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,
Hi had my FET 2/22/2016 of 2 5day blastocyst embryo, I have no pregnancy symptoms at all, I cheated and took a home pregnancy test 6 dpt and it was negative, I’m very sad, I already had a failed fresh embryo transfer a few months ago, my beta hcg is set for 3/2/2016, what are the chances that I can still be pregnant? I’m hoping for a little good news. Thank you and hope to hear from you soon
You really should defer reaching a conclusion until the blood test because a urine test is very insensitive.
Whenever a patient fails to achieve a 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)
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
•Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
•Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
•IVF Failure and Implantation Dysfunction: The Role of Endometrial Thickness, Uterine Pathology and Immunologic Factors
•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)
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
Dr. Sher,
Thank you so much for allowing this kind of open forum.
I am 37, and trying for a second. I have a four year old, conceived without problem, but over the past two years, I’ve had 3 losses. We just did IVF, and it appears it did not work (positive home tests are getting lighter; trigger is out). We have had all testing, and I have DOR.
I wanted to ask about protocol options, because my RE has been clear that #2 would be the same. I felt over suppressed, as I have had more follicles on IUI cycles (did 3 and got pregnant on 1, with a loss at 10w).
Estrogen patches for suppression starting CD22-30 (I made it to only CD26 as I have short cycles)
Micro dose Lupron, 20u morning and night starting CD2
Gonal-F 300iu AM, Menopur 150iu PM
Omnitrope added in the last 4 nights of stims (they didn’t have me take it after trigger)
Ovidrel trigger x2
I had only 3 follicles, and we contemplated IUI conversion, but my husband’s backup sample was not very good, so we did IVF. 2 retrieved and mature, but only 1 fertilized overnight; we did use ICSI. That one was a perfect blast on day 3 and transferred, but it was moving a little fast, and jumped from 10 to 12 cells the morning of transfer.
Thank you so much!
In my opinion, “microdose” (“flare”) Lupron protocols, the use of clomiphene or Letrozole, and high dosage Menopur protocols, should best NOT be used in women with DOR (see below). It surges LH and with it ovarian testosterone as the stimulation begins and this can have a deleterious effect on egg quality/competency…especially in women who have DOR. You need a modified, robust, long pituitary down-regulation protocol. I would use an agonist/antagonist conversion protocol with human growth hormone (HGH) augmentation and would recommend Staggered IVF with embryo banking of PGS (next generation gene sequencing)-normal blastocysts, to make hay while the sun still shines.
It is one thing for a woman who has never been able to conceive (primary infertility) to come to grips with undergoing In Vitro Fertilization. It is quite another matter for someone who has successfully achieved a pregnancy in the past having to come to terms with a subsequent inability to conceive (secondary infertility). When this happens, it raises issues of guilt, a declining sense of self-worth and ultimately self-recrimination. The ramifications often impact family relationships involving partners and siblings. The truth is that secondary infertility can be just as difficult for individuals and family to deal with as primary infertility.
There are many factors that contribute to the problem of secondary infertility. These include:
Social and marital factors: In this modern day and age where at least one in two marriages ends in divorce, it is not surprising that there would be an inevitable hiatus in childbearing. This often results in a considerable delay in re-initiating family building. Since the biological clock keeps on ticking in the interim, advancing age can, and often does, have a profound affect on a woman’s ability to subsequently conceive and successfully complete a pregnancy. In my experience, this is one of the most common reasons for secondary infertility. In addition, by the time a decision is made to enter a new relationship, many men and women will have undergone a prior sterilization procedure which now needs to be addressed. To make matters worse, many such men and women first opt for surgical reversal of their occlusive surgery, only to learn in the end that the procedures were not successful, and they now need to consider in vitro fertilization (IVF) in one form or another.
Financial factors: Here, the cost of raising a child often weighs heavily, especially in this present tough economic climate. This is becoming more of an issue as women playing an ever increasing role as a primary bread winner.
Career demands: There can be little doubt that when it comes to climbing the career ladder, women are considerably disadvantaged by the fact that pregnancy and the immediate demands of child rearing take away from their ability to compete with men. As such, many women choose to delay having another child until such time as they have been able to make up for prior lost opportunity.
Medical barriers to fertility: Certain common medical conditions, while not absolutely precluding pregnancy, make it much more difficult to conceive.
Endometriosis: It is not uncommon for women with endometriosis to achieve a pregnancy, but find difficulty in doing so again at a later date. The reason for this is that while most women with endometriosis have patent fallopian tubes, the environment surrounding their tubes is compromised due to pelvic toxins that are produced by the endometriotic implants. These toxins compromise egg fertilization potential, making it more difficult for sperm in the fallopian tube to fertilize the egg upon its arrival there. As such, endometriosis is one of the commonest causes of secondary infertility.
Tubal damage due to prior pelvic inflammatory disease: In first world countries, the early and often indiscriminate use of antibiotics for the slightest symptom has led to the point where an acute attack of pelvic inflammatory disease is often masked. As such, less than 30% of American women with tubal damage have knowledge that their tubes are compromised and that they might have subsequent difficulty in conceiving. Since, in many such cases the tubal damage will not have totally blocked both tubes, some of the women so affected might experience a pregnancy but have difficulty in conceiving again later down the line.
Dysfunctional ovulation: Since ovulation as well as normal hormonal support of the early implanting embryo are both essential for a healthy pregnancy to occur, it follows that women with irregular or dysfunctional ovulation (e.g., polycystic ovarian syndrome – PCOS, persistent follicular luteal phase deficiencies or post birth control pill ovulatory problems) might sporadically conceive and thereupon find it difficult to do achieve another pregnancy later on.
Immunologic Implantation Dysfunction (IID): has become ever more apparent that immunologic factors play an important role in achieving healthy implantation. Women with endometriosis (regardless of its severity), those with a personal or family history of autoimmune diseases such as lupus erythematosus, rheumatoid arthritis and thyroid autoimmunity (TAI), and some cases where the man and the woman share certain genetic similarities (alloimmune implantation dysfunction), will have activated CTL/NK cells that can inhibit or compromise healthy implantation. This is an often overlooked cause of secondary infertility. Most such autoimmune/alloimmune cases require selective immunotherapy and IVF.
Antisperm Antibodies: Although infrequent, some cases of secondary infertility might also be caused by the woman harboring antisperm antibodies. In such cases IVF is mandated.
Previous post-pregnancy uterine infection: Retention of products of conception after the birth of a child, miscarriage, or abortion can so damage the uterine lining as to result in subsequent implantation failure. Unless specifically looked for, this will usually be unknown to the patient, who will simply present with secondary infertility. Treatment is often difficult because such patients might not respond adequately to surgical removal of intrauterine scar tissue or to hormonal or Viagra therapy
Male immunologic factors: Most men who have undergone a previous vasectomy more than 10 years earlier, will have antisperm antibodies that will interfere with fertilization. Such cases require IVF with intracytoplasmic sperm injection (ICSI). Here we offer a few words of caution to men who are considering undergoing surgical reversal of vasectomy. Always first have a test done to exclude the presence of circulating antisperm antibodies, because in such cases, even if the reversal is successfully performed, they will not be able to initiate a pregnancy without IVF/ICSI.
Whatever the cause, secondary infertility often affects older couples disproportionately, creating a sense of urgency and even desperation in achieving a viable pregnancy before time runs out. It is for this reason that IVF becomes the treatment of choice in such cases. However, even IVF becomes progressively less successful with advancing age of the woman (whose eggs are being fertilized). In such cases it is important for the couple to be realistic with regard to their expectations. Here, options that include embryo banking and egg donation should be carefully considered.
Another important point is that whenever a regularly ovulating younger woman (under 36 years of age) with patent fallopian tubes is diagnosed with secondary infertility, it is essential to consider underlying endometriosis or non-obstructive tubal disease as a possible cause. In such cases, IVF is again the treatment of choice.
Please visit my new Blog at o to http://goo.gl/4hvjoP , 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)
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Frozen Embryo Transfer (FET): What Does it Involve?
•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.
•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
•Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
•Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report)
•
I invite you to call 702-699-7437 or 800-780-7437 or go online on this site and set up a one hour Skype consultation with me to discuss your case in detail.
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
Good morning Dr. Sher.
Can you pls provide your valuable advice on this.
I had my follicular scan yday after which I was asked to take my intralipids dose.
In today’s scan , my doc said that in case we don’t get enough embryos , we would do a back to back cycle and bank the embryos.
please let me know if my current intralipids dose would suffice if the ET was to happen in the next cycle or should we do another round of intralipids (7-10 days) before ET when it finally happens.
Thank you in advance, Dr. Sher.
With warm Regards
You would ideally in my opinion need a repeat IL infusion about 10-14 days prior to that ET.
Geoff Sher
Dear Dr. Sher,
I am very confused. I had an LH surge showing on home test and still RE said it is the IVF meds. I felt it was a accurate surge because I have been very consistent in my cycle surges happening 12 to 14 days after CD1 with or without IVF meds. However based on their advice I went in for retrieval. The eggs did not fertilise and they said to stop everything and to expect period in 2 weeks from egg retrieval. However as I guessed I got my period 1 week after egg retrieval (14 days after the LH home test that showed surge which I believe was a genuine surge). After I got my period again I monitored for LH surge again with home test and got surge on CD11. Bloods were consistent with a surge. Mucus also showed consistency with ovulation but then Mucus patterns again started to look like ovulation, so on CD18 and CD19 I checked again and I had a surge on home test. To see what was happening I did a blood test again and blood test show I am having LH surge again on CD18 and 19. What is happening as I have never had like this before? I have never had so many LH surges.
This could well be “premature Luteinization in my opinion.
women with diminished ovarian reserve, and those with polycystic ovarian syndrome, tend to have more biologically active LH in circulation. LH causes production of male hormone (androgens, predominantly testosterone), by ovarian connective tissue (stroma/theca). A little testosterone is needed for optimal follicle development and for FSH-induced ovogenesis (egg development). Too much LH activity compromises the latter, and eggs so affected are far more likely to be aneuploid following meiosis.
Women with the above conditions have increased LH activity and are thus more likely to produce excessive ovarian testosterone. It follows that sustained, premature elevations in LH or premature luteinization (often referred to as a “premature LH surge”) will prejudice egg development. Such compromised eggs are much more likely to end up being complex aneuploid following the administration of the hCG trigger, leading to fruitless attempts at retrieval and the so called “empty follicle syndrome.”
The developing eggs of women who have increased LH activity (older women, women with diminished ovarian reserve, and those with PCOS) are inordinately vulnerable to the effects of protracted exposure to LH-induced ovarian testosterone. Because of this, the administration of medications that provoke further pituitary LH release (e.g., clomiphene and Letrozole), drugs that contain LH or hCG (e.g., Menopur), or protocols of ovarian stimulation that provoke increased exposure to the woman’s own pituitary LH (e.g., “flare-agonist protocols”) and the use of “late pituitary blockade” (antagonist) protocols can be prejudicial.
The importance of individualizing COS protocol selection, precision with regard to the dosage and type of hCG trigger used, and the timing of its administration in such cases cannot be overstated. The ideal dosage of urinary-derived hCG (hCG-u) such as Novarel, Pregnyl and Profasi is 10,000U. When recombinant DNA-derived hCG (hCG-r) such as Ovidrel is used, the optimal dosage is 500mcg. A lower dosage of hCG can, by compromising meiosis, increase the risk of egg aneuploidy, and thus of IVF outcome
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)
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
•The Role of Nutritional Supplements in Preparing for IVF
I invite you to call 702-699-7437 or 800-780-7437 or go online on this site and set up a one hour Skype consultation with me to discuss your case in detail.
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
Hi Dr. Sher,
Thank you for your informational blog post on “The Sperm Chromatin Structure Assay (SCSA): A Measure of the Potential of Sperm to Help Propagate a Viable Pregnancy.” I am currently testing for SCSA due to a recent unexplained IVF failure. I am a 35 year old male with male factor infertility (very low morphology, motility and count). After reading your article, I had the following questions:
1. Can sperm with high DNA fragmentation/damage still successfully fertilize eggs with ICSI? During our cycle we had a fantastic fertilization rate (24 out of 26 eggs fertilized with ICSI and all looked good on Day 3). However, only 2 very poor quality blasts remained on Day 5 and everything else had arrested. Could this drastic drop-off be indicative of a sperm DNA fragmentation issue or would that be more likely to reveal itself at the fertilization stage?
2. I understand there are some existing procedures used in addition to ICSI that may be helpful to improve outcomes in IVF cycles where the male has abnormal SCSA results. I have heard about both Preselective Intracytoplasmic Sperm Injection (PICSI) and Intracytoplasmic Morphologically Selected Sperm Injection (IMSI). Do you recommend either of these sperm selection techniques to try to improve outcomes if there is an underlying sperm DNA fragmentation issue? Do you think one is better than the other? We’d like to do whatever we can to improve our chance of success next cycle.
Thank you kindly for your thoughts, Dr. Sher.
1. Can sperm with high DNA fragmentation/damage still successfully fertilize eggs with ICSI? During our cycle we had a fantastic fertilization rate (24 out of 26 eggs fertilized with ICSI and all looked good on Day 3). However, only 2 very poor quality blasts remained on Day 5 and everything else had arrested. Could this drastic drop-off be indicative of a sperm DNA fragmentation issue or would that be more likely to reveal itself at the fertilization stage?
A: The simple answer is yes!. However, I would issue a word ofcaution to simply assume that this is all due to a sperm issue. It is important to rule out the possibility that the protocol used for ovarian stimulation might in part or completely be the reason (see below).
2. I understand there are some existing procedures used in addition to ICSI that may be helpful to improve outcomes in IVF cycles where the male has abnormal SCSA results. I have heard about both Preselective Intracytoplasmic Sperm Injection (PICSI) and Intracytoplasmic Morphologically Selected Sperm Injection (IMSI). Do you recommend either of these sperm selection techniques to try to improve outcomes if there is an underlying sperm DNA fragmentation issue? Do you think one is better than the other? We’d like to do whatever we can to improve our chance of success next cycle.
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)
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
•Generation Gene Sequencing (NGS): Method of Choice.
•IVF Failure and Implantation Dysfunction: The Role of Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Why did my IVF Fail
•Male Factor Infertility
•The Sperm Chromatin Structure Assay (SCSA): A Measure of the Potential of Sperm to Help Propagate a Viable Pregnancy
I invite you to call 702-699-7437 or 800-780-7437 or go online on this site and set up a one hour Skype consultation with me to discuss your case in detail.
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
A: In our experience, there is no benefit to either IMSI ir PICSI.