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, I am wondering if you know of any reasons why I do not ovulate on Femara. I’ve had mid-cycle scans showing mature follicles but my body never has a natural LH surge while on Femara. I did not have a problem ovulating without medication.
Is there any explanation as to why this would happen?
Thank you.
I should add that my RE has ended up using Ovidrel the past 2 cycles when no LH surge is detected but both cycles have ended in chemical pregnancy.
Hi Kelsey,
I would need a great deal more information to comment authoritatively.
Geoff Sher
Is there any case that you recommend IVIG for?
Not really!
There is an ever growing realization, recognition and acceptance of the fact that uterine immunologic dysfunction can lead to immunologic implantation dysfunction (IID) with “unexplained infertility”, “unexplained IVF failure” and “recurrent pregnancy loss (RPL)”. Although many factors that contribute to such implantation dysfunction, in the final analysis it is activated “functional” uterine natural killer cells (NKa) in association with cytotoxic-T cells (CTL), which through the production of cytotoxic cytokines (see below) damage the “root system” (trophoblast) of the embryo causing the pregnancy either to be immediately rejected, or so compromising placentation that early pregnancy loss occurs. Both immunoglobulin-G (IVIG) and intralipid (IL) therapy given in combination with corticosteroids (e.g. dexamethasone, prednisone, and prednisolone) are used to effectively reduce/down-regulate activated NK cells.
NK cells” reach the uterus from the woman’s bone marrow, early in the menstrual cycle, as so called “parental” or “progenitor” cells. There these early NK cells proliferate under the effect of estrogens. Only upon being exposed to progesterone do they begin to propagate “functional” NK cells that release cytokines and promote implantation. The concentration of functional NK cells in the endometrium is maximal about 7 days after exposure to natural(endogenous), or synthetic (exogenous) progesterone ….i.e. corresponding to the time the time when the embryo implants into the uterine lining (endometrium).
Functional uterine natural killer (NK) cells as well as T-helper cells are immune cells that frequent the uterine lining. They produce growth factors known as cytokines that regulate orderly implantation of the embryo and facilitate placentation (development of a functional placenta……the baby’s life line).There are of two varieties of uterine cytokines: a) TH-2 (humoral) cytokines that promote permeation of the uterine wall by the embryo’s trophoblast (“root system and, b) TH-1 (cellular) cytokines that oppose trophoblastic proliferation and permeation of the uterine wall by culling interstitial trophoblastic cells. Orderly implantation and formation of a functional placenta (lifeline of the baby) requires that TH-1 and TH2 activity be in equilibrium
There are two categories of immunologic implantation dysfunction (IID) linked to NK cell activation (NKa).
•Autoimmune IID. Here, there is often a personal or family history of autoimmune conditions such as Rheumatoid arthritis, Lupus Erythematosus, and thyroid autoimmune activity (e.g. Hashimoto’s hypothyroidism) etc. Autoimmune IID also occurs in about one third of cases of endometriosis (regardless of its severity).
•Alloimmune IID. Here uterine NK cell activation results from uterine exposure to an embryo derived through fertilization of an egg by a spermatozoon which shares certain genetic (HLA/DQ alpha)characteristics with that of the mother or embryo recipient.
In both autoimmune and alloimmune IID, the end point is excessive NKa/CTL, TH-1 release that damages the embryos trophoblast, resulting in failed implantation or early pregnancy loss.
It is important to bear in mind that measurement of the concentration of blood NK cells has little or no relevance when it comes to assessing NK cell activation (NKa). Rather it is the degree of NK cell activation (cytotoxicity) that matters. In fact there are certain conditions (such as with endometriosis) where the NK cell blood concentrations is normal or well below normal and NK cell activation is markedly increased.
There are several methods by which NK cell activation (cytotoxicity) can be assessed in the laboratory. Methods such as immunohistochemical assessment of uterine NK cells and/or TH-1 and TH-2 cytokines have been used with some success. However, use of the K-562 target cell test remains the gold standard. With this test, NK cells are isolated from the woman’s blood using Flow Cytometry and are incubated in the presence of specific “target cells”. These are then incubated together. The percentage (%) of “target cells” killed through exposure to NKa/CTL-TH1 cytokines is then quantified.
Currently, there are less than a half dozen Reproductive Immunology Reference Laboratories in the U.S.A that are capable of performing the K-562 Target cell test reliably. I have for 20 + years been working with Reproductive Immunology Associates (RIA) in Van Nuys, CA and preferentially recommend them to my patients.
There exist a pervasive but blatant misconception on the part of many, that the addition of IL/IVIG can have an immediate down-regulatory effect on NK cell activity. This has established a demand that Reproductive Immunology Reference Laboratories report on NK cell activity before and following exposure to IVIG and/or IL. However, the fact is that activated “functional” NK cells (NKa) cannot be deactivated in the laboratory. Effective down-regulation of activated NK cells can only be adequately accomplished if their activated “progenitor/parental” NK cells are first down-regulated. Thereupon once these down-regulated “precursor” NK cells are exposed to progesterone, they will begin spawning normal and functional NK cells. This process takes about 10-14 days. It follows that to assess for a therapeutic response to IVIG/IL therapy would require that the patient first be treated (10-14 days prior to embryo transfer) and thereupon, about 2 weeks later, be retested. While at 1st glance this might seem to be a reasonable approach, it is in reality would be of little clinical benefit because even if blood were to be drawn 10 -14 days after IL/IVIG treatment it would require an additional 10 days to receive results from the laboratory and by that time it would be far too late to be of practical advantage.
Neither IVIG nor IL is capable of significantly suppressing already activated “functional NK cells”. For this to happen, the IL/IVIG would have to down-regulate progenitor (parent) NK cell” activity. Thus it should be infused several days prior to ovulation or progesterone administration so that the down-regulated “progenitor/precursor” NK cells” can propagate a sufficient number of normally regulated “functional NK cell” to be present at the implantation site 7 days later.
It is very regrettable that so many patients are being denied the ability to go from “infertility to family” simply because (for whatever reason) so many reproductive specialists refuse to embrace the role of immunologic factors in the genesis of intractable reproductive dysfunction. Hopefully this will change …and the sooner the better.
Geoff Sher
800-780-7437
Hi Dr Sher, why is it an issue to have high sperm volume? My partner’s sperm volume ranges between 5-9ml (normally above 5.5ml). Surely it’s good to have more sperm? But I was told it should be lower than 5.5ml
It is definitely NOT an issue!
Geoff Sher
Hi Dr. Sher,
Currently in first IVF cycle, 1 day post ER. Age 31 and diagnosed with low ovarian reserve (AMH 0.5). Was on an aggressive protocol. Of the 6 eggs that were retrieved yesterday, 4 were mature and just found out that only 1 has fertilized. Any reason we would want to ask about a 3 day transfer rather than 5 day? 3 day hasn’t been brought up by the doctor, so I’m assuming there’s reasons and don’t want to offend them…. but definitely interested in your thoughts.
Thank you!
Alli
In my opinion, it is always better to do ma day 5-6 transfer. Embryos that dont makle it to blastocyst would not have propagated a viable pregnancy had they been transferred earlier.
With IVF, embryos may be transferred at the cleaved stage, 2 days following fertilization (2-4 cell stage) or 3 days post-fertilization (5-10 cell stage or alternatively, 5-6 days following fertilization, at the blastocyst stage (>100 cells). Blastocyst embryo transfer thus requires extending the embryo culturing duration for an additional 2-3 days.
With blastocyst transfer, the chance of pregnancy is significantly higher than with cleaved embryo transfers. This is because many numerically chromosomally abnormal (aneuploid) embryos arrest in development before they reach the blastocyst stage.
Previously (and to a large extent even today), IVF doctors and embryologists have intuitively believed that the uterus provides a more “natural” and favorable environment for embryo development, than the petri dish and incubator and accordingly have held that the sooner an embryo is transferred to the uterus, the better off it would be. By this belief an embryo transferred as on day 2 -3 post-fertilization rather than as a blastocyst (on day 5 or 6) would have a better chance of resulting in a live birth. We now know this to be erroneous.
Background information: Before the freshly fertilized egg, starts to cleave (divide), it is called a zygote. After the first 24 hours, (Day 1) the embryo has divided into 2 cells. By Day 2 the embryo has 4 cells blastomeres and by the third day, there should be between 6 and 9 cells. Up to that point, embryonic development is under the control of maternal genes in the egg. Around the 8 cell stage, the embryo’s own genes (embryonic genome) begin to take over control of development. By the fourth day, the embryo has between 16 and 32 cells. At this point it looks like a mulberry and is called a morula. Until the morula stage, all of the embryo’s cells are the same and are “totipotential” (i.e. they have the ability to ultimately develop into any tissue or organ type). By day 5 post-fertilization, differentiation of the embryo begins. A fluid-filled cavity blastocoel forms in the center of the conglomerate of blastomeres. This blastocoel will eventually become the amniotic sac and the fluid surrounding the conceptus in the uterus.
The cells around the outside of the morula develop into the trophectoderm, which will eventually form the placenta and fetal membranes, while the cells on the inside of the morula aggregate and group together to form the inner cell mass, which ultimately develops into the fetus. This complex creation is now called a blastocyst. By this stage the embryo comprises more than 100 cells. As the blastocoel fills with fluid, the blastocyst expands, its walls thin out and it eventually breaks through (hatches) its envelopment zona pellucida. The trophectoderm then begins to invade the uterine lining (implantation) by the 6th to 8th day after ovulation (or egg retrieval in the case of IVF treatment).
Human embryos are very fickle. They have specific metabolic requirements in order to survive. The earliest type of artificial embryo culture media developed for IVF purposes was relatively simple in composition and could only support limited embryonic development in the Petri dish and incubator. Thus, the majority of embryos cultured in such media could only survive to the third day, whereupon their development would usually arrest. Subsequent improvements in media composition allowed for more reliable embryo development to the third day…which became and remained the standard time at which embryos were transferred for more than two decades.
In the mid-1990s, researchers in Australia, Scandinavia and the USA simultaneously developed a new generation of culture media that could support the growth of embryos to the fifth or sixth day. This development was based on a clearer appreciation of the metabolic needs of the early embryo. Now, contingent upon the age of the egg provider, approximately 30-40% of morphologically “good quality” day 3 embryos (comprising 5-9 cells with minimal/no fragmentation) can be grown to the blastocyst stage using such advanced culturing methods.
A few years ago I and my research partner, Levent Keskintepe PhD, reported on the fact that embryos that failed to develop into blastocysts were almost always aneuploid and incapable of propagating a viable pregnancy (i.e. “incompetent”). However, not all embryos that developed into expanded blastocyst were chromosomally normal and “competent”. As such, embryos that fail to develop in the laboratory to the expanded blastocyst (advanced preimplantation) stage by day 5-6 post-fertilization, would not have developed into a viable pregnancy had they been transferred to the uterus earlier on in the cleaved stage (day 2-4 post-fertilization). Accordingly, there is in my opinion, little justification for transferring embryos that have not developed into fully expanded blastocysts by day 5-6 post-fertilization. Since many aneuploid (“incompetent” embryos are culled out during the developmental stage, it follows that blastocysts are much more likely to be “competent” than are cleaved, earlier stage embryos. Thus blastocyst transfer reduces the incentive on the part of IVF doctors to transfer multiple embryos in order to bolster their success rates, and the process this reduces the risk of high order multiple pregnancies (triplets or greater) with its incumbent risks to both mother and babies.
As mentioned earlier on, the older the egg provider, the lower the chance that her fertilized eggs with develop into blastocysts. In fact, in spite of the introduction of specialized culture systems and other new techniques, at best (even in younger women) 40% of “good quality” day 3 embryos (those that are 6-9 cells and have little fragmentation) will develop into expanded blastocysts by day 5-6 post-fertilization in younger women. And the blastocyst conversion rate declines rapidly as the woman ages beyond 35 years, such that by age 40 years, the conversion rate is about 15-20% and by 43 years of age it is <10-15%. Since blastocysts are much more likely than cleaved embryos to implant following embryo transfer (ET), the transfer of 1-2 good quality blastocysts will in any age category, proportionately yield a far better IVF success rate
The new found ability to safely freeze blastocysts using a new ultra-rapid process known as vitrification which does not compromise their subsequent (post-thaw) ability to propagate a viable pregnancy, has led to many IVF programs to preferentially cryobank vitrified blastocysts for transfer in one or more subsequent frozen embryo transfer (FET) cycles. Also, the introduction of Preimplantation genetic sampling (PGS) with full numerical chromosomal assessment (full karyotyping) using methods such as comparative genomic hybridization (CGH) and next generation gene sequencing or (NGS) now permits the identification and selective transfer of only the most competent blastocysts, thereby improving IVF outcome substantially. This allows many older women and those with diminished ovarian reserve(DOR) who are averse to doing egg donation-IVF, to have their embryos biopsied and then bank (stockpile) their embryos over several cycles, in the hope of subsequently transferring only those that are determined through PGS to be the most “competent” ones
For all these reasons (and there are probably many others) most IVF centers of excellence have graduated from transferring cleaved embryos to blastocyst transfers.
Other than patient preference and easing pressure on doctor and/or patient, there is in my view seldom a justification for transferring embryos on day 2 or day 3. In light of the aforementioned revelations and developments I therefore hold that blastocyst transfer should be the embryo transfer method of choice.
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.
Geoff Sher
hi,
i had 4 failed Ivf fresh and 2 failed transfer, last transfer i finally conceive but the baby died at 9 weeks and4 days according to the ultrasound as i was having my 12 week ultrasound i had a d and c the same day we’ve found out as it was needed. this is what they found on the specimen. Sorry as it is long. I am going to see a specialist but since I live in a thirt world country with limited knowledge in fertility i thought you might be able to advise me. As i am now desperate and really down at the moment.
specimen consist of tan spongy and membranous tissue with blood clot 35x50x15 mm in aggregater dimention. No foetal parts seen. There are possible villi. representative sections in blocks a1 and a2.
Description: Section show placental villi of early pregnancy together with a moderate amount of inflamed decidua as well as one large fragment of weakly secretory endometirum. Some of the placental villi are hydropic. Occasional villi contain inconspicous empty fetal blood vessels. There is trophoblast proliferation without atypia.The endometrial fragment appears to be derived from the isthmic portion with glands of irregular shape showing weak secretory activity embedded in an abundant dense stroma. One area of the A. A fragment of endometrium shows increased numbers of thick walled blood vessels with narrowed lumena filled with red blood cells. No obvious vascular occlusion is seen in this fragment. Features are suggestive of a benign endometrial (isthmic) polyp.
No fetal tissue is identified. There is no evidence of malignancy or of trophoblast decease.
Diagnosis: UTERINE CURETTINGS – product of conception
The pathology report does unfortunately not shed light on the underlying cause of the losses.
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
ANNOUNCEMENTS:
1.About my Retirement by mid-2018:
After > 30 years in the field of Assisted Reproduction (AR), the time is approaching for my retirement. 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.
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