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.
I was just recently diagnosed with stage 2 endometriosis and a lap showed that both my tubes are blocked due to hematosalpinx. I’ve read online about hydrosalpinx and that when doing ivf this can damage the embryo they implant. Is this the same for hematosalpinx? I’m worried that when I am ready for ivf they’ll want to remove my blocked tubes and I don’t think my insurance will cover it.
Indeed, hematosalpinx can also compromise IVF outcome and needs to be addressed surgically before the IVF treatment cycle.
Endometriosis is associated with an immunologic implantation dysfunction in 1/3 of cases, regardless of its severity and this too needs to be addressed if applicable in your case. More than half of women who have endometriosis harbor antiphospholipid antibodies (APA) that can compromise development of the embryo’s root system (trophoblast). In addition and far more serious, is the fact that in about one third of cases endometriosis, regardless of its severity is associated with NKa and cytotoxic uterine lymphocytes (CTL) which can seriously jeopardize implantation. This immunologic implantation dysfunction (IID) is diagnosed by testing the woman’s blood for APA, for NKa (using the K-562 target cell test or by endometrial biopsy for cytokine activity) and, for CTL (by a blood immunophenotype). Activated NK cells attack the invading trophoblast cells (developing “root system” of the embryo/early conceptus) as soon as it tries to gain attachment to the uterine wall. In most cases, this results in rejection of the embryo even before the pregnancy is diagnosed and sometimes, in a chemical pregnancy or an early miscarriage. As such, many women with endometriosis, rather than being infertile, in the strict sense of the word, often actually experience repeated undetected “mini-miscarriages”.
Women who harbor APA’s often experience improved IVF birth rates when heparinoids (Clexane/Lovenox) are administered from the onset of ovarian stimulation with gonadotropins until the 10th week of pregnancy. NKa is treated with a combination of Intralipid (IL) and steroid therapy: Intralipid (IL) is a solution of small lipid droplets suspended in water. When administered intravenously, IL provides essential fatty acids, linoleic acid (LA), an omega-6 fatty acid, alpha-linolenic acid (ALA), an omega-3 fatty acid.IL is made up of 20% soybean oil/fatty acids (comprising linoleic acid, oleic acid, palmitic acid, linolenic acid and stearic acid) , 1.2% egg yolk phospholipids (1.2%), glycerin (2.25%) and water (76.5%).IL exerts a modulating effect on certain immune cellular mechanisms largely by down-regulating NKa.
The therapeutic effect of IL/steroid therapy is likely due to an ability to suppress pro-inflammatory cellular (Type-1) cytokines such as interferon gamma and TNF-alpha. IL/steroids down-regulates NKa within 2-3 weeks of treatment the vast majority of women experiencing immunologic implantation dysfunction. In this regard IL is just as effective as Intravenous Gamma globulin (IVIg) but at a fraction of the cost and with a far lower incidence of side-effects. Its effect lasts for 4-9 weeks when administered in early pregnancy.
The toxic pelvic environment caused by endometriosis, profoundly reduces natural fertilization potential. As a result normally ovulating infertile women with endometriosis and patent Fallopian tubes are much less likely to conceive naturally, or by using fertility agents alone (with or without intrauterine (IUI) insemination. The only effective way to bypass this adverse pelvic environment is through IVF. I am not suggesting here that all women who have endometriosis require IVF! Rather, I am saying that in cases where the condition is further compromised by an IID associated with NKa and/or for older women(over 35y) who have diminished ovarian reserve (DOR) where time is of the essence, it is my opinion that IVF is the 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.
•The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•The Fundamental Requirements For Achieving Optimal IVF Success
•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?
•The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
•Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
•Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
•Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
•Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
•Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
•Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
•Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
•A personalized, stepwise approach to IVF
•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.
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.
Hello Dr Sher, I would like to thank you very much for this webpage it is really helpful and all the information are valuable.
I would like to have your opinion in my protocol.
First, I would like to speak about myself briefly, I have PCOS, my weight is 60 kg, I am 31 years old. tried several times IVF 3 times with 5000 IU trigger shot I got no eggs, 2 times short protocol with 10000 IU trigger shot they got only the cells around the egg. during all attempts, I was very good responder and I got many follicles and 2 times I was hyper-stimulated. last time we planned to use the long DR protocol as follows:
– to take 42 days birth control pills.
– the last four days of birth control pills I start decapeptyl 0.1 mg daily for 13 days.
– after 13 days of decapeptyl I start with puregon injection 50 IU and the decapyptyl reduced to the half ( day yes day no).
– after three days of puregon 50 IU , I start Menupor 75IU.
– after 4 days of menupor I do the scan.
In this cycle I got bad response .. a lot of follicles and the size is not good. so we stopped the cycle.
I was not taking metformin as I should.
What do you think the reason of bad responding? If we increase the first shot of puregon to be 75 IU Do you think it will be better? because we are planning to use the same protocol comes after 32 pills of birth control pills at the end of this month, please doctor what is your opinion? and Is there anything that might increase the success rate of the treatment?
Thank you very much
Ovarian hyperstimulation syndrome (OHSS) is a life-endangering condition that occurs following ovarian stimulation for the treatment of infertility. It occurs due to overstimulation of the ovaries with the development of numerous follicles in susceptible women. Systemic effects can be very serious and can lead to life-endangering complications. Thus every effort must be made to avoid the condition and when it does threaten, to take the necessary steps to mitigate its effects, and at the same time attempt to protect egg quality which often is adversely affected as well. Prevention starts with recognizing those women who are at the greatest risk of developing OHSS. They include:
•Those with a history of having hyperstimulated on fertility drugs in the past.
•Younger women (<25y)
•Women who have biochemical indicators that suggest they are so at risk of developing OHSS (e.g. An AMH of >5ng/ml; basal FSH of <5MIU/ml; basal LH level being significantly higher than LH; Antral follicle count of >25)
•Women who have dysfunctional or absent ovulation.
•Women diagnosed with polycystic Ovarian Syndrome (PCOS)
In such cases, it is prudent to minimize the dosage of gonadotropins administered, but alas, this often will not eliminate risk of OHSS developing anyway. Aside from the risk that OHSS places the woman at, it can also have a devastating effect on egg quality/competency. Thus, all too often, the measures taken (see below) to reduce maternal risk come at a price.
PRESENTATION AND MANAGEMENT OF OHSS:
The onset of OHSS, heralded by the presence of large numbers (>25) of developing ovarian follicles and rapidly rising plasma estradiol levels, often exceeding 3000pg/ml within 7 or 9 days of stimulation, and rapidly peaking above 6,000 pg/ml prior to hCG administration. When this happens, the risk of OHSS developing is above 80%. The fear of this escalating often leads physicians to prematurely administer hCG in an attempt to abruptly arrest the process and prevent escalation of risk to the patient. However, the premature administration of the “trigger” shot arrests egg development and adds to the problem of poor egg/embryo quality in such cases.
Symptoms and signs of OHSS include: abdominal distention due to fluid collection (ascites), fluid in the chest cavity (hydrothorax), rapid weight gain (of a pound or more per day) due to tissue fluid retention, abdominal pain, lower back ache, nausea, diarrhea, vomiting, visual disturbances such as blurred vision and spots in front of the eyes (scotomata), a rapidly declining urine output, cardiovascular collapse and failure of blood to clot which sometimes results in severe bruising (ecchymosis) and frank bleeding. These symptoms and signs may appear before pregnancy can be diagnosed. If pregnancy occurs, the condition is likely to worsen progressively over a period of 3-5 weeks whereupon it rapidly resolves spontaneously over a few days. If no pregnancy occurs, the symptoms and signs all disappear spontaneously within 10-12 days of the hCG injection.
When increasing fluid collection in the abdominal cavity (ascites) starts to compromise breathing raising the head of the bed rose slightly by placing a 4-6 inch block at the base of each head post and using a few additional pillows, will sometimes help ameliorate the problem. In cases where this does not help or symptoms become severe, all or most of the fluid can readily and safely be drained through t transvaginal sterile needle aspiration (vaginal paracentesis-performed once or sometimes twice a week) can be performed once or twice weekly . The problem will usually self corrects within 10-12 days of the hCG shot if pregnancy does not occur or, by the 8th week of pregnancy.
Urine output should be monitored daily to see if it drops below about 500ml a day (about two cups and a half). A chest X-ray, to evaluate for fluid collection in the chest and around the heart should be done weekly along with blood tests for hematocrit, BUN, electrolytes, creatinine, platelet count and fibrin split products (FSP). If indicated on the basis of a deteriorating clinical situation, hospitalization might be needed for close observation and if necessary, to provide intensive care.
In all case of OHSS, the ovaries and contain numerous theca-lutein cysts and will invariably be considerably enlarged. This is irrelevant to the final outcome, unless ovarian torsion (twisting of the ovary on its axis), an extremely rare complication occurs. The latter would usually require surgical emergency surgical intervention.
Human chorionic gonadotropin (hCG) “Fans the flames “ of OHSS. That is why the occurrence of pregnancy worsens the condition. In women who do not conceive, the clinical severity of OHSS will usually peak 7-10 days after the hCG “trigger”, plateaus for another 3-4 days and thereupon rapidly improves within the ensuing week. Thus in the absence of hCG the condition is “self-limited”. Sometimes severe symptoms due ascites make it imperative to drain the fluid transvaginally (often repeatedly). This brings immediate relief but it can be short-lived requiring repeated drainage a few days later until the condition resolves. If the woman conceives following a fresh embryo transfer, the rising hCG blood levels can exacerbate the OHSS for several weeks, but either way, it usually disappears spontaneously by the 8th to 9th harrowing week of pregnancy. This is why there is a growing tendency to avoid fresh embryo transfers, preferring to do FET’s later once the woman is out of risk. It is also the reason for a move to avoid using 10,000U of hCG for the “trigger shot” or to avoid to supplant hCG with an “agonist” trigger. But this comes at a price…see below.
OHSS ANF POOR EGG/EMBRYO QUALITY/COMPETENCY:
OHSS is also associated with e poor egg/embryo quality. This is especially so in women with high ovarian LH-induced testosterone (e.g. those with PCOS). The often present with poorly developed (“dysmorphic”) eggs, with reduced fertilization potential and yielding “poor quality embryos”. However, in the author’s opinion (which admittedly runs contrary to popular opinion), this is unlikely to be due to an intrinsic deficit in egg quality. Rather, it more likely relates to intra-ovarian hormonal changes brought about by hyperstimulation and which compromise egg development. This effect, in my opinion, can often be significantly reduced through implementation of an individualized or customized ovarian stimulation protocols that minimize exposure of the developing follicles and eggs to excessive LH-induced ovarian androgens. This can be best achieved by limiting the use of LH-containing gonadotropins such as Menopur through selective institution of “prolonged coasting” (see below). Approaches to preventing OHSS include:
1.PROLONGED COASTING (My preferred approach) : My approach is to use a long pituitary DR protocol coming off up to 2 months on the BCP, overlapped in the last 3 days with the agonist, Lupron. The BCP is intended to lower LH and thereby reduce stromal activation (hyperthecosis) in the hope of controlling ovarian androgen (predominantly, testosterone) production and release. I then stimulate with low dosage FSHr (Follistim/Gonal-F/Puregon) to which I add a smidgeon of LH/hCG (Luveris/Menopur) from the 3rd day. Then, starting on day 7 of ovarian stimulation, I perform serial blood estradiol (E2) and ultrasound follicle assessments, watching for the # of follicles and [E2]. If there are > 25 follicles, I keep stimulating (regardless of the [E2] until 50% of all follicles reach 14mm. At this point, provided the [E2] reaches at least >2,500pg/ml, I stop the agonist as well as gonadotropin stimulation and track the blood E2 (without continuing US, follicle measurements) ) daily. The [E2] will almost invariably increase for a few days. I watch the E2 rise (regardless of how high a blood concentration it reaches) and then track it coming down again. As soon as the [E2] drops below 2500pg/ml (and not before then), I administer a “trigger” shot of 10,000U hCGu (Profasi/ Novarel/Pregnyl) or hCGr (Ovidrel/Ovitrel-500mcg) and perform an egg retrieval 36 hours later. ICSI is a MUST because “coasted” eggs usually have no cumulus oophoris envelopment and eggs without a cumulus will not readily fertilize naturally. Moreover, they also tend to have a “hardened” envelopment (zona pellucida), making spontaneous fertilization problematic in many cases. All fertilized eggs are cultured to blastocyst (up to 6 days) and are then either vitrified and preserved for subsequent transfer in later hormone replacement cycles or up to two (2) fresh blastocysts are transferred transvaginal under US guidance.. The success of this approach depends on precise timing of the initiation and conclusion of “prolonged coasting”. If you start too early, follicle growth will stop and the cycle will be lost. If you start too late, you will encounter too many post-mature/cystic follicles (>22mm) that usually harbor abnormally developed eggs. Use of “Coasting” avoids unnecessary cycle cancellation, severe OHSS, and optimizes egg/embryo quality. The worst you will encounter is mild to moderate OHSS and this too is uncommon. The obvious remedy for these adverse effects on egg and endometrial development is to employ stimulation protocols that limit ovarian over-exposure to LH and allowing the time necessary for the follicles/eggs to develop optimally, prior to administering hCG through the judicious implementation of “Prolonged coasting” (PC).
2.MULTIPLE FOLLICLE ASPIRATION: In some cases, where because of mean follicle size exceeding 16mm or when “coasting” fails to effectively lower the [E2} below 2,500pg/ml within 3 days, the number of developing follicles can effectively and drastically reduced through target transvaginal aspiration, 1-3 PRIOR to planned the hCG trigger. This will almost invariably be accompanied by a rapid and significant drop in the plasma [E2] and in the process will drastically reduce reduce the risk of OHSS occurring without significantly compromising egg/embryo quality. The drawback of this effective approach is the fact that it interjects an additional surgical intervention into an already complex and stressful situation. i
3.TRIGGERING WITH LOW DOISAGE hCG; Because of the fact that hCG augments the development of OHSS (unless preceded by “coasting”), may RE’s prefer to use a lower dosage of hCG for the “trigger. This is either done by administering 5,000U (half the traditional dosage) or by administering, a 250mcg (rather than 500mcg) of DNA recombinant form of hCGr (Ovidrel/Ovitrel. Some clinicians, when faced with a risk of OHSS developing will deliberately elect to reduce the “trigger” dosage of hCG administered (from 10,000U to 5,000U or 250mcg of recombinant hCG-Ovidrel) in the hope that by doing so the risk of critical OHSS developing will be lowered. While this might indeed be true, it is my opinion, that such a reduced dosage is usually insufficient to optimize the efficiency of egg meiosis, e3specially when there are so many follicles present. While the use of a reduced “trigger” dosage of hCG does indeed reduce the risk and occurrence of OHSS-related life-endangering complications, the price to be paid is reduced egg quality/”competency”.
4.“TRIGGERING” WITH A GnRH AGONIST (E.G. “LUPRON/BUSERELIN): More recently, an increasing number of RE’s prefer to trigger meiosis by way of an agonist (Lupron/Buserelin/Superfact () “trigger” rather than through the use of hCG. The idea is to mimic what happens in natural cycles to promote egg maturation (meiosis) and ovulation, namely to have the agonist cause a “surge” in the release of body’s own pituitary LH to trigger egg meiosis (maturation) .But the amount of LH released in by the pituitary gland is often insufficient to optimize meiotic egg maturation and thus, while this approach also lowers the risk of OHSS it again comes at the expense of egg quality/competency.
A word of caution: I do not use long term administration of antagonists (Ganirelix/Cetrotide/Orgalutron), such as with the agonist/antagonist conversion protocol (A/ACP) in high responders whom are at risk of developing OHSS prolonged in-cycle administration of because it can interferes with the E2 assay (often causing the value to be understated), and serial measurement of E2 is a vital part of monitoring patients undergoing “coasting”
I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
•The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•The Fundamental Requirements For Achieving Optimal IVF Success
•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?
•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.
Hi Dr. Sher,
I’m wondering if grade 2 and 3 5-day frozen blastocysts could ever implant and go on to result in a successful pregnancy?
Do they have to be grade 1s to be successful?
Hope your enjoying Africa. It’s always been a dream of mine.
Sincerely
Molly
Grade 1-2 blastocysts do equally well in my opinion!
Geoff Sher
First of all, thank you Dr. Sher for being such a huge resource for so many women struggling with fertility issues!
I’m a fit and healthy just newly turned 40 year old. Although I seem to be able to get pregnant, I have had difficultly remaining pregnant as I experienced 3 miscarriages in the past year and half. So my husband and I decided to give ivf a try last month. Everything started off well as AMH number was above normal for my age and from the my scans I had a lot of follicles.
My doctor decided to start me on an antagonist protocol (i.e., follistim at 375 for 2 days, then dose was lowered at which point I started Menopur then to Ganirelix–a little less than 2 weeks later I gave myself an HCG trigger shot then headed off to the retrieval 36 hours later). They were able to retrieve 25 eggs, of those only 11 were mature and 10 fertilized. From there 6 made it to day 3 (2 ten cell, 2 eight cell, 2 six cell) and then by day 5 all stopped growing and we had no embryos to transfer/freeze.
My doctor indicated my eggs quality looked poor (some dark and grainy and misshapen) and found the immature to mature ratio to be high. He believes that this is an inherent problem I have been suffering from and believes I will unlikely be able to produce very many healthy eggs, if at all. However, he did strongly recommend I try one more cycle (this time the long cycle with Lupron) with the hope that we might be able to get one maybe two better quality eggs. He also added that even if we were able to retrieve a healthier egg which then would make it to day 5 for freeze, there was a 80% chance that it would come back abnormal after PGS testing.
This all sounds like a very steep up hill battle for us. I am now wondering why we would even try another round if he felt like even the one or two would come back abnormal. Dr. Sher do you think a longer protocol could help someone like me? Why would my doctor come to the conclusion that I may have an inherent egg quality problem? From what I described would you also come to the same conclusion?
Thank you Dr. Sher for your help,
Blake
There is little doubt that the older a woman gets, the poorer the likelihood of chromosomally normal embryos. This can only be partially compensated for by using a very individualized approach to ovarian stimulation. Women wo hyper-respond as you did, often have their cycles cut short or get triggered with a lower dosage of hCG or Ovidrel. Some receive an agonist (Lupron.Superfact/Buserelin) trigger and while such approaches may lessen the risk of severe ovarian hyperstimulation and thus protect the woman, this comes at the expense of egg/embryo quality.
In my opinion, the protocol used for ovarian stimulation, against the backdrop of age, and ovarian reserve are the drivers of egg quality and egg quality is the most important factor affecting embryo “competency”.
Older women tend to have increased LH biological activity which often results in excessive LH-induced ovarian testosterone production which in turn can have a deleterious effect on egg/embryo “competency”.
Certain ovarian stimulation regimes either promote excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), augment LH/hCG delivered through additional administration (e.g. high dosage menotropins such as Menopur), or fail to protect against body’s own/self-produced LH (e.g. late antagonist protocols where drugs such as Ganirelix/Cetrotide/Orgalutron that are first administered 6-7 days after ovarian stimulation has commenced).
I try to avoid using such protocols/regimes (especially) in older women favoring instead the use of a long pituitary down-regulation protocol (augmented by adding supplementary human growth hormone (HGH). I further recommend Staggered IVF with embryo banking of PGS (next generation gene sequencing/NGS)-normal blastocysts in such cases. This type of approach will in my opinion, optimize the chance of a viable pregnancy per embryo transfer procedure and provide an opportunity to capitalize on whatever residual ovarian reserve and egg quality still exists, allowing the chance to “make hay while the sun still shines”.
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.
•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?
•Staggered IVF: An Excellent Option When. Advancing Age 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
•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.
Geoff Sher
Hi Dr. Sher. Happy New Year! At 34 I had my first successful transfer of 2 pgs normal embryos on day 5. My twins are now 5 months old. I’m now 35 and took my twins to see my RE. He says the clinic guidelines have changed. Now age 37 and <, they only let patients transfer 1 embryo. We're doing another transfer Fall 2017. I do not like that I can only transfer 1 pgs normal blastocyst. Is there a way of going around this? I'm in the middle of nowhere and there aren't any clinics I can transfer to without having to drive 2 hours. I'm a good candidate for a double embryo transfer. Any thoughts on this? Thank you.
I can understand their position. Even twins are more risky than singletons but not that much more. Thus I still transfer 2 embryos (but no more).
Sorry I cannot help here.
Geoff Sher