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 have diminished ovarian reserve and I am wondering how injected estrogen improves a stimulation cycle. Does it improve egg quality? Does it increase the number of antral follicles that develop into mature eggs? Can it be counterproductive since estrogen is not at a constant level during the follicular phase of an unstimulated cycle? Please let me know how it works. Thank you.
Older women, and those who have diminished ovarian reserve (DOR) with resistance to ovarian stimulation (“poor responders” are often labeled as being producers of “poor quality eggs and embryos, and advised to seek IVF with egg donation. In fact, in my opinion such “recipe” or “one size fits all” attitude towards ovarian stimulation is not always justified. In my opinion it should be replaced by a customized approach that addresses specific individualized needs on a case by case basis. This article addresses my personal preference in selecting a stimulation protocol in such cases.
The older a woman becomes, the more likely it is that her eggs will be chromosomally/genetically “incompetent” (not have the potential upon being fertilized and transferred, to result in a viable pregnancy). That is why, the likelihood of failure to conceive, miscarrying and of giving birth to a chromosomally defective child (e.g. with Down Syndrome) increases with the woman’s advancing age. In addition, as women age beyond 35Y there is commonly a progressive diminution in the number of eggs left in the ovaries, i.e. diminished ovarian reserve (DOR). So it is that older women as well as those who (regardless of age) have DOR have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production of LH biological activity which can result in excessive LH-induced ovarian male hormone (predominantly testosterone) production which in turn can have a deleterious effect on egg/embryo “competency”.
While it is presently not possible by any means, to reverse the age-related effect on the woman’s “biological clock, certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can make matters worse. Similarly, the amount/dosage of certain fertility drugs that contain LH/hCG (e.g. Menopur) can have a negative effect on the development of the eggs of older women and those who have DOR and should be limited.
I try to avoid using such protocols/regimes (especially) in older women and those with DOR, favoring instead the use of the agonist/antagonist conversion protocol (A/ACP), a modified, long pituitary down-regulation regime, augmented by adding supplementary human growth hormone (HGH).
•The Agonist/Antagonist Conversion Protocol Women who have a tendency to overproduce LH (i.e poor responders, older women) require a form of pituitary blockade (with GnRH agonist or an antagonist) throughout the stimulation period to prevent the progressive and excessive rise in LH –induced ovarian male hormones …(.mainly testosterone) can adversely influence egg development, resulting in compromised embryo quality. However, prolonged administration of GnRH agonists (e.g. Lupron/Lucrin/Buserelin/Superfact/Decapeptyl) starting several days prior to the initiation of gonadotropin therapy (the long protocol) and then continued through the gonadotropin stimulation phase (until the day of the hCG trigger) has one possible down side, namely that the agonist can compete for FSH binding sites on follicle cell FSH receptors and thereby blunt the response to gonadotropin stimulation. Obviously this is the last thing that women who have DOR (“poor responders”) need. It is for this reason that I, some time back developed the Agonist/Antagonist Conversion Protocol (A/ACP) With this protocol, the women starts by taking a combined BCP for 8 or more days, whereupon a GnRH agonist is overlapped with the pill for two days. The BCP is then stopped and daily agonist administration continues until the onset of menstruation (usually within 3-6 days). At this point the agonist is completely supplanted with daily injections of 125mcg, antagonist (Ganirelix/Cetrotide/Orgalutron). Commencing within a few days of initiating antagonist therapy, daily FSH-gonadotropins (usually Folistim) injections are commenced. A few days later daily injections of Menopur 75U daily is added. Gonadotropin and antagonist therapy are both discontinued on the day of the hCG trigger
•Agonist/antagonist conversion protocol combinred with Estrogen “priming”: The addition of parenteral estradiol valerate (E2V) for about a week following the initiation of the agonist/antagonist conversion protocol (A/ACP), prior to commencing FSH-dominant gonadotropin stimulation appears to further enhance ovarian response, presumably by up-regulating ovarian FSH-receptors. Accordingly, for women with severely diminished ovarian reserve (“very poor responders”) he adds “estrogen priming” by administering of estradiol valerate (Delestrogen) during the 1st week of antagonist therapy. This appears to enhance ovarian follicular response to gonadotropins. Following one week of “estrogen priming”, gonadotropin therapy is commenced and is this is continued along with antagonist therapy (as above) until the day of the hCG trigger. In my opinion, in cases of severe DOR with very poor response to stimulation, the use of A/ACP + “estrogen priming ” there is in my experience a relatively low (<15%) cycle cancellation rate. In fact , a significant number of patients who previously had been advised to give up and switch to egg donation subsequently achieved viable pregnancies using the A/ACP with “estrogen priming”.
•Augmentation of ovarian stimulation with Human Growth Hormone (HGH) Several researchers have shown that the administration of human growth hormone (HGH), as an adjunct to ovarian stimulation, enhances follicle response in older women and those with DOR and so can help optimize egg quality. It is thought that HGH hormone by increasing the production of insulin-like growth factor 1 (IGF-1), improves follicle development, estrogen hormone production and egg maturation. Two basic mechanisms have been proposed: 1) improving the response to gonadotropin therapy by up-regulating the FSH receptors on the granulosa cells that form the inner lining of follicles and, 2) through a direct enhancing effect of HGH on the egg’s mitochondrial activity. While human eggs do have HGH receptors, those retrieved from older women show decreased expression of such receptors (as well as a reduction in the number of functional mitochondria) as compared with those derived from younger women. In fact, it has recently been shown that older women treated with HGH showed a marked increase in functional mitochondria in their eggs along with improved egg quality. My personal experience in selectively prescribing HGH as an adjuvant to women with DOR, older women and those with unexplained egg quality deficits, is that if used in combination with the A/ACP it seems to indeed enhance egg quality and ovarian response, culminating in improved IVF outcome.
•Embryo Banking: I further recommend that such women be offered access to embryo banking of PGS (next generation gene sequencing/NGS)-selected normal blastocysts, the subsequent selective transfer of which by allowing them to to capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” could significantly enhance the opportunity to achieve a viable pregnancy
“When designing an individualized ovarian stimulation protocol woman with diminished ovarian reserve and/or older women the primary objective is to optimally regulate the intraovarian testosterone environment by: 1. avoiding protocols of stimulation that cause increased LH exposure, using predominantly FSH-dominant medications such as Follistim/Gonal-F and Puregon, limiting the administration of LH-containing gonadotropins, augmenting the protocol by adding HGH accurately timing the hCG trigger to coincide wit optimal follicle/egg development and offering such women access to “Embryo Banking with the selective transfer of PGS-selected embryos..
Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•The Fundamental Requirements For Achieving Optimal IVF Success
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
• A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
•Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
•Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
•Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Blastocyst Embryo Transfers Should be the Standard of Care in IVF
•Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
•Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
•Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
•Preimplantation Genetic Testing (PGS) in IVF: It Should be Used Selectively and NOT be Routine.
•Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
•PGS in IVF: Are Some Chromosomally Abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
•PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
•Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
•How Many Embryos should be transferred: A Critical Decision in IVF.
•The Role of Nutritional Supplements in Preparing for IVF
•Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
•IVF Egg Donation: A Comprehensive Overview
I invite you to arrange to have a Skype or an in-person consultation with me to discuss your case in detail. If you are interested, please contact Julie Dahan, at:
Email: Julied@sherivf.com
OR
Phone: 702-533-2691
800-780-7437
I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Thank you for this response.m
My husband and I have been trying for a baby for 3.5years, I am 35 and my husband is 36. After various testing and exploratory surgeries no issues were found; tubes were flushed, no endometriosis, no polyps etc, everything physically looked fine. We were diagnosed as unexplained infertility by our local Reproductive Endocrinologist. We did an IVF stim cycle, got 10 eggs, all fertilised, 5 of which made it to day 5&6 blasts.
After a couple of failed IVF transfers we went on to see a Reproductive Immunologist in Sydney Australia named Prof. Gamal Matthias (studied under Dr Beer). After further testing, we have now been told that I most likely have activated natural killer cells (auto-immune), but due to costs of sending blood to the USA for testing, I am being treated as though they are activated without having done the test. Also, my husband and I have some HLA matches (allo-immune), as well as me having some matches within my own DNA. We have been told we have approx. 70% chance of conceiving a baby with treatment. Also that there is 50% chance of any embryo having a HLA match and therefore failing. I have never had a positive pregnancy test or chemical pregnancy.
We are about to try our second FET cycle on our current immune protocol of:
0.5mg Dexmethsone, 3 tabs a day, from Day 1-21
40mg Clexane Injections, once a day, 7 days before transfer
Progesterone Pessaries, 3 times a day, from Transfer to Period
I had an intralipid infusion prior to the last FET cycle 2 months ago along with the above.
I have two main questions:
1.Is it best to only transfer one embryo at a time in case the HLA match prevents either of 2 embryos implanting or will the medications I am taking make this a non issue? In our case, does 2 embryos mean more chance that one will implant or higher chance that both will fail?
2.Is it best to abstain from trying naturally during the IVF cycle to ensure no negative affect is had on the transferred embryo as far as the possibility of match in a natural embryo causing both to fail. Or is it best to go for it naturally too and try on both fronts?
After this transfer we only have one frozen embryo left. We want to make sure we are giving this one and the last one every chance. Any further advice you have for us would be much appreciated. Thanks.
1. Is it best to only transfer one embryo at a time in case the HLA match prevents either of 2 embryos implanting or will the medications I am taking make this a non issue? In our case, does 2 embryos mean more chance that one will implant or higher chance that both will fail?
A: In thed case of a partial DQ alpha match + NKa it would in my opinion be advisable to transfer one at a time (see below)
2. Is it best to abstain from trying naturally during the IVF cycle to ensure no negative affect is had on the transferred embryo as far as the possibility of match in a natural embryo causing both to fail. Or is it best to go for it naturally too and try on both fronts?
A: If there is DQ alpha match plus NKa+, I would not recommend an attempt a pregnancy without appropriate reproductive immunotherapy such as intralipid + steroids on board.
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 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)
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
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.
Last year I had a chemical pregnancy. After that we were unable to conceive again and were eventually diagnosed with 2 blocked tubes. First IVF in Feb this year resulted in 5 blastocysts, a top grade was transferred but no implantation and some spotting prior to test date. In June we did a frozen embryo transfer of a hatching blastocyst, added steroids, had a scratch and added a progesterone injection at lunch time along with pessaries. No spotting this time and a chemical pregnancy. We have 3 frozen blastocysts left is it worth trying again. Are chemical pregnancys bad luck or do you think given 2 chemicals and a failed implantation that there is something underlying preventing proper implantation? Should we be looking at karotyping, more immunes or hidden infection testing (given the blocked tubes)
I have seen dr lower to rule out Ashermans syndrome as possible cause
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.
•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 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)
•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:
•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.
Hello Dr Sher,
I am 41 (going 42 in sept). My partner is 48. We just started ivf to start a family (never of us had kid, had any infertility issues). We had done our tests and all came back normal for our age, no sperm issue a de for me I am average for my age. I understand that my chance of still having good quality eggs is very slim so this is why we just turn to ivf before I turn 42 and become too late. So first attempt (I could only afford 1 attempt), they use icsi because i was worried with little number to risk no fertilisation at all (there is no issue with the sperm mobility). I got 6 follicles (7 one was too small). 6 eggs retreived, 4 matured, 3 fertilized and 2 embryos: 1 was a day 5 blastocyst good quality and secone a day 6 blastocyst good quality (the icm starting showing on day6). So we had one embryo transfer on day 5 and the second was good to be frozen on day6.
Unfortunately the hcg was negative, the nurse told me there was no trace (<0.01).
So does it mean my egg are bad, good enough to fertilize and get a good quality blastocyst but stop developing in my womb? I suppose if no trace of hcg there was no implantation at all? They said my uterine lining was perfect.
I am wondering if the second frozen day 6 Embryo could serving thawing and if it could implant or because it took longer to develop my chance are not looking good at all?
In your experience what are you thoughts of possible cause and chance of a FET success?
If all failed, can we simply continue in a natural way under a Clomiphene treatment monitored at least to get a chance of more than 1 egg per natural cycle or this type of treatment is only working of younger women?
Thanks in advance for your opinion.
Hi Dr. Sher,
I just transferred two frozen BB6 embryos from a donor cycle. My lining was 9.1. I forgot the type, but every monitoring appointment my doctor said everything looks great. Transfer went smoothly. My estrogen and progesterone were checked three days after transfer, and nurse said my levels were fine- so I continued with 2 estrace pills 2x day and 1mlg of progesterone in oil. My test came back negative.
(I prepped for the frozen transfer with estrogen, progesterone, medrol, and doxcyline.)
My doctor was surprised by the result. He’s reviewing my file and we are having a consult. However, I reviewed my file too and when I started this journey my prolactin was elevated. He retested twice (with fasting an no nipple stimulation) and eventually it was lowered to 24.
I’m wondering if maybe they did not retest my prolcatin before this cycle and it effected implantation. Isn’t implantation effected by high prolactin?
Any information would be helpful.
Thank you,
Elyse
A raised prolactin can be associated with an underlying clinical or subclinical thyroid deficiency. The reason this could be relevant is because this is oftyen due to an underlying autoimmune thyroid process and about 50% of women who have antithyroid antibodies will in addition have activated uterine natural killer cells which can lead to an immunologic implantation dysfunction.
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
•Why did my IVF Fail
•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)
•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:
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
•IVF Egg Donation: A Comprehensive Overview
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.