Ask Our Doctors – Archive
Our Medical Directors are outstanding physicians that you will find to be very personable and compassionate, who take care to ensure that you have the most cutting-edge fertility treatments at your disposal. This is your outlet to ask your questions to the doctors.
Hi Dr. Sher –
I just experienced my first failed IVF (fresh transfer). Prior to this I was diagnosed with stage 2 endometriosis and underwent laparoscopy surgery in March 2014. A few months later, we conceived naturally, twice but they ended in a miscarriage. The last miscarriage was in June 2015 and a year later we have not been able to conceive again. I am 35 and my spouse is 37 (MFI). In this last year we also had 4 IUI attempts that failed, which the doctor gave me the same protocol each time. Maybe IUI was not the best option for success anyways. We took 4 months off and just started IVF, which the first one failed. Just before we went into this my doctor said my AMH was high which indicated I had DOR. I had 9 follicles, 6 mature, 4 fertilized. We transferred two (4AA and 4BB I think) embryos. I am stunned that they did not stick. My lining was 9mm.
Do you see an advantage to doing a 2nd attempt almost back to back (2 cycles) for those that have DOR?
Do you think we should do another lap surgery to see if the endometriosis is posing challenges or does endometriosis not “correct” IVF? In other words IVF helps bypass the issue of endometriosis?
My doctor said he maxed my doses given the fact that I have DOR and felt it wasn’t terrible but on the lower side. He does not feel we should change the protocol for the 2nd attempt? Your opinion?
Could it be me and having implantation problems or is it the embryos that don’t implant? He also mentioned I’ve undergone several tests (for reoccurring miscarriages) and nothing is coming back that stands out to him. He said there is a test for chromosomal abnormality but its extremely rare and doesn’t feel its necessary to test that.
With my DOR, I just don’t want to do 3-4 rounds of IVF to find out that there was something else. He also mentioned that if it doesn’t work the first 3 times there is a likeliness that it will not work thereafter. I’m not sure I agree as I’ve heard several women who have attempted this 4 + times and were successful.
Could you please share any advice. I am stuck! Thank you so much!
Back to back IVF is not uideal. You need to rest a cycle between. Also, unless you have an anatomical issue that neeeds attention, a laparoscopy is not needed.
Indeed, endometriosis can be assoaciated with an immunologic implantation dysfunction.
When women with infertility due to endometriosis seek treatment, they are all too often advised to first try ovarian stimulation (ovulation Induction) with intrauterine insemination (IUI) ………as if to say that this would be just as likely to result in a baby as would in vitro fertilization (IVF). Nothing could be further from reality It is time to set the record straight. And hence this blog!
Bear in mind that the cost of treatment comprises both financial and emotional components and that it is the cost of having a baby rather than cost of a procedure. Then consider the fact that regardless of her age or the severity of the condition, women with infertility due to endometriosis are several fold more likely to have a baby per treatment cycle of IVF than with IUI. It follows that there is a distinct advantage in doing IVF first, rather than as a last resort.
So then, why is it that ovulation induction with or without IUI is routinely offered proposed preferentially to women with mild to moderately severe endometriosis? Could it in part be due to the fact that most practicing doctors do not provide IVF services but are indeed remunerated for ovarian stimulation and IUI services and are thus economically incentivized to offer IUI as a first line approach? Or is because of the often erroneous belief that the use of fertility drugs will in all cases induce the release (ovulation) of multiple eggs at a time and thereby increase the chance of a pregnancy. The truth however is that while normally ovulating women (the majority of women who have mild to moderately severe endometriosis) respond to ovarian stimulation with fertility drugs by forming multiple follicles, they rarely ovulate > 1 (or at most 2) egg at a time. This is because such women usually only develop a single dominant follicle which upon ovulating leaves the others intact. This is the reason why normally ovulating women who undergo ovulation induction usually will not experience improved pregnancy potential, nor will they have a marked increase in multiple pregnancies. Conversely, non-ovulating women (as well as those with dysfunctional ovulation) who undergo ovulation induction, almost always develop multiple large follicles that tend to ovulate in unison. This increases the potential to conceive along with an increased risk multiple pregnancies.
So let me take a stab at explaining why IVF is more successful than IUI or surgical correction in the treatment of endometriosis-related infertility:
1.The toxic pelvic factor: Endometriosis is a condition where the lining of the uterus (the endometrium) grows outside the uterus. While this process begins early in the reproductive life of a woman, with notable exceptions, it only becomes manifest in the 2ndhalf of her reproductive life. After some time, these deposits bleed and when the blood absorbs it leaves a visible pigment that can be identified upon surgical exposure of the pelvis. Such endometriotic deposits invariably produce and release toxins” into the pelvic secretions that coat the surface of the membrane (the peritoneum) that envelops all abdominal and pelvic organs, including the uterus, tubes and ovaries. These toxins are referred to as “the peritoneal factor”. Following ovulation, the egg(s) must pass from the ovary (ies), through these toxic secretions to reach the sperm lying in wait in the outer part the fallopian tube (s) tube(s) where, the sperm lie in waiting. In the process of going from the ovary(ies) to the Fallopian tube(s) these eggs become exposed to the “peritoneal toxins” which alter s the envelopment of the egg (i.e. zona pellucida) making it much less receptive to being fertilized by sperm. As a consequence, if they are chromosomally normal such eggs are rendered much less likely to be successfully fertilized. Since almost all women with endometriosis have this problem, it is not difficult to understand why they are far less likely to conceive following ovulation (whether natural or induced through ovulation induction). This “toxic peritoneal factor impacts on eggs that are ovulated whether spontaneously (as in natural cycles) or following the use of fertility drugs and serves to explain why the chance of pregnancy is so significantly reduced in normally ovulating women with endometriosis.
2.The Immunologic Factor: About one third of women who have endometriosis will also have an immunologic implantation dysfunction (IID) linked to activation of uterine natural killer cells (NKa). This will require selective immunotherapy with Intralipid infusions, and/or heparinoids (e.g. Clexane/Lovenox) that is much more effectively implemented in combination with IVF.
3.Surgical treatment of mild to moderate endometriosis does not usually improve pregnancy potential:. The reason is that endometriosis can be considered to be a “work in progress”. New lesions are constantly developing. So it is that for every endometriotic seen there are usually many non-pigmented deposits that are in the process of evolving but are not yet visible to the naked eye and such evolving (non-visible) lesions can also release the same “toxins that compromise fertilization. Accordingly, even after surgical removal of all visible lesions the invisible ones continue to release “toxins” and retain the ability to compromise natural fertilization. It also explains why surgery to remove endometriotic deposits in women with mild to moderate endometriosis usually will fail to significantly improve pregnancy generating potential. In contrast, IVF, by removing eggs from the ovaries prior to ovulation, fertilizing these outside of the body and then transferring the resulting embryo(s) to the uterus, bypasses the toxic pelvic environment and is therefore is the treatment of choice in cases of endometriosis-related infertility.
I am not suggesting that all women with infertility-related endometriosis should automatically resort to IVF. Quite to the contrary…. In spite of having reduced fertility potential, many women with mild to moderate endometriosis can and do go on to conceive on their own (without treatment). It is just that the chance of this happening is so is much lower than normal.
In young ovulating women (< 35 years of age ) with endometriosis, who have normal reproductive anatomy and have fertile male partners, expectant treatment is often preferable to IUI or IVF. However, for older women, women who (regardless of their age) have any additional factor (e.g. pelvic adhesions, ovarian endometriomas, male infertility, IID or diminished ovarian reserve-DOR) IVF should be the primary treatment of choice. ` I strongly recommend that you visit 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
•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?
•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)
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
•Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
•Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
•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
•Endometriosis and Infertily
•Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.
•Treating Ovarian Endometriomas with Sclerotherapy.
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.
I have just had a failed IVF cycle with donor eggs. This was my first cycle with donor eggs but I am wondering if there is any point for me to go through this again. I knew before the test that I was not pregnant as nothing in the cycle was straight forward. I am 42 and I have been treated and told I am cured of Asherman’s syndrome. The doctor who treated me was very surprised I had Ashermans as I have had none of the surgeries/infections that cause it. Also despite being treated my period is still brown in colour rather than red. Anyway to my question – the lining of my womb was slow to build to the required 7.5mm so at the end I was on 5 x 2mg Fematab, 4 x 200mg cyclogest, 1 x viagra, 1 x 50mg gestone injection, 1 x 75mg aspirin, 1 x 100mg esatradot and follic acid every day. I had two blastocysts transferred – 12 eggs collected 4 survived to blastocyst stage with my husband’s sperm. So with all this medication and the donor eggs the result was failure. Am I wasting my time and money trying again? Could my age and previous history of Ashermans mean this is just not going to work for me. The clinic did recheck that my ashermans was gone and during the process the lining was triple layer. I just don’t know what to do?
If you are unable to propagate an 8t least an 8mm lining in spite of best effort, it would in my opinion not be a good idea to keep on trying.
A normal uterine cavity and endometrial lining are essential in order to conceive and maintain a pregnancy. Scar tissue in the uterine cavity (Asherman’s syndrome) can interfere with conception, or increase the risk of miscarriage. The condition is often so severe that it destroys most of the basal (germinal) layer of the endometrium from which the uterine lining (endometrium) develops each month. When most of the basal endometrium is incapacitated, no regeneration of the endometrium can take place and amenorrhea (cessation of menstruation) or infertility can follow. The condition often results in fusion/adhesion of the opposing endometrial surfaces, but can also simply destroy the basal layer of endometrium without resulting in adhesions (non-adhesive Asherman’s).
Asherman’s syndrome most commonly results from post-partum or post-abortal inflammation involving the uterine lining (endometritis), but it can also occur (although infrequently) following uterine surgery such as removal of fibroid tumors (myomectomy) that encroach upon (or penetrate into) the uterine cavity.
The treatment of adhesive Asherman’s syndrome is resection of scar tissue by hysteroscopy. A hysteroscope is a telescope-like instrument that is introduced via the vagina and cervix into the uterine cavity allowing visualization of and access to the entire uterine cavity, enabling surgical resection of scar tissue. The objective is to remove as much scar tissue as possible and to free adhesions that fuse the walls of the uterine cavity together, so as to enable viable basal endometrium to resume growth and progressively cover as much of the surface of the uterine cavity as possible. Post-operatively, a small balloon is often placed in the uterine cavity for a day or two, to keep the opposing surfaces separated in the hope of preventing recurrence of adhesion formation. The woman usually receives supplemental estrogen to encourage endometrial growth.
Endometritis of a severity sufficient to produce Asherman’s Syndrome often scars and blocks the uterine entrances into the Fallopian tubes. However it is not always the case. The lining can be damaged while the tubes remain open. In such cases, if the uterine lining cannot support proper embryo implantation, a pregnancy could still implant in a Fallopian tube leading to an ectopic (tubal) pregnancy. Unless it is diagnosed early (by blood testing in combination with ultrasound examination) and treated medically or surgically, the ectopic pregnancy will rupture with serious and potentially life endangering consequences.
About 8 years ago, we reported on the use of Viagra vaginal suppositories to improve blood flow and hence enhanced delivery of estrogen to the endometrium. In this manner, we have been able to improve endometrial development in about 75% of women who otherwise were unable to develop an “adequate” uterine lining. Most of these women had undergone several failed IVF attempts. Many of the women who were successfully treated with Viagra subsequently conceived following IVF and went on to deliver healthy babies. One such case immediately comes to mind. It involved a woman who was from Singapore and who following 15 failed IVF attempts due to poor endometrial development conceived on her first IVF-Viagra attempt with us following Viagra therapy.
But Viagra is often ineffective in thickening the uterine lining in women with Asherman’s syndrome. The reason is that with Asherman’s there is often such widespread destruction of the basal endometrium (from which fresh endometrial cells must be generated), that regardless of the improvement in uterine blood flow and improved estrogen delivery, the endometrium just can’t respond. In such cases, the woman should consider using a gestational surrogate or pursuing adoption
I hope this helps!
Good luck!
Geoff Sher
I’m a 32 year old male currently taking OxyContin for chronic pain related to a car accident. Would my use of this painkiller affect IVF?
Dr sher
1. Is dhea supplementation advisable in someone who
Is mildly pcos?
2. Does quiet ovaries or small follicle in mid chcle in one observation significant or indicate anything
3. Most doctors implant embryos some five days after retrieval. Have you heard and give credence to
Recent credence on optimal Windows and testing related to
That. When is such testing justified e.g after a number of failure to implant
4. What are your thoughts on debate on elevated progesterone levels prior to implantation and why that occurs. Is this likely to occur under specific protocols or in specific people. If the latter how can this ocuranvce be reduced
5. What are hour views on supplementation and use of supplements such as ubiquinol, maca root etc to boost egg quality or balance hormones .
1. Is dhea supplementation advisable in someone who
Is mildly pcos?
A: No…not in my opinion.
2. Does quiet ovaries or small follicle in mid chcle in one observation significant or indicate anything.
A: Not really …except that you likely would be capable of responding in a subsequent stimulation cycle.
3. Most doctors implant embryos some five days after retrieval. Have you heard and give credence to
Recent credence on optimal Windows and testing related to
That. When is such testing justified e.g after a number of failure to implant
A: Women with repeated IVF failure, women undergoing “embryo banking”, women with recurrent pregnancy loss of chromosomally abnormal concepti
4. What are your thoughts on debate on elevated progesterone levels prior to implantation and why that occurs. Is this likely to occur under specific protocols or in specific people. If the latter how can this ocuranvce be reduced
A: Raised progesterone levels prior to the hCG trigger could point to “premature luteinization” and when this occurs it can have a damaging effect on egg/embryo competency (see below).
5. What are hour views on supplementation and use of supplements such as ubiquinol, maca root etc to boost egg quality or balance hormones .
A: Probably does no harm but there is no objective evidence of benefit.
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
•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
•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?
•Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
•The Role of Nutritional Supplements in Preparing for IVF
•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.
I am a healthy 30 year old with only one ovary and DOR. We did two IVF cycles when I was 28 y/o. I am also a poor responder and took the highest dose of bravelle, lupron, and menupor. The first one was a day 5 transfer as they looked great on day 3 but on day 5 they weren’t so great. I was simply told poor progression. Round two, we did a day three transfer which resulted in my healthy almost two year old child. Currently we are up for round three, would you recommend a day 3 transfer in my case? This round i am still doing lupron and menupor but Gonal in place of bravelle. Thank you for your time.
If there are few (2 or less) embryos available, a day 3 transfer is OK…however please bear in mind that embryos that fail to make it to blastocyst by day 5-6 are almost always abnormal and would with very few exceptions not have made a viable pregnancy had they been transferred earlier.
Geoff Sher
Immunology Results.
Hi Dr. Sher,
I am an immunology patient undergoing a FET currently. I am on 10 mg of prednisone and 500mg of metformin. I just had my labs drawn and they were:
–NK assay 50:1 16.6 target range is 15 or less (improved from 32.5)……….
–cd56 3.7 target range is 12 or less………
–Th1/Th2 Cytokines:…… TNF 38.9 target range is 30.6 or less……….
–IFN 26.1 target range is 20.5 or less……….
–CBC, Chemistry, Aptt and Thyroid panel all reassuring.
My doctor recommended IVIG or increasing to 20mg of Prednisone in anticipation of my transfer on July 22. I started the prednisone/metformin on June 16 and the blood draw was July1.
I am already having a hard time with the prednisone and I can’t afford IVIG. Are these numbers really THAT far off or can I keep taking 10mg of prednisone and hope that more time passes and the numbers go down? Or have I reached my “peak” in terms of how low they will go without adding more Prednisone?
Thank you for weighing in!
Erin
It certainly sounds as if you have NKa+. Problem is that I do not know whether it is autoimmune or alloimmune in nature and treatment would differ depending on the cause. In my opinion, IVIG can be supplanted with intralipid which is just as effective, relatively risk free and not associated with significant side effects….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.
•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)
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
•Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
•Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
•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 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.