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!
please can you shed more light on membranous dysmenorrhoea as regards the etiology, complications,effects on fertility and treatment if any. I have an extensive history of the condition which does not seem to match other cases.
This is (as you probably know) a very painful type of menses. It is associated with the passage of the entire endometrial cast. The cause is unknown. Treatment would be to try using a BCP for a while. The pain should respond to NSAI such as Aleve and Ibuprophen.
Geoff Sher
Dr Sher thank you for all the support. For my FET my E2 levels are 2155 and lining is 9mm. They are cutting my daily estradiol to half the dose. I am starting my progesterone shots today. What are your thoughts?
Sounds right to me!
Geoff Sher
Hi Dr Sher. I thought I posted but it’s not showing up, so sorry if this is duplication.
I have wrote you a few times. I recently had a FET, this was my first and do acupuncture as well. I’m currently 14dp5dt. I had a normal pgs embryo that was of excellent quality and hatching when transferred. I had my beta on Monday and received solid results hcg 273 and progesterone was 21. The week before I had some cramping and light brown spotting. I took this as implantation. My second HCG Wednesday was 223 so I was devastated. I’m repeating tomorrow but I’ve been down this road a few too many times. Of note in my background, my husband and I started ttc in Feb 2014. didn’t have a lot of at home positive opks. finally that October I had a positive pregnancy test but mc at 5 wks. I was then dx with Hashimotoes. My antibodies were 160’s-not sure if that is significant? I’ve seen some in the thousands. That following Feb I had an Us showing few follicles and a slight uterine septum. I did 4 months of clomid which thinned my lining. Switched to femara and then 2nd month of femara had iui and was pregnant but had missed mc noted at 8 weeks, only saw a gestational sac. Then I went to an RE. Had rpl panel that was negative. She did a hysteroscopic septoplasty in December. Then March 2016 had IUI, pregnant, parital molar. HB was seen at 6 weeks but slow. Then d & c. Both my husband & I had negative karyotypes. In the midst of monitoring the parital molar, I became pregnant in late july/august my hcg was 80 and then repeat 2 days later in the 40s. the surprisingly pregnant in later August/September but same thing happened. The RE did an US at 5 weeks showing my lining at a 3. She had me do another hysteroscopy, a few septal cells had returned and she removed them. We did 3 IUIs after that & all BFN. We moved to IVF with pgs and that’s where Im at now. I’ve had 3 early losses, one pending, and 2 losses at 8 weeks. I’m kind of at a loss of what to do. My clinic doesn’t do intralipids or prednisone. I had a consultation at one of the Sher clinics in IL prior to my IUIS. Dr Emmi wanted me to get labs but nothing was covered by INS and at the point wanted to be able able to afford IVF if needed which isn’t covered either. Based on the way the FET looked, I feel like it appears there was implantation with a good hcg value. Any advice about what to change? I’m not sure if they would do a transfer if I had intralipids and prednisone from elsewhere. Do you think the intralipids & prednisone would be beneficial-just tx empirically? During this time, I’ve been on estradiol 2mg TID and PIO. Not sure if aspirin would be helpful? Could it be that though the embryos we have look good, they have a mitochondrial issue and then at some point don’t have enough energy to keep dividing? Or could this really just be that bad of luck? I’ve read through a lot of your material in regards to RPL. Also, my husband’s semen analysis have been great. Any advice would be greatly appreciated. Thanks in advance.
I responded to this post earlier today
Geoff Sher
Hi Dr Sher,
I have wrote to you a few times. I recently had a FET, this was my first and do accupuncture as well. I’m currently 14dp5dt. I had a normal pgs embryo of excellent quality and was hatching when transferred. I had my beta on Monday and received solid results hcg was 273 and progesterone was 21. The week before I had some cramping and light brown spotting, I took this as implantation. My second HCG Wednesday was 223 so I was devastated, I’m repeating tomorrow but I’ve been down this road a few too many times. Of note in my background, my husband and I started ttc in Feb 2014. Didn’t have a lot of at home positive opks. Finally that October I had a positive pregnancy test but mc at around 5 wks. I was then dx with Hashimotos. My antibodies were in the 160’s-not sure if this is significant? I’ve seen some in the thousands. That following Feb I had an US showing few follicles and a slight uterine septum. I did 4 months of clomid that thinned my lining. Switched to femara and then then 2nd month had IUI and was pregnant but had a missed mc noted at 8 weeks, only saw a gestational sac. Then I went to an RE. Had rpl panel which was negative. She had me fix my uterine septum. Then march 2016 I was pregnant again-partial molar, did have a low heartbeat then d/c. In the midst of being monitored I became pregnant in late july/august. @ 5 weeks my hcg was 80 and then repeat 2 days later in the 40s. Then surprisingly pregnant in late august/sept and the same thing happened with the hcg. my lining as she had me do an us showed it was 3 when I was 5 weeks so very thin. They had me do another hysteroscopy and the septal cells returned. I did 3 iuis after that and negative tests so we went on to IVF. So now Ive had 4 early pregnancy losses and two noted around 8 weeks. I’m kind of at a loss of what to do. My clinic does not do intralipids or prednisone. I had a consultation at one of the Sher clinics in IL regarding this and Dr Emmi wanted me to get labs done but nothing was covered by INS and at that point we wanted to be able to afford IVF if needed which isn’t covered by INS either. Based on the way the FET looked, I feel like it appears there was implantation with the good hcg value. Any advice about what to change. I’m not sure if they would do a transfer if I had intralipids and prednisone from elsewhere. Do you think the intralipids and prednisone would be beneficial-just treating empirically? During this time I’ve been on estradiol 2mg tid and PIO. Not sure if aspirin would be helpful? Could it be that though the embryos we have look good, they have mitochondrial issues and then at some point don’t have enough energy to keep dividing? Or could this really just be that bad of luck? I’ve read through a lot of your material in regards to recurrent pregnancy loss. Any advice would be greatly appreciated. Thanks in advance.
All I can say is that this sounds characteristic of an implantation dysfunction rather tan an embryo issue. Having said this, whether it is due to an endometrial lining issue and/or immunologic would need to be fully evaluated. I can tell you that 50% of women who have autoimmune hypothyroidism (Hashimoto’s) have activation of uterine natural killer cells (NKa) which definitely has a very adverse effect on implantation. Also, an endometrial lining of <8mm is usually not compatible with healthy 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 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
ANNOUNCEMENTS:
1.About my Retirement by mid-2018:
After > 30 years in the field of Assisted Reproduction (AR), the time has finally come for me to plan on retiring from full-time clinical medicine within a year. If you are interested in my medical services prior to my retirement, 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.
2.The 4th edition of my newest book ,
“In Vitro Fertilization, the ART of Making Babies” is now available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Geoffrey Sher MD
Good afternoon,
My name is Cornelia. I am 45 year old and I lost several pregnancies, they all stopped from evolution befor maximum 10 weeks. For several years I made a lot of tests and analysis to see the causes, but unfortunately no one could find the cause und unfortunately menopause installed in the years.
Now I reading about PRP therapy for ovaries.
Please, telll me about ovarian rejuvenation. Is this possible?
Yours faithfully!
Unfortunately there is NO METHOD whereby eggs can be rejuvenated. Your age makes the likelihood of any given egg being genetically/chromosomally normea <5%. You need to consider egg donation and if that is not an option then consider the following.
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”.
Older women as well as those who (regardless of age) have diminished ovarian reserve (DOR) tend to produce fewer and less “competent” eggs, the main reason for reduced IVF success in such cases. The compromised outcome is largely due to the fact that such women tend to have increased LH biological activity which often results in excessive LH-induced ovarian testosterone production which in turn can have a deleterious effect on egg/embryo “competency”.
Certain ovarian stimulation regimes either promote excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), augment LH/hCG delivered through additional administration (e.g. high dosage menotropins such as Menopur), or fail to protect against body’s own/self-produced LH (e.g. late antagonist protocols where drugs such as Ganirelix/Cetrotide/Orgalutron that are first administered 6-7 days after ovarian stimulation has commenced).
I try to avoid using such protocols/regimes (especially) in older women and those with DOR, favoring instead the use of a modified, long pituitary down-regulation protocol (the agonist/antagonist conversion protocol-A/ACP) augmented by adding supplementary human growth hormone (HGH). I further recommend Staggered IVF with embryo banking of PGS (next generation gene sequencing/NGS)-normal blastocysts in such cases. This type of approach will in my opinion, optimize the chance of a viable pregnancy per embryo transfer procedure and provide an opportunity to capitalize on whatever residual ovarian reserve and egg quality still exists, allowing the chance to “make hay while the sun still shines”.
I strongly recommend that you visit 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.
•The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
•Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
•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?
•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
•Implications of “Empty Follicle Syndrome and “Premature Luteinization”
•Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
ANNOUNCEMENTS:
1.About my Retirement by mid-2018:
After > 30 years in the field of Assisted Reproduction (AR), the time has finally come for me to plan on retiring from full-time clinical medicine within a year. If you are interested in my medical services prior to my retirement, 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.
2.The 4th edition of my newest book ,
“In Vitro Fertilization, the ART of Making Babies” is now available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Geoffrey Sher MD