids and IVIG.
Before conceiving in’97 through you, I had a premature son after 7 years of infertility treatments. I had many failed IUIs, 7 unsuccessful GIFTs, 1 failed ZIFT and possibly one chemical pregnancy. I eventually conceived my son though IUI and a daily baby ASA. After positive cardiac activity, I had a massive bleeding episode at 6 weeks and then went into preterm labor at 23 weeks.
Now for the tricky part. Prior to my twin’s birth in 97′ through your clinic, I had a trigeminal neuralgia affecting all of my teeth with intermittent excruciating episodes of tooth pain. The neuralgia was possibly triggered by a root canal. During the course of your treatment with IVIG, glucocorticoids, heparin and ASA 81 mg, the neuralgia went away and never came back. I think the glucocorticoids and IVIG were the reason it went away.
In January of 2017, I had a face lift and now once again have a trigeminal neuralgia that is affecting my ears bilaterally. The neuralgia symptoms started one day post op and may be attributed to the movement of nerves and/or nerve compression. This excruciating pain is lancinating and burning. My neurologist thinks that the cause is autoimmune and wants to treat me with IVIG and steroids. What blood tests should she order and what is your recommendation for treatment? She wants to find a reason to give me IVIG.
Prednisone 2o mg qd, started 4/17 helped initially, however, it is not enough. I had a work up by a Rheumatologist for a systemic disorder that came back negative, with the exception of some positive ANA antibodies. I am desperate for treatment. Should my neurologist test for those same antibodies that you did in ’97? My records are not available. What antibodies should she test for? Treatment wise, what do you recommend in terms of how many IVIG infusions, dose of glucocorticoids and any other medications. I am desperate and have been to a least 12 specialists. This neuralgia has been going on for 19 months. Lyrica helps with the pain, however, the side effects are horrible.
Thank you so much for your advice!
Candace
Hi Candace,
I am afraid I cannot help here as I have no experience when it comes to trigeminal neuralgia and a basis for autoimmune disease in this settimg.
Sorry…good luck!
Geoff Sher
I have just finished my second round of ivf. My first attempt ended in a chemical. My second I transferred 2 and sadly just miscarried at 6 weeks. I have low amh of .849 I am soon to be 37. I have one available frozen non tested embryo. My question is how many ivf attempts should I do. What’s the average of cycles to get a successful pregnancy. I would like to think I have some good eggs left. I dont know if I should go ahead with the frozen transfer or try to get my insurance to cover another egg retrieval. What do u think? Thanks for your help
I would first consider the following before making the decision of whether or not to do the FET before doing another ER.
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