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.
We are really heartbroken after a second “unsuccessful” cycle. I also haven’t really seen a lot of info about the issues we are having: I’m 38 he’s 33. Good egg reserve, slight morphology problem, response to drugs “seemed great”
first attempt: Antagonist – 11 eggs, 7 ICSI’d – all but one arrested overnight only 1 embryo frozen
attempt 2: Micro flare – 10 eggs, only 4 were fully mature, even though the others appeared to be on the scans, ZERO fertilized w ICSI
I haven’t really seen many people having issues w ICSI not working! Is there just no way for this to work? Or are there factors that can provoke this kind of response that we are unaware of?
And also, if we do consider implanting that one embryo, should we do this at another clinic?
Hi Steph,
Sorry to hear about your disappointment. I cannot advise you regarding the transfer of your one blastocyst, but I can say that in my opinion your poor egg/embryo yield this could have more to do with stimulation. There is no doubt that this is the most important determinant of egg/embryo yield and quality…and thus also IVF outcome. It must be reviewed carefully and perhaps significantly revised. I think this is a more pressing decision than where/wnen to transfer the one blastocyst you have because of your age and the biological clock….see below!
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
•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.
•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
•Optimizing Response to Ovarian Stimulation in Women who Have Compromised Ovarian Response to Ovarian Stimulation in Women who Have Compromised Ovarian Reserve: A Personal Approach.
•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
•Why did my IVF Fail?
•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
•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
•Implications of “Empty Follicle Syndrome and “Premature Luteinization”
•Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
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.
Good morning Dr. Sher.
(My question has disappeared.)
I’m a 25 year old with Endometriosis and PCOS. My husband has also been diagnosed with a borderline Morphology percentage of 3%-5%. In your opinion, what are our chances with IVF? What is IVF like for someone with both Endo and PCOS?
Endometriosis is a complex condition where, the lack or relative absence of an overt anatomical barrier to fertility often belies the true extent of reproductive problem(s). All too often the view is expressed that the severity of related infertility is directly proportionate to the anatomical severity of the endometriosis itself, the implication being that the primary reason for endometriosis –related infertility is anatomical interference with egg transport to the Fallopian tube(s). This over-simplification and an erroneous view is often used to justify the performance of many unnecessary surgeries for the removal of small innocuous endometriotic lesions, on the basis of such “treatment” evoking an improvement in subsequent fertility.
It is indeed indisputable that even the mildest form of endometriosis can compromise fertility. It is equally true that, mild to moderate endometriosis is by no means a cause of absolute “sterility”. Rather, when compared with normally ovulating women of a similar age who do not have endometriosis, women with mild to moderate endometriosis are about three to four times less likely to have a successful pregnancy. Two important reasons for such reduction in fertility potential are:
a) Toxic Pelvic Environment: Endometriosis is associated with the presence of local pelvic toxins that significantly reduces the fertilization potential of eggs as they pass from the ovary to the fallopian tube via the pelvic cavity and,
b) Immunologic Implantation Dysfunction (IID): Given that the pathogenesis of endometriosis almost certainly involves an abnormal immune response. In about one third of cases, activation of uterine natural killer cells (NKa) causes the uterus to reject the embryo (fertilized egg) as it attempts to gain attachment to the uterine lining (endometrium).
The reported annual birth rate for normally ovulating women under 35 yrs who are free of endometriosis or any other pelvic disease, is about 70-80%. For women 35-40yrs of age, the comparable annual rate is about 40-50%, for women in their early 40’s, it is probably less than 20% and by the mid-forties, …around 10%. In contrast women in similar age categories who have even the mildest degree of endometriosis can expect a 3-4-fold reduction in the annual birth rate.
Since, the reason for women with mild to moderate endometriosis having a much poorer reproductive performance has little to do with ovulation dysfunction or anatomical disease, it should come as no surprise that the use of fertility drugs, surgery to ablate small endometriotic deposits and minor adhesions, and/or intrauterine insemination is unlikely to any improvement in pregnancy rate over no treatment at all. Women under 35 years who fit this profile, and who conceive following fertility hormone therapy, intrauterine insemination (IUI) or surgery, should consider that they probably conceived in spite of (rather than due to), such treatment. Failure to recognize this reality carries with it the risk that when it comes to planning for another baby, the woman will erroneously belief that having conceived before means that there should be no difficulty in doing so again and be lulled into a false sense of complacency. In reality, the achievement of a viable pregnancy by a woman with mild/moderate endometriosis, whether it occurred spontaneously or following such treatment probably does not improve her subsequent ability to conceive.
Younger women (under 30 yrs) with mild/moderate pelvic endometriosis (who have patent fallopian tubes, are ovulating normally and have fertile male partners), have about a 40% chance of having a baby within 3-4 years. Accordingly they justifiably can choose taking a “wait and see “approach, avoiding surgery, fertility drugs and intrauterine insemination (which in my opinion would be unlikely to improve the chance of a successful pregnancy over no treatment at all) and In Vitro Fertilization which by involving the direct extraction of eggs from the ovaries and initiating the fertilization process in the Petri dish/incubator, the IVF procedure facilitates fertilization, is much likely to be successful, but might have been avoided by a “wait and see approach”.
Finally, I wish to point out that in addition to an inevitable toxic “peritoneal factor” present in all women with endometriosis, about 1/3 of women with endometriosis (regardless of its severity), also have an immunologic barrier to implantation involving NKa and possibly the action of antiphospholipid antibodies. This population of women are not likely to achieve a viable pregnancy conceive until/unless the IID is addressed through selective immunotherapy involving Intralipid, heparinoids (Lovenox/Clexane) and low dosage (short term) steroid therapy. It therefore behooves all women with endometriosis who are planning to have a family to be thoroughly tested which in my opinion should be performed in a reproductive immunology reference lab of which to my knowledge no more than a half dozen in the United States, capable of performing these tests with the required sensitivity. I preferentially use Reproductive Immunology Associates (RIA) in Van Nuys, CA.
Given the effect of the accelerating biological clock, women over 35yrs who have endometriosis-related infertility, do not have time to waste and should, in my opinion do IVF as a first line approach, regardless of their immunologic status. In the absence of clear evidence of increased NK cell activity, I often recommend a conservative approach in women under 35years (who potentially can afford the time to wait). However, regardless of age, women who have increased NK cell activity, should in my opinion undergo IVF accompanied with immunotherapy with Intralipid (and sometimes heparin, Clexane or Lovenox) because without such treatment they are not likely to conceive regardless of the approach to treatment) undergo IVF.
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”
•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.
•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 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
•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
•Male Factor Infertility
•Routine Fertilization by Intracytoplasmic Sperm Injection (ICSI): An Argument in FavorHormonal Treatment of Male Infertility
•Endometriosis and Infertily
•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
•Treating Ovarian Endometriomas with Sclerotherapy.
•Understanding Polycystic Ovarian Syndrome (PCOS) and the Need to Customize Ovarian Stimulation Protocols.
•“Triggering” Egg Maturation in IVF: Comparing urine-derived hCG, Recombinant DNA-hCG and GnRH-agonist:
•The “Lupron Trigger” to Prevent Severe OHSS: What are the Pro’s and Con’s?
•Micro-IVF: Often Preferable to Ovarian Stimulation with or Without IUI
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.
Dear Dr. Sher,
We would appreciate your expertise in overlooking our case.
We have been through 7 transfers (ICSI; IMSI; Cryo) with negative results and still have not received a diagnosis or a professional support for our way forward.
We would kindly ask you to review our case and make a first diagnosis based on the general summary outlined below. There is a more detailed summary (tests) available, if required. We are planning our next treatment in the USA, as we see more individual options in treatment.
Sincerely yours Mina and Tai
Medical history male (age 28):
February 2012: Diagnosed with PNET (primitive neuroectodermal tumor)
Sperm cryopreservation prior to initiating chemotherapy and radiotherapy
End of chemotherapy August 2012, End of radiotherapy October 2012
Frequent routine checks involving CT scan and colonoscopy
Medical history female (age 29):
Hashimoto-Thyroiditis / Hypothyroiditis (2003)
Hyperprolactinaemia (2004-2011), no checkup after 2011 (normal blood level prolactin 8 ng/ml)
Vitamin D deficiency (2015: 34.5 ng/mL)
Hypothalamic ovarian insufficiency
Insulin resistance (got worse despite medication and better lifestyle)
AMH 2.21 (2014)
Height: 168cm
Weight: 54kg (weight gain 3kg through IVF)
Current Medication female:
L-Thyroxin 75 Henning
Contraceptive pill “Juliette“ (2 mg Cyproteron acetat (1,8 mg Cyproteron), 0,035 mg Ethinylestradiol)
Prenatal Multivitamin (i.a. Metafolate 800 µg)
Metformin 2x500mg
Dekristol (20000 IE 1x/week)
Summary – In total 7 transfers with 12 blastocysts and 1 morula:
ICSI 1 (Start November 2014)
Cryopreserved sperm from 2012
In total 9 ova collected
6 ova in mature state
4 ova in pronucleus stage
2 transferred (Day 3)
Abdominal cramps
Withdrawal bleeding
No blood test performed
ICSI 2 (Start December 2014)
Cryopreserved sperm from 2012
In total 20 ova collected
19 ova in mature state
17 ova in pronucleus stage
11 ova in pronucleus stage and 2 blastocysts cryopreserved
2 blastocysts transferred
Abdominal cramps
Withdrawal bleeding
Blood test: HCG: 0.02 IU/L; Progesterone: 3.51 ng/mL
Cryo 1 (Start April 2015)
Cryopreserved sperm from 2012
2 blastocysts transferred
Abdominal cramps
Blood test 1: HCG-Wert: 4.28 IU/L; Progesterone: 4.83 ng/mL
Blood test 2: HCG-Wert: 22.49 IU/L; Progesterone: 5.51 ng/mL
Blood test 3: HCG-Wert: 7.56 IU/L; Progesterone: 4.99 ng/mL
Withdrawal bleeding
Cryo 2 (Start May 2015)
Cryopreserved sperm from 2012
2 blastocysts transferred
Blood test 1: HCG-Wert: 33.06 IU/L; Progesterone: 5.6 ng/mL
Blood test 2: HCG-Wert: 179.1 IU/L; Progesterone: 10.76 ng/mL
Blood test 3: HCG-Wert: 944.8 IU/L; Progesterone: 11.09 ng/mL
Abdominal cramps, followed by withdrawal bleeding
HCG-Wert: 554 IU/L; Progesterone: 7.82 ng/mL
Cryo 3 (Start August 2015)
Cryopreserved sperm from 2012
1 Morula transferred
Blood test: HCG-Wert: 0.57 IU/L; Progesterone: 15 ng/mL
Withdrawal bleeding
Scratching utilized as preparation for next treatment
IMSI + Kryo 4 + Kryo 5
IMSI (Start September 2015)
In total 15 ova collected
14 ova in mature state
9 ova in pronucleus stage
6 blastocysts for pre-implantation genetic analysis of chromosomal aberrations by aCGH
3 blastocysts good quality and cryopreserved
Cryo 4 (Start October 2015)
Fresh sperm from 2015 (Cryopreserved September 2015)
2 blastocysts transferred (5BA + 5BC)
Blood test: HCG < 1.2 IU/L, Progesterone: 5.6 ng/ml, Estradiol (E2): 349 pg/ml
Withdrawal bleeding
Hysteroscopy performed (no medical indication)
Cryo 5 (Start January 2016)
Fresh sperm from 2015 (Cryopreserved September 2015)
1 blastocyst transferred (5AB)
Withdrawal bleeding
Blood test: HCG < 1.2 IU/L
All treatments performed in accordance with antagonist protocol.
Thank you for this communication. In my opinion, given that you did have access to cryobanked good sperm and taking into account that you also have autoimmune hypothyroidism (Hashimoto’s Disease) which is associated with immunologic implantation dysfunction in 50% of cases (see below), I beliweve that an implantation dysfunction plus the protocols used (and there implementatio) could provide the explanation (s) for your repeated IVF failures…see below:
1. Unexplained IVF failure:
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).
My answer to patients who ask me when is the time to stop undergoing IVF is ….Aside from the weight of the financial burden, the time to stop is when in spite of thorough and comprehensive evaluation, there is no remediable and treatable explanation for repeated failure.
2. Thyroid autoimmune disease and IVF:
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.
•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
•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 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
•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
•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
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.
Dear Dr Sher
I have had persistent thin lining issues: We have 6 euploid blasts on ice, but are struggling to get my endometrium to play ball to put one back
It seems my lining only responds to high levels of endogenous oestrogen, as it’s only ever grown in my fresh IVF cycles
My lining got to 11mm in my last IVF cycle – which was freeze all for PGS
However in a medicated FET (oestrogen pills & patches) it didn’t get much above 6mm, and not triple line – cycle cancelled
We tried an ovulation induction FET (plus supplementary oestrogen) and the same again
We tried oral viagra and unsurprisingly weren’t successful
A G-CSF wash significantly improved the quality & appearance of the endometrium in the most recent cycle – however at only 7mm thickness we weren’t going to risk a transfer
So, we find ourselves doing a full stimulated cycle, to create lots of endogenous oestrogen, in the hope my lining thickens up as it has done in the past
We have managed to source one pharmacy in the UK which will make up vaginal viagra pessaries (hurrah!) so will be adding those in to the protocol
We will be repeating the G-CSF wash on day of hCG trigger and egg retrieval
We will add in vaginal oestrogen / patches to the stims if needed
I’m taking 6g L-Arginine and 1000iu tocopherol
My lining thickened up before, so we hope it can do it again…
Is there anything else you would recommend that we’to support a temperamental endometrium?!
Kindest regards and very many thanks in advance
Katy
In my opinion, the fact that you do not get a good lininhg with FET suggests that the reason could reside in the HRT method used to prepare your uterus. The estrogen therapy should preferably be administered subdermally and not orally. Also, I would recommmend estradiol Valerate and not estrace. Finally viagra must be compounded and administered vaginally.
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
•Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
•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 apologize, my intention was to have a more detailed question than my previous post. I’m 25 years old, I have Endometriosis, PCOS and my husband was told he has a borderline morphology percentage (3-4%). I have had an HSG test and Laparoscopy, I have taken Clomid and have undergone Lupron treatment. I also take Metformin for my PCOS. My husband and I are trying to prepare ourselves financially before scheduling something with you! As a Nurse Aide, would I be eligible for the First Responder Discount (not usually but doesn’t hurt to ask)? What can you tell me about IVFs in couples with our conditions?
I think my response before addressed the medical issues.
Good luck and G-d bless!
Geoff Sher