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 was hoping you could help me with a few queries.
I am 40 years old and considering doing medicated IUI inbetween ivf cycles (I am single and using donor sperm). I generally have an endometrial thickness of 65-70mm in a natural cycle.
What drug would you recommend to use?
I also have 3 aneuploid embryos from prior ivf cycles which are all -22. Have you ever transferred monosomy 22 and had success ?
Many thanks for taking the time to answer.
Natalie
You should not do IUI at 40y , in my opinion. The chance of success is only about 1:40. You don’t have the time to waste on such a poor chance. IVF is by far your best option.
In my opinion, your monosomy 22 embryos could be mosaics…but because of your age this is highly unlikely. Again, time is your enemy.
Perhaps we should talk first. Call my assistant Patti at 702-533-2691 for an online consultation.
Geoff Sher
Good evening,
I am gearing up for my third IVF cycle. Kaiser Permanente would like me to have their typical fertility work up done. I have endometriosis and endometrial hyperplasia. My concern is that they would like me to have another HSG. I’ve had 4 in my lifetime. Each time led to a bad reaction. Immediately after the 3rd time I developed a cyst that continued to grow and leak in my POD. I have imaging that shows it wasn’t there prior to this procedure. Imaging immediately after shows it grew to 10 times the volume of my left ovary. I had difficulty walking/intercourse. They said not was wrong and ignored my complaints of pain. It finally burst a few months later and I immediately gained 10 lbs in less than a week, stretch marks on the front of my thighs, and looked pregnant. It has been hard to maintain my weight since. My weight has never fluctuated prior at the time I was 33. I am now approaching 35. My inflammation/endometriosis was controlled at this point as I had excision surgery in 1 year prior in October 2018. After this procedure I could feel inflammation traveling up my abdominal wall and up my back. I developed back acne that traveled down to my waist for the first time. They also stated that my fallopian tubes appeared closed. I had another HSG 4 months later Dec 2019 to confirm this diagnosis. The 4th time my menstruation and inflammation became so bad. I begin vomiting uncontrollably during the first day prior and during menstruation. The pain was always bad, but I never vomited from it prior to this. I would vomit from the pain of gas trapped/traveling through my intestine every 30 mins at times. At this time I did not undergo any IVF treatment or change in medication. My IVF cycles were the following year in 2020.
My question – Is endometriosis or endometrial hyperplasia a counterindication for HSG? Why would any doctor advise an HSG for a woman that already has endometriosis? I didn’t voice my concern the last two times. However, I am very hesistant to undergo an HSG a 5th time. Isn’t a diagnostic hysteroscopy and vaginal ultrasound a better alternative? I could not find any information for this online.
In my opinion, If you do not have a hydrosalpinx(which is not common with endometriosis , unless you had concomitant pelvic inflammatory disease, your tubal status is irrelevant and an HSG is of no value. You need IVF. However, endometriosis affects IVF outcome (see below).
When women with infertility due to endometriosis seek treatment, they are all too often advised to first try ovarian stimulation (ovulation Induction) with intrauterine insemination (IUI) ………as if to say that this would be just as likely to result in a baby as would in vitro fertilization (IVF). Nothing could be further from reality It is time to set the record straight. And hence this communication!
Bear in mind that the cost of treatment comprises both financial and emotional components and that it is the cost of having a baby rather than cost of a procedure. Then consider the fact that regardless of her age or the severity of the condition, women with infertility due to endometriosis are several fold more likely to have a baby per treatment cycle of IVF than with IUI. It follows that there is a distinct advantage in doing IVF first, rather than as a last resort.
So then, why is it that ovulation induction with or without IUI is routinely offered proposed preferentially to women with mild to moderately severe endometriosis? Could it in part be due to the fact that most practicing doctors do not provide IVF services but are indeed remunerated for ovarian stimulation and IUI services and are thus economically incentivized to offer IUI as a first line approach? Or is because of the often erroneous belief that the use of fertility drugs will in all cases induce the release (ovulation) of multiple eggs at a time and thereby increase the chance of a pregnancy. The truth however is that while normally ovulating women (the majority of women who have mild to moderately severe endometriosis) respond to ovarian stimulation with fertility drugs by forming multiple follicles, they rarely ovulate > 1 (or at most 2) egg at a time. This is because such women usually only develop a single dominant follicle which upon ovulating leaves the others intact. This is the reason why normally ovulating women who undergo ovulation induction usually will not experience improved pregnancy potential, nor will they have a marked increase in multiple pregnancies. Conversely, non-ovulating women (as well as those with dysfunctional ovulation) who undergo ovulation induction, almost always develop multiple large follicles that tend to ovulate in unison. This increases the potential to conceive along with an increased risk multiple pregnancies.
So let me take a stab at explaining why IVF is more successful than IUI or surgical correction in the treatment of endometriosis-related infertility:
1.The toxic pelvic factor: Endometriosis is a condition where the lining of the uterus (the endometrium) grows outside the uterus. While this process begins early in the reproductive life of a woman, with notable exceptions, it only becomes manifest in the 2ndhalf of her reproductive life. After some time, these deposits bleed and when the blood absorbs it leaves a visible pigment that can be identified upon surgical exposure of the pelvis. Such endometriotic deposits invariably produce and release toxins” into the pelvic secretions that coat the surface of the membrane (the peritoneum) that envelops all abdominal and pelvic organs, including the uterus, tubes and ovaries. These toxins are referred to as “the peritoneal factor”. Following ovulation, the egg(s) must pass from the ovary (ies), through these toxic secretions to reach the sperm lying in wait in the outer part the fallopian tube (s) tube(s) where, the sperm lie in waiting. In the process of going from the ovary(ies) to the Fallopian tube(s) these eggs become exposed to the “peritoneal toxins” which alter s the envelopment of the egg (i.e. zona pellucida) making it much less receptive to being fertilized by sperm. As a consequence, if they are chromosomally normal such eggs are rendered much less likely to be successfully fertilized. Since almost all women with endometriosis have this problem, it is not difficult to understand why they are far less likely to conceive following ovulation (whether natural or induced through ovulation induction). This “toxic peritoneal factor impacts on eggs that are ovulated whether spontaneously (as in natural cycles) or following the use of fertility drugs and serves to explain why the chance of pregnancy is so significantly reduced in normally ovulating women with endometriosis.
2.The Immunologic Factor: About one third of women who have endometriosis will also have an immunologic implantation dysfunction (IID) linked to activation of uterine natural killer cells (NKa). This will require selective immunotherapy with Intralipid infusions, and/or heparinoids (e.g. Clexane/Lovenox) that is much more effectively implemented in combination with IVF.
3.Surgical treatment of mild to moderate endometriosis does not usually improve pregnancy potential:. The reason is that endometriosis can be considered to be a “work in progress”. New lesions are constantly developing. So it is that for every endometriotic seen there are usually many non-pigmented deposits that are in the process of evolving but are not yet visible to the naked eye and such evolving (non-visible) lesions can also release the same “toxins that compromise fertilization. Accordingly, even after surgical removal of all visible lesions the invisible ones continue to release “toxins” and retain the ability to compromise natural fertilization. It also explains why surgery to remove endometriotic deposits in women with mild to moderate endometriosis usually will fail to significantly improve pregnancy generating potential. In contrast, IVF, by removing eggs from the ovaries prior to ovulation, fertilizing these outside of the body and then transferring the resulting embryo(s) to the uterus, bypasses the toxic pelvic environment and is therefore is the treatment of choice in cases of endometriosis-related infertility.
4.Ovarian Endometriomas: Women, who have advanced endometriosis, often have endometriotic ovarian cysts, known as endometriomas. These cysts contain decomposed menstrual blood that looks like melted chocolate…hence the name “chocolate cysts”. These space occupying lesions can activate ovarian connective tissue (stroma or theca) resulting in an overproduction of male hormones (especially testosterone). An excess of ovarian testosterone can severely compromise follicle and egg development in the affected ovary. Thus there are two reasons for treating endometriomas. The first is to alleviate symptoms and the second is to optimize egg and embryo quality. Conventional treatment of endometriomas involves surgical drainage of the cyst contents with subsequent removal of the cyst wall (usually by laparoscopy), increasing the risk of surgical complications. We recently reported on a new, effective and safe outpatient approach to treating endometriomas in women planning to undergo IVF. We termed the treatment ovarian Sclerotherapy. The process involves; needle aspiration of the “chocolate colored liquid content of the endometriotic cyst, followed by the injection of 5% tetracycline hydrochloride into the cyst cavity. Such treatment will, more than 75% of the time result in disappearance of the lesion within 6-8 weeks. Ovarian sclerotherapy can be performed under local anesthesia or under conscious sedation. It is a safe and effective alternative to surgery for definitive treatment of recurrent ovarian endometriomas in a select group of patients planning to undergo IVF
I am not suggesting that all women with infertility-related endometriosis should automatically resort to IVF. Quite to the contrary…. In spite of having reduced fertility potential, many women with mild to moderate endometriosis can and do go on to conceive on their own (without treatment). It is just that the chance of this happening is so is much lower than normal.
IN SUMMARY: For young ovulating women (< 35 years of age ) with endometriosis, who have normal reproductive anatomy and have fertile male partners, expectant treatment is often preferable to IUI or IVF. However, for older women, women who (regardless of their age) have any additional factor (e.g. pelvic adhesions, ovarian endometriomas, male infertility, IID or diminished ovarian reserve-DOR) IVF should be the primary treatment of choice. 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. •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) •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! •Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas •Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year •A personalized, stepwise approach to IVF •How Many Embryos should be transferred: A Critical Decision in IVF? •Endometriosis and Immunologic Implantation Dysfunction (IID) and IVF •Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice. •Endometriosis and Infertility: The Influence of Age and Severity on Treatment Options •Early -Endometriosis-related Infertility: Ovulation Induction (with or without Intrauterine Insemination) and Reproductive Surgery Versus IVF •Treating Ovarian Endometriomas with Sclerotherapy. •Effect of Advanced Endometriosis with Endometriotic cysts (Endometriomas) on IVF Outcome & Treatment Options. •Deciding Between Intrauterine Insemination (IUI) and In Vitro Fertilization (IVF). •Intrauterine Insemination (IUI): Who Needs it & who Does Not: Pro’s & •Induction of Ovulation with Clomiphene Citrate: Mode of Action, Indications, Benefits, Limitations and Contraindications for its use •Clomiphene Induction of Ovulation: Its Use and Misuse! ______________________________________________________ ADDENDUM: PLEASE READ!! INTRODUCING SHER FERTILITY SOLUTIONS (SFS) Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.
If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or, enroll online on then home-page of my website (www.SherIVF.com).
PLEASE SPREAD THE WORD ABOUT SFS!
Geoff Sher
I’m 36 years old with pcos. I have 3 daughters. 1st was concieved with clomid and iui. 2nd was concieved 8 years later on 3rd round of letrozole. 3rd was concieved 2 months after my second was born. Naturally. Pregnancy 4 was also Naturally but ended in miscarriage due to trisomy 16. Pregnancy 5 was Naturally as well. Healthy baby boy we lost him at 14 weeks gestation. Pregnancy 6.. 100 mg of clomid..another healthy boy.. we lost him at 12 weeks. Pregnancy 7. 7.5 mg of letrozole.. a baby girl ended in miscarriage as well. Cause was triploid at 7 weeks.
I am starting letrozole again and just had cycle day 3 labs done. Total testosterone came back high at 86.6 ng/dl and dheas came back low at 44 ug/dl.
My dr wants me to take a dhea supplement.. wouldn’t this increase my testosterone that is already high, and hinder my chances of conception.. is it safe to take this cycle that I’ve taken letrozole. Today is cycle day 8…
What could cause dheas to be low and testosterone to be high.. this doesn’t make sense to me.
My preference would be to avoid DHEA.
Dehydroepiandrosterone (DHEA), is steroid hormone produced by the adrenal glands and ovary. It is involved in producing the male hormones, androstenedione testosterone and also estrogen. DHEA blood levels tend to decline naturally with age.
Under the effect if luteinizing hormone (LH), DHEA is metabolized to testosterone in ovarian connective tissue (theca/stroma). Thereupon the testosterone is transported to the granulosa cells that form the innermost layer of the ovarian follicles where, under the influence of follicle stimulating hormone (FSH)-induced desmolase and aromatase enzymatic activity the testosterone is converted to estradiol. As this happens, granulosa cells multiply, follicle fluid volume increases along with estrogen output and egg development is promoted.
It is recognition of the essential/indispensable role that male hormones (mainly testosterone) play in follicle and egg development that prompted the belief that by giving DHEA and boosting ovarian testosterone production might benefit follicle/egg development. This belief was given some credence by an Israeli study that in 2010 reported on improved fertility when a group of infertile women were given the administration of 75mg of oral DHEA for 5 months. However, this study was seriously flawed by the fact that it did not separate out women who had diminished ovarian reserve, older women and those with PCOS, all of whom have increased LH-induced production of testosterone. In fact, we recently completed a study (currently being processed for publication) where we conclusively showed that when follicular fluid testosterone levels exceeded a certain threshold, egg quality was seriously prejudiced as evidenced by a marked increase in the incidence of egg chromosomal defects (aneuploidy).
Consider the following: Ovarian testosterone is needed for follicular development. However, the amount required is small. Too much ovarian testosterone spills over into the follicular fluid and has a deleterious effect on egg/follicle development. Some women (women with diminished ovarian reserve –DOR, older women and those with polycystic ovarian syndrome-PCOS) who tend to have increased LH biological activity, already over-produce testosterone. To such women, the administration of DHEA to such women, by “adding fuel to the fire” can be decidedly prejudicial, in my opinion. Young women with normal ovarian reserve do not over produce LH-induced ovarian testosterone, and are thus probably not at significant risk from DHEA supplementation. It is noteworthy that to date, none of the studies that suggest a benefit from DHEA therapy have differentiated between young healthy normal women with normal ovarian reserve on the one hand and older women, those with DOR and women with PCOS on the other hand.
In Some countries DHEA treatment requires a medical prescription and medical supervision. Not so in the U.S.A where it can be bought over the counter. Since DHEA is involved in sex hormone production, including testosterone and estrogen, individuals with malignant conditions that may be hormone dependent (certain types of breast cancer or testicular cancer) should not receive DHEA supplementation. Also, if overdosed with DHEA some “sensitive women” might so increase their blood concentrations of testosterone that they develop increased aggressive tendencies or male characteristics such as hirsuites (increased hair growth) and a deepening voice. DHEA can also interact other medications, such as barbiturates, corticosteroids, insulin and with other oral diabetic medications.
BUT the strongest argument against the use of routine DHEA supplementation is the potential risk of compromising egg quality in certain categories of women and since there is presently no convincing evidence of any benefit, why take the risk in using it on anyone.
Finally, for those who in spite of the above, still feel compelled to take DHEA, the best advice I can give is to consult their health care providers before starting the process.
Addendum: One potential advantage of DHEA therapy if used appropriately came from a study conducted by Washington University School of Medicine in St. Louis, MI and reported in the November 2004 issue of the “Journal of the American Medical Association” which showed that judicious (selective) administration of 50mg DHEA daily for 6 months resulted in a significant reduction of abdominal fat and blood insulin in elderly women.
Geoff Sher
.
I have had 2 miscarriages in the past so I do worry but I am pregnant. My first hcg level was 148 and 2 days late it is 342. Does this sound okay? I am just so worried. I don’t have an ultrasound until July 12.
I think this could turn out to be na keeper!
Good luck!
Geoff Sher
Hi Dr Sher!
We recently got our results back from the HLA DQ panel screen but no one is able to tell us if we are a DQ Alpha gene match or not. Do you take consults for people wanting results explained? Thank you
Yes…but it also depends on which laboratory performed the tests and whether/where/how you had NK cell activation assessed.
Central to making a diagnosis of an immunologic implantation dysfunction (IID) is a need for the appropriate interpretation of Natural Killer Cell Activity (NKa). In this regard, one of the commonest and most serious errors, is interpret the blood concentration of natural killer cells as being relevant. Rather it is the activity (toxicity) of NK cells that matters as mentioned. This activity can best be measured using the blood, K-562 target cell test (the gold standard). and/ or endometrial biopsy for cytokine activity.
With the K-562 test, the most important consideration is the percentage of target cells “killed” in the “native state”. In most cases a level of >10% killing should be regarded with suspicion and >12% overtly abnormal. In addition to reporting the result of the K-562 test, in the “native state” (without adding, Immunoglobulin-G (IVIG) or Intralipid (IL) which many Laboratories erroneously do to try and determine whether either or both of these immune therapies would have a therapeutic benefit or is/are unlikely to be of clinical value. The entire premise upon which this assertion is based, is in my opinion flawed. Clinically such NK cell deactivation can only be significantly affected in vivo as it takes more than a week following infusion to occur. Thus, what happens to the percentage of target cells killed with the K-562 test, by adding IVIG or IL is in my opinion irrelevant
Another way to assess endometrial NKa is by measuring TH-1 and TH-2 cytokines in endometrial tissue derived through biopsy.TH-1 cytokines kill the trophoblast (the root system of the embryo). Thus if is an excess of TH-1 cytokine activity is found with/without a disruption in the TH-1: TH-2 ratio, this points to NK cell activation.
There are basically two causes of immunologic implantation dysfunction (IID), a) Autoimmune (85%) & , b) Alloimmune (15%). The former occurs when the body reacts to its own tissue and the latter (far less common) when the male and female partners share certain genotypic similarities involving DQ alpha and HLA genes. In both cases IID results in rejection of the pregnancy due to uterine Natural Killer (NK) Cell and T-cell activation leading to the release of an excessive amount of TH-1 cytokines. These, “toxins” attack the embryo’s root system (trophoblast), killing the cells and causing implantation to fail.
Autoimmune Implantation Dysfunction: Autoimmune implantation dysfunction, most commonly presents with presumed “infertility” due to such early pregnancy losses that the woman did not even know she was pregnant in the first place. Sometimes there as an early miscarriage. Tests required are: a) blood levels of all IgA, IgG and IgM-related antiphospholipid antibodies (APA’s) directed against six or seven specific phospholipids, b) both antithyroid antibodies (antithyroid and antimicrosomal antibodies), c) a comprehensive reproductive immunophenotype (RIP) and, c) most importantly, assessment of Natural Killer (NK) cell activity (rather than concentration) by measuring by their killing, using the K-562 target cell test and/or endometrial cytokine activity tests.
It is important to recognize that currently there are only about 3 or 4 Reproductive Immunology Reference Laboratories in the U.S.A that, are capable of reliably analyzing the required elements with a sufficient degree of sensitivity and specificity. I use a Reprosource, a laboratory located in Boston,MA.
Patients with Alloimmune implantation Dysfunction usually present with a history of unexplained (usually repeated) miscarriages or secondary infertility (where the woman conceived initially and thereupon was either unable to conceive again or started having repeated early miscarriages. However, it can also present as “presumed” primary infertility. Alloimmune dysfunction is diagnosed by testing the blood of both the male and female partners for matching DQ alpha genes and NK/CTL activation. It is important to note that any DQ alpha match (partial or complete) will only result in an IID when there both a DQa/HLA match exists along with NK cell activation. With the exception of cases where both partners have a total (absolute DQa match and treatment requires the use of sperm from a non-matching sperm donor, about 90% of cases alloimmune implantation will have a partial match where 1: 2 embryos will match the woman’s DQa genotype and half will not. In cases of an alloimmune dysfunction (with associated NKa), treatment with IL or IVIG will in my opinion, will not protect against a matching embryo being rejected. It can only clear the NK environment for an embryo that does not match the woman’s DQa genotype. For this reason, it is my opinion that only 1 embryo should be transferred at a time because, given the fact that i:2 embryos will match, transferring >1 embryo at a time creates a risk that the matching embryo will evoke a local NKa/’cytokine response that will “muddy the water” for both. Thus, in cases of a “partial” DQa match I recommend against transferring more than a single embryo at a time.
.
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.
Between 2% and 5% of women of the childbearing age have reduced thyroid hormone activity (hypothyroidism). Women with hypothyroidism often manifest with reproductive failure i.e. infertility, unexplained (often repeated) IVF failure, or recurrent pregnancy loss (RPL). The condition is 5-10 times more common in women than in men. In most cases hypothyroidism is caused by damage to the thyroid gland resulting from of thyroid autoimmunity (Hashimoto’s disease) caused by damage done to the thyroid gland by antithyroglobulin and antimicrosomal auto-antibodies.
The increased prevalence of hypothyroidism and thyroid autoimmunity (TAI) in women is likely the result of a combination of genetic factors, estrogen-related effects and chromosome X abnormalities. This having been said, there is significantly increased incidence of thyroid antibodies in non-pregnant women with a history of infertility and recurrent pregnancy loss and thyroid antibodies can be present asymptomatically in women without them manifesting with overt clinical or endocrinologic evidence of thyroid disease. In addition, these antibodies may persist in women who have suffered from hyper- or hypothyroidism even after normalization of their thyroid function by appropriate pharmacological treatment. The manifestations of reproductive dysfunction thus seem to be linked more to the presence of thyroid autoimmunity (TAI) than to clinical existence of hypothyroidism and treatment of the latter does not routinely result in a subsequent improvement in reproductive performance.
It follows, that if antithyroid autoantibodies are associated with reproductive dysfunction they may serve as useful markers for predicting poor outcome in patients undergoing assisted reproductive technologies.
Some years back, I reported on the fact that 47% of women who harbor thyroid autoantibodies, regardless of the absence or presence of clinical hypothyroidism, have activated uterine natural killer cells (NKa) cells and cytotoxic lymphocytes (CTL) and that such women often present with reproductive dysfunction. We demonstrated that appropriate immunotherapy with IVIG or intralipid (IL) and steroids, subsequently often results in a significant improvement in reproductive performance in such cases.
The fact that almost 50% of women who harbor antithyroid antibodies do not have activated CTL/NK cells suggests that it is NOT the antithyroid antibodies themselves that cause reproductive dysfunction. The activation of CTL and NK cells that occurs in half of the cases with TAI is probably an epiphenomenon with the associated reproductive dysfunction being due to CTL/NK cell activation that damages the early “root system” (trophoblast) of the implanting embryo. We have shown that treatment of those women who have thyroid antibodies + NKa/CTL using IL/steroids, improves subsequent reproductive performance while women with thyroid antibodies who do not harbor NKa/CTL do not require or benefit from such treatment.
I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
•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.
•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) Why did my IVF Fail
•Recurrent Pregnancy Loss (RPL): Why do I keep losing my Pregnancies
•Genetically Testing Embryos for IVF
•Staggered IVF
•Staggered IVF with PGS- Selection of “Competent” Embryos Greatly Enhances the Utility & Efficiency of IVF.
•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.
•IVF: Selecting the Best Quality Embryos to Transfer
•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?
•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!
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
•Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year.
•A personalized, stepwise approach to IVF
•Nutritional supplements in IVF
______________________________________________________
ADDENDUM: PLEASE READ!!
INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.
If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or, enroll online on then home-page of my website (www.SherIVF.com).
PLEASE SPREAD THE WORD ABOUT SFS!
Geoff Sher