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.
Hello Dr Sher,
I conceived naturally 12 years ago but miscarried at 11 weeks, this was before i met my Husband. We tried naturally together for 6 years no pregnancy. told no reason why except husband sperm had a low 24 hour survival rate and his results varied from normal to borderline. Had ICSI in 2014 and only retrieved one egg despite normal AMH for my age (i am 39 now). Resulted in pregnancy but Blighted Ovum miscarriage found at 6 weeks. Only had progesterone support. Moved to Donor as i responded badly.We had 2 donor FET’s both with a single a-CGH tested grade 1 embryo. The first resulted in another Blighted Ovum and the second no implantation.I had clexane, progesterone and steroids support for the first and for the second cycle i had steroids (medrol 8mg), Clexane & intralipids a week before and on day of transfer and aspirin from CD 1.
8 weeks after the failed implantation i conceived naturally (positive test 10 weeks after) I took progesterone and aspirin from around 4+5 weeks and up till 12 weeks everything seemed fine but the baby was found to have severe abnormalities and termination advised. The issues were Spina Bifida & very rare Cloacal Exstrophy we were told this was not genetic and just ‘bad luck’ We have since had genetic testing on both of us no issues, and also clotting blood tests all normal. Thyroid is stable and just under 1 (i take thyroxine for under active).
I just had another donor FET with 2 top grade embryos in a natural cycle, lining triple line, everything looked great, but no implantation for the second time. I only had progesterone support no other drugs.
Do you have any advice and also could the intralipids and steroids have had an effect 8-10 weeks later to allow me to conceive naturally? And if so why did the FET fail when i had them in the first place? I am just lost in what to try next. Thank you for your time.
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.
Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•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)
•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?
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
•Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
•Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
•Preimplantation Genetic 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?
•IVF Failure and Implantation Dysfunction: The Role of Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
•Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
•Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
•Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
•Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
•Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
•Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
•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.
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
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.
Also, I am taking synthroid and NK Killer celles are inactive. Thanks Dr Sher.
Remember, it is NOT the concentration of NK cells that matters. Rather it is their activation (preferably) as measured by the rK-562 target cell test.
Geoff Sher
Dear Dr. Sher,
In your experience is there a connection between thyroid antibodies and unexplained infertility and recurrent ivf failure with no implantation? If so, what treatment is available?
Thanks,
Stacey
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.
Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•IVF Failure and Implantation Dysfunction: The Role of Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Why did my IVF Fail
•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)
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
•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
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.
Geoff Sher
Thank you in advance!
Background: I have been seeing an RE for two years, starting just after I turned 40 (I recently turned 42.) I have one child conceived naturally and have not had any trouble getting pregnant (at 39 we lost euploid twins.) We have been carefully AVOIDING pregnancy (until very recently.) Our goal was to bank 5 day blastocysts for genetic screening and later transfer, because we hope for a large family (though that hope is dwindling.) With this RE, I underwent a surgery for a uterine septum (he told me he did not measure the length.) We also did two rounds of IVF/ICSI, both antagonist protocols, but retrieved six and five eggs (despite follicle counts of ~25 and ~22.) Only one blastocyst (which the clinic cannot confirm they still have as of yesterday.) Since age 40 in 2014 to now, my ‘numbers’ have been: AFCs from 17 to >25, AMH greater than 8, FSH less than 7 and my BMI around 20. Forgive my lack of proper units usage – I am in the U.S. & am trying to be more brief. I have many concerns about my doctor and clinic at this point, but will try to limit myself to my most pressing and frightenening concerns. I had an appointment to plan my next cycle yesterday morning. I was/am 3 weeks and a few days pregnant (a both happy and frightening accident.)
Questions:
(i) During TVS the RE counted six (quite large) follicles. He later explained that in the past two months my ovarian reserve had dropped from excellent to extremely poor. The follicles were too large to be antral, and no AFs were seen. It was my understanding that this is normal in pregnancy – follicles from that cycle become atresic and the ovaries do not show much activity and AFCs are not reliable until after pregnancy. But now I am honestly terrified. Can you explain or direct me to references please? Does this mean I will have no chance at IVF with my own eggs after this pregnancy?
(ii) My quantitative beta HCG came back at 51 which the doctor stated (through a nurse,) is borderline positive for pregnancy (but the lab ranges showed anything above 6 was positive.) Is that indicative of any early loss or too low to confirm? I am very concerned and confused.
(iii) Progesterone came back at 12.1. The RE communicated through the nurse that this was very low and prescribed IM progesterone daily. An OB friend said he would not supplement unless under 10 or if dropping in a second assay. Again, I am confused and frightened. Is this value too low at ~3.5 weeks pregnant as an absolute? My estradiol was 263, is it low considering this figure? Is there possibility of harm to the pregnancy with this supplementation?
(iv) How long after birth can I resume IVF treatment? When can I begin planning and consulting?
(v) The RE stated I had an arcuate uterus yesterday. I reminded him he had performed a surgery, and asked if that meant the septum had not been completely removed. He said it had but some remained (confusing.) I asked if an arcuate uterus posed risk to this pregnancy and he said, “well, we will find out!”. Is it possible this is scar tissue? What is the danger to this pregnancy?
(vi) This RE has told me on many occasions that my follicles, for the most part, simply do not contain eggs at all. This contradicts everything I have read and every opinion I have sought, including a post by you. Is this due to poor in quality or protocol or perhaps both in my case, in your opinion?
Thank you so much for you time and help for so
many of us – I have not written before myself, but have learned so much reading your comments, posts and articles.
All Best, Kathrine
Questions:
(i) During TVS the RE counted six (quite large) follicles. He later explained that in the past two months my ovarian reserve had dropped from excellent to extremely poor. The follicles were too large to be antral, and no AFs were seen. It was my understanding that this is normal in pregnancy – follicles from that cycle become atresic and the ovaries do not show much activity and AFCs are not reliable until after pregnancy. But now I am honestly terrified. Can you explain or direct me to references please? Does this mean I will have no chance at IVF with my own eggs after this pregnancy?
A: In my opinion, there is no merit in assessing AFC or AMH in pregnancy or for several weeks thereafter.
(ii) My quantitative beta HCG came back at 51 which the doctor stated (through a nurse,) is borderline positive for pregnancy (but the lab ranges showed anything above 6 was positive.) Is that indicative of any early loss or too low to confirm? I am very concerned and confused.
A: hCG levels should double every 2 days in early pregnancy. Theareafter after 6 weeks and US examination is definitive.
(iii) Progesterone came back at 12.1. The RE communicated through the nurse that this was very low and prescribed IM progesterone daily. An OB friend said he would not supplement unless under 10 or if dropping in a second assay. Again, I am confused and frightened. Is this value too low at ~3.5 weeks pregnant as an absolute? My estradiol was 263, is it low considering this figure? Is there possibility of harm to the pregnancy with this supplementation?
A: A P4 level of 12 in early pregnancy is on the low side, especially if it is declining. I would treat sooner rather than later.
(iv) How long after birth can I resume IVF treatment? When can I begin planning and consulting?
A: IVF treatment should in my opinion be delayed until at least 2 natural cycles have passed.
(v) The RE stated I had an arcuate uterus yesterday. I reminded him he had performed a surgery, and asked if that meant the septum had not been completely removed. He said it had but some remained (confusing.) I asked if an arcuate uterus posed risk to this pregnancy and he said, “well, we will find out!”. Is it possible this is scar tissue? What is the danger to this pregnancy?
A: An arcuate uterus will not compromise implantation. However, in my opinio, operating on a partial uterine septum for infertility is not helpful and will often, by causing local scarring, be counter-productive.
(vi) This RE has told me on many occasions that my follicles, for the most part, simply do not contain eggs at all. This contradicts everything I have read and every opinion I have sought, including a post by you. Is this due to poor in quality or protocol or perhaps both in my case, in your opinion?
Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•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)
•Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to 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
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.
Hi Dr Sher,
I have Hashimoto’s. My thyroid levels are closely monitored by an endocrinologist (TSH between 1 and 2 and T3 and T4 levels in optimal range).
1. Does having Hashimoto’s mean I have a higher amount of NK cells and could this could be a reason for our unexplained infertility? Or do my thyroid meds control NK cell activity?
2. Would I be able to stay on Armour or do you recommend switching back to synthetic (Synthroid) before starting the IVF procedure and/or getting pregnant?
Many thanks for your time.
Fist, as long as the treatment keeps your TSH in the normal range, it sdoes not matter which thyroid medication you take.
Second, 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.
Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly
•Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
•Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
•Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
•Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
•Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
•Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
•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
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.