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.
Dear Dr. Geoffrey,
My wife has DOR. Her AMH – 0.662, FSH – 12.1, LH 5.5.
She has undergone Clomiphene 50mg from days 2 for 5 days, menotrophin – 75 IU on day 6 and 8, HCG 10000 IU on day 12, this was done for 2 cycles for IUI. She developed a folicle of 7 mm in both cycles but it failed.
A cycle of Clomiphene 50mg from days 2 for 5 days, letrozole 150 IU on day 6, HCG 10000 IU on day 12, this was done for 1 cycle for IUI. She developed a folicle of 8.7 mm (25×24) in Lt. ovary. IUI was done on day 14 but she did not conceive.
Now we changed the Dr. and he is only doing Clomiphene 50mg from days 2 for 5 days, HCG 10000 IU on day 12 and IUI on day 14. We tried this for 2 cycles but no success.
My sperm count are low. It is 18 mill/ml and total sperm count is 36mil / ejaculate. So, our Dr. is doing IUI. Apart from that he has put her on DHEA 75mg a day, which she is taking from last 3 months and we await to see its benefits on egg quality now.
Can you please help by guiding on how should we proceed ? Which protocol should we use. I asked Dr. about IVF but he is saying chances are less with her own eggs and we should go for donor eggs.
Can she conceive naturally?
her age is 32.
Respectfully, IUI is in my opinion totally inadequate for someone like your wife who has diminished ovarian reserve (AMH=0.66ng/ml) and or in cases where there is male factor. Also in my opinion, clomiphene should not be used in cases o DOR. Given the adverse effect of progressive DOR on egg quantity as well as on egg quality (unless an optimal protocol for stimulation is implemented), time is of the essence….see below!
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”.
Women who (regardless of age) have DOR have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production of LH biological activity which can result in excessive LH-induced ovarian male hormone (predominantly testosterone) production which in turn can have a deleterious effect on egg/embryo “competency”.
While it is presently not possible by any means, to reverse the effect of DOR, certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can in my opinion, make matters worse. Similarly, the amount/dosage of certain fertility drugs that contain LH/hCG (e.g. Menopur) can have a negative effect on the development of the eggs of older women and those who have DOR and should be limited.I try to avoid using such protocols/regimes (especially) in women with DOR, favoring instead the use of the agonist/antagonist conversion protocol (A/ACP), a modified, long pituitary down-regulation regime, augmented by adding supplementary human growth hormone (HGH). I further recommend that such women be offered access to embryo banking of PGS (next generation gene sequencing/NGS)-selected normal blastocysts, the subsequent selective transfer of which by allowing them to capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” could significantly enhance the opportunity to achieve a viable pregnancy
Please visit my new Blog on this very site, https://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
• 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 Approach
• 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?
• Blastocyst Embryo Transfers should be the Standard of Care in IVF
• Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
• 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 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
• 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
• Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
• IVF Egg Donation: A Comprehensive Overview
•Male Factor Infertility
•Routine Fertilization by Intracytoplasmic Sperm Injection (ICSI): An Argument in Favor
•Hormonal Treatment of Male Infertility
•Intrauterine Insemination (IUI): Who Needs it & who Does Not: Pro’s & Con’s!
•IUI-Reflecting upon its Use and Misuse : Time for a Serious “Reality Check”.
I invite you to arrange to have a Skype or an in-person consultation with me to discuss your case in detail. If you are interested, please contact Julie Dahan, at:
Email: Julied@sherivf.com
OR
Phone: 702-533-2691
800-780-7437
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, thank you sooo much for taking the time to answer our questions. I can’t express in words how grateful I personally am for your support in this difficult journey.
Please could you advise whether you think we should do blood Karyotype tests as we have not been able to get PGS normal embryos? In what situations do you normally recommend doing the Karyotype test? As we have had conflicting opinions from two different doctors. Thanks so much in advance!
Blood Karyotyping is rarely of benefit in the evaluation of treatment for infertility. The notable exceptions are where there have been repeated pregnancy losses and you want to exclude translocation as a cause and in cases where there is a suspicion of a particular type of chromosomally transmitted genetic disorder. Karyotyping of the embryo is another matter altogether.
Geoff Sher
Hello Dr. Sher. I have read some of your articles online about empty follicle syndrome and wanted to share my recent experience with you to get your take on it. I am 38 years old and my husband is 49. We have been diagnosed with MFI. My husband’s count is 9 million, motility is 55%, and morphology is 3%. After being checked out and trying to find a cause it is unexplained. My FSH is 7.6, AMH is 3.84, estradiol is 42, and antral follicle count is 18. So everything with me came out good. Tubes are good, uterus is good, no polyps. Neither my husband nor myself have ever conceived. My RE recommended my husband go on Clomid and we try IUI first since he felt I had plenty of time yet. We opted instead to go straight to IVF/ICSI to be as aggressive as possible and have the best chance the first time. I was on 150 of Menopur and 150 of Gonal f starting on cd3. No BC as it might suppress me too much. After 4 days of stimming, I added Cetrotide. I was responding really well, but almost too well they said. On day 6 of stims, my doses were dropped in half to 75 & 75. Day 8, Gonal f was eliminated entirely. I only stimmed for 8 days and then triggered with Ovidrel. After 8 days of stims, my estradiol was 1865 and I had 35 follicles, 20 of which were over 15mm. The nurse said I would only lose one to being over mature. The morning after the trigger shot my estradiol was 2900. So everything looked great. However, at retrieval only 7 eggs were retrieved and 6 were mature. 5 fertilized thru ICSI, and we had a 3 day transfer of two 8 cell embryos with minimal fragmentation. The other 3 were a 6 cell, a 7 cell, and a 10 cell, all with less than 10% fragmentation. None of the remaining 3 made it to day 5 for freezing. Our beta unfortunately was negative. I meet with my doctor tomorrow to see what he thinks, but I wanted to get an outside perspective. I’m concerned that I may be someone who looks good on paper but really has poor quality eggs. I’m hoping that that is not the case of course and that maybe the medication is to blame for our failed cycle. Could I still have a chance for success with a different protocol? Also, if the embryos look good on day 3 but arrest before day 5 is that due to the egg or the sperm or both? Could my husband’s sperm quality be an issue with why they didn’t survive to day 5 or does ICSI completely eliminate any issues with sperm? Does the issue with the “empty follicles” mean the eggs that we got were probably low quality? With a different protocol could we get healthier eggs that mature properly? Was there a chance that I could’ve gotten pregnant with such a strange outcome from retrieval? I mean the fact that we only got 20-25% of the eggs that we expected from the ultrasound seemed like a bad prognosis to me from the get go. But could we still have achieved pregnancy with one of those eggs? Also, I’ve never been diagnosed with PCOS but I’m wondering if this is a sign of that? I have always had normal cycles and my weight is within healthy limits but I have always struggled with acne and I also have PMDD. Plus, my AMH seemed a little on the high end to me and I did have 35 follicles after 8 days of stimming which seems like I am a fast responder. Just a thought. Also, I did make a mistake and got a double dose of Gonal f the first night so it was actually 300 instead of 150. I went in sooner for blood work though and they said it would be ok. Wondering if that caused any problems. Thank you so much for your time and I appreciate any insight you can give me into my situation.
I also wanted to add a few more facts about my failed IVF treatment. We did assisted hatching as well. This was a decision we had to make beforehand and our doc said it benefits some people and others it makes no difference but there is no way of knowing that. We decided to go ahead and do it if we had a 3 day transfer due to my age. The embryologist actually said our embryos had nice thin zonas so I feel it may not have been necessary but they did it anyway since we agreed to it ahead of time. The embryologist said it never hurts. But due to the added cost of $975 I am thinking about skipping it next time. Unfortunately they don’t skip it if you agree to it ahead of time, even if it doesn’t look like it’s necessary. What are your thoughts on assisted hatching, especially since we had thin zonas the first time around? And I also wanted to share some of my symptoms following retrieval. Even though only 7 eggs were retrieved I had quite a bit of discomfort. I’m guessing that’s because I actually had 35 follicles. I had a lot of difficulty urinating the day of the retrieval and was close to having to have a catheter, but it slowly started to improve. I also had extreme bloat for 2 days after the retrieval, like my abdomen could not distend any further. It ended up taking almost 2 weeks to go back to normal. Also, I was using crinone from the day after retrieval until my negative test. Just wanted to make sure you had all my info. Thanks.
Respectfully, if you had that many follicles and you were triggered on day 8 of stimulation with an E2 of <2,000 pg/ml, then it was done too early. I would have expected the E2 to be >4,000pg/ml. The reason you were triggered prematurely was likely to prevent further follicle growth that would have increased the risk of severe ovarian hyperstimulation syndrome (OHSS). I further suspect that your trigger dosage of hCG was reduced (either 5,000U rather than the usual 10,000U or that you received 250mcg of Ovidrel (rather than 500mcg). While such an approach would certainly reduce the risk of OHSS, this would come at the expense of egg quality. When eggs are complex aneuploid, they often are unable to transmit the trigger signal, to cause the surrounding cells that bind them to the inner wall of the follicles to disperse , allowing them to be easily aspirated at ER. The result is that they remain attached and the follicle yields no egg..leading to them being erroneously labled as being “empty”. What you need is a complete review and revision of the protocol used for ovarian stimulation as well as its revision. I believe that given your age and circumstances, this needs to be effected ASAP.
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
•Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
•A personalized, stepwise approach to IVF
•Preventing Severe Ovarian Hyperstimulation Syndrome (OHSS) with “Prolonged Coasting.
•“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?
•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 Doctor Sher,
We started trying to get pregnant from August 2014. In August 2015 our GP referred us to a Fertility Clinic in Ireland. We had our consultation, bloods, scans, etc and it was decided ICSI was the best way for us. They did notice I had a fibroid on my left hand side, but after internal scan, ultrasound and another internal scan they decided it would not effect a pregnancy. We started our cycle in January 2016 where I started on a nasal spray and then started on Gonal F, 200 from what I remember. I went in for collection and they collected 7 eggs, 6 fertilised and on day 5 they transferred one. The other two didn’t grow enough to be frozen. The one they transferred ended up not even reaching blastocyst stage and all embryos were a poor quality. The clinic said they wouldn’t change any meds for the next cycle, and then also suggested maybe it was the fibroid that was an issue, and asked for me to go for an MRI. We were extremely unhappy with the outcome with the clinic so in May 2016 we had a consultation with a European clinic and after 5 hours with them we thought they were perfect to help us. As soon as they saw the fibroid on the scan they suggested an MRI, which I had done the end of May 2016 and Spain were happy that the fibroid would not interfere with pregnancy
Priming phase with IVF Spain started in July with 3 days of Letrozol, I then took the pill for 2 weeks in August. Once my period came, I then started 225UI Pergoveris. For egg collection in September, I had 6 eggs, 5 fertilised and 1 made it to blastocyst. The following day we had a catch up meeting with the clinic and they said that they wanted me to take a human growth hormone to hopefully improve the quality of the embryos. So for November egg collection (part of 2 round embryo banking process) I started taking Saizen(Somatropin), a human grown hormone daily from 10th October until collection. On 12th November I started Pergoveris 225IU and then we were back over in Spain the middle of November for collection around the 25th November. We had 7 eggs collected this time 6 fertilised and by day 5 we had 2 blastocysts and day 6 we had another blastocyst. So we had 4 embryos that were biopsied for PGS testing.
Unfortunately we found out just before Christmas that none of our embryos passed the testing and Spain suggest for us, as the issue is my egg quality, that Donor Egg would be our only option.
Also, just to mention, in November 2009 I did get pregnant but miscarried after 5-6 weeks.
AMH was 1.01ng/ml and the last sperm count on the second cycle was 2 mL, 6 mill/mL, 45% motility total. FACS 16%. SCSA 34%.
Any help or suggestions would be greatly appreciated.
I agree that a modest sized fibroid that does not encroach on the uterine cavity will not have an adversarial effect on IVF outcome. It obviously has nothing to do with the number or quality of your eggs/embryos. It sounds as if you have diminished ovarian reserve to boot. Almost certainly this really is likely to be a stimulation issue.
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”.
Women who (regardless of age) have DOR have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production of LH biological activity which can result in excessive LH-induced ovarian male hormone (predominantly testosterone) production which in turn can have a deleterious effect on egg/embryo “competency”.
While it is presently not possible by any means, to reverse the effect of DOR, certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can in my opinion, make matters worse. Similarly, the amount/dosage of certain fertility drugs that contain LH/hCG (e.g. Menopur) can have a negative effect on the development of the eggs of older women and those who have DOR and should be limited.I try to avoid using such protocols/regimes (especially) in women with DOR, favoring instead the use of the agonist/antagonist conversion protocol (A/ACP), a modified, long pituitary down-regulation regime, augmented by adding supplementary human growth hormone (HGH). I further recommend that such women be offered access to embryo banking of PGS (next generation gene sequencing/NGS)-selected normal blastocysts, the subsequent selective transfer of which by allowing them to capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” could significantly enhance the opportunity to achieve a viable pregnancy
Please visit my new Blog on this very site, https://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
• 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 Approach
• 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?
• Blastocyst Embryo Transfers should be the Standard of Care in IVF
• Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
• 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 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
• 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
• Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
• IVF Egg Donation: A Comprehensive Overview
I invite you to arrange to have a Skype or an in-person consultation with me to discuss your case in detail. If you are interested, please contact Julie Dahan, at:
Email: Julied@sherivf.com
OR
Phone: 702-533-2691
800-780-7437
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 desperately need your help. I’m a healthy 42 yr old with an AMH of 46.7 (very high) but I do not have PCOS.
I have had 5 cycles of IVF:
Cycle 1 Gonal F 300, orgalutran from day 5 and Ovidrel 250mcg trigger. 16 eggs collected 11 mature ICSI (9 fertilise). PGD (2 blastocysts tested 1 normal and 1 abnormal. So 1 frozen normal embryo but my fertility specialist tells me there is only 50% chance it will develop into a life baby.
Cycle 2. Gonal F 300 Orgalutran from day 5, Ovedril 250mcg trigger. 13 eggs, ICSi – 9 fertilise, 2 blastocysts and nil normal on PGD testing
Cycle 3 Gonal F 300 Orgalutran from day 5, Small second daily doses of LH towards end of cycle, Ovedril trigger 19 eggs collected IVF instead of ICSI 16 fertilise and 3 blastocysts biopsied (day 6), nil normal
Cycle 4. Gonal F 300 Orgalutran from day 5, Lucrein trigger 22 eggs collected IVF 18 fertilised 1 day 5 blast biopsied and 1 day 6- nil normal
Cycle 5 Gonal F 300 orgalutran from day 5, Lucrein trigger and it doesn’t work!!! Go to theatre- 7 follicles emptied from L every , all empty. Procedure stopped- LH tested and its 2! Dose of goal f given after coming out of theatre and overdid trigger that night and back to theatre 2 days later. 16 eggs from r ovary (left not touched though follicles were there), 15 fertilised, 12 day 3, nil able to be biopsied as didn’t reach blast stage!
Next cycle my Dr wants to used Menopur (FSE,LH,BHGC) 300IU and an ovedril trigger. Would really appreciate your opinion with regards what you think would be best for me medication wise! I’m really finding it hard to be positive and your help would be greatly appreciated. I look forward to hearing back from you about what i can do differently and why i have so many eggs and none of them are good (when statistically there should be some good ones amongst this lot).
Please help!
Best wishes, Ann-Maree
Age is definitely a factor that invariably affects egg quality. However, in your case I very respectfully do not agree with the protocol used for stimulation, also not the use of a 250mcg Ovidrel and/or an agonist trigger (see below). In my opinion your protocol needs to be reviewed carefully and then revised. You need alsom fo consider staggered IVF with embryo banking.
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”.
Women who (regardless of age) have DOR have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production of LH biological activity which can result in excessive LH-induced ovarian male hormone (predominantly testosterone) production which in turn can have a deleterious effect on egg/embryo “competency”.
While it is presently not possible by any means, to reverse the effect of DOR, certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can in my opinion, make matters worse. Similarly, the amount/dosage of certain fertility drugs that contain LH/hCG (e.g. Menopur) can have a negative effect on the development of the eggs of older women and those who have DOR and should be limited.I try to avoid using such protocols/regimes (especially) in women with DOR, favoring instead the use of the agonist/antagonist conversion protocol (A/ACP), a modified, long pituitary down-regulation regime, augmented by adding supplementary human growth hormone (HGH). I further recommend that such women be offered access to embryo banking of PGS (next generation gene sequencing/NGS)-selected normal blastocysts, the subsequent selective transfer of which by allowing them to capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” could significantly enhance the opportunity to achieve a viable pregnancy
Please visit my new Blog on this very site, https://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
• 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 Approach
• 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?
• Blastocyst Embryo Transfers should be the Standard of Care in IVF
• Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
• 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 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
• 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
• Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
• Preventing Severe Ovarian Hyperstimulation Syndrome (OHSS) with “Prolonged Coasting.
•“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?
I invite you to arrange to have a Skype or an in-person consultation with me to discuss your case in detail. If you are interested, please contact Julie Dahan, at:
Email: Julied@sherivf.com
OR
Phone: 702-533-2691
800-780-7437
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.