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 again Dr. Sher,
I was able to talk to me RE about moving forward with another cycle after both cycles ended in all my embroyrs arresseting. He now want to put me on a down regulation protocol. In your opinion is that one that is seen or shown to work in women of my age of 40 and had embryos arrest?
I really do value your opinions.
Dear Dr Sher,
Does metformin raise or in any way affect FSH in non PCOS and non diabetic patients? I was put on it for endometriosis and I’m wondering if it’s what made my FSH rise. Thank you
I do not think it will affect ovarian reserve, but I do question why you were put on it for endometriosis!
Geoff Sher
I have my last periods on 15th sep 2017. I did beta hcg test on 23 oct 2017 which shows 5 weeks pregnancy . Ultimately went for ultrasound on 1 nov 2017 shows 5 weeks and 1 day pregnancy . However , as per calculations it would be 6 weeks and 5 days . Should i need to worry about?? Or it happens?? Any diet for growth
Sometimes the assessment is less than accurate. Repeat the ultrasound in 1 week!
Good luck!
Geoff Sher
Hello Dr. Sher,
I’ve read your blog post on using sildenafil to thicken lining. You indicated that the pills were compounded into vaginal suppositories. Does the compounding into suppositories help with absorption, versus just inserting the pill in it’s original form?
I’m hoping to use sildenafil to attempt to thicken my lining, but the doctor didn’t indicate that they should be compounded.
Yes Leanna, this facilitates absorption.
Geoff Sher
Hi Dr Sher,
Thank you for taking the time to answer my questions! I am 29 years old (partner 28 years old) and trying to conceive my 2nd via IVF. (After 4 clomid cycles and 2 IUIs with Menopur failed.) I have been diagnosed with lean PCOS with irregular periods of >50 days after polycystic ovaries were sighted on ultrasound and with results from my day 2 LH/FSH profile since I was 19.
My protocol was as follows:
Day 3-6: Cetrotide
Day 6 – Day 10: Gonal F (112.5iu)
Day 11 – Day 15: Gonal F (150iu) + Cetrotide
Day 15: Trigger Shot of Pregnyl 10,000 units
Day 17: Egg retrieval
I had a Day 5 transfer with a beautiful triple stripe uterine lining and the transfer went very smoothly.
Despite my PCOS diagnosis and a antral follicle count of 54 – I am confused as to why only 14 eggs were retrieved from 20 follicles and out of those only 9 were mature. 6 successfully fertilized with ICSI. I had one blastocyst with grading CB transferred and that unfortunately didn’t take. None of my other 5 embryos made it to freeze as I was told by the embryologist that they were of low quality and will not survive the freeze/thaw.
Despite my PCOS, my 1st child was conceived naturally with my current partner. I also have naturally conceived once prior to my first child with another partner. I have no known endometriosis, Immune/Thyroid issues, uterine abnormalities (other than a accurate uterus). What can be the possible reason for my IVF failure in this case? Could Metformin possibly improve my outcome and is ICSI better than natural fertilization in my case?
Thank you!
I think your reduced yield of eggs is likely the result of the protocol used for ovarian stimulation. PCOS women tend to be more vulnerable (when it comes to egg quality and follicle development) than are their non-PCOS counterparts. As such a very individualized approach needs to be taken to controlled ovarian stimulation (COS).
PCOS is a common hormonal system disorder among women affecting between 5% and 10% of women of reproductive age worldwide. Women with PCOS may have enlarged ovaries that contain multiple small collections of fluid (subcapsular microcysts) that are arranged like a “string of pearls” immediately below the ovarian surface (capsule).interspersed by an overgrowth of ovarian connective tissue (stroma). The condition is characterized by abnormal ovarian function (irregular or absent periods, abnormal or absent ovulation and infertility, androgenicity (increased body hair or hirsutism, acne) and increased body weight –body mass index or BMI.
Women with PCOS are at increased risk that ovarian stimulation with gonadotropins will result in the, of development of severe ovarian hyperstimulation syndrome (OHSS), a life-endangering condition that is often accompanied by a profound reduction in egg quality. Such eggs will upon fertilization often yield an inordinately high percentage of “incompetent” embryos which have a reduced potential to propagate viable pregnancies.
Concern and even fear that their PCOS patients will develop of OHSS often leads the treating RE to take measures aimed at reducing these risks. In this regard, it is my opinion that the most important consideration is the selection and proper implementation of an individualized or customized ovarian stimulation protocol.
What follows is a critical assessment of methods to prevent OHSS and/or limit its severity:
1. PROLONGED COASTING…my preferred approach: My preferred approach is to use a long pituitary down-regulation protocol coming off the BCP which during the last 3 days is overlapped with the agonist, Lupron/Buserelin/Superfact. The BCP is intended to lower LH and thereby reduce stromal activation (hyperthecosis) in the hope of controlling LH-induced ovarian androgen (predominantly, testosterone) production and release. I then stimulate my PCOS patients using a low dosage of recombinant FSH-(FSHr) such as Follistim/Gonal-F/Puregon. On the 3rd day of such stimulation a smidgeon of LH/hCG (Luveris/Menopur) is added. Thereupon, starting on day 7 of ovarian stimulation, I perform serial blood estradiol (E2) and ultrasound follicle assessments, watching for the number and size of the follicles and the blood estradiol concentration [E2]. 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 concentration daily. The [E2] will almost invariably increase for a few days. I closely monitor the [E2] as it rises, plateaus and then begins to decline. As soon as the [E2] drops below 2500pg/ml (and not before then), I administer a “trigger” shot of 10,000U Profasi/ Novarel/Pregnyl or 500mcg Ovidrel/Ovitrel. This is followed by an egg retrieval, performed 36 hours later. Fertilization is accomplished using intracytoplasmic sperm injection (ICSI) because “coasted” eggs usually have little or no cumulus oophoris enveloping them 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 the blastocyst stage (up to day 5- 6 days) and thereupon are either vitrified and preserved for subsequent transfer in later hormone replacement cycles or (up to 2) blastocysts are transferred to the uterus, transvaginally under transabdominal ultrasound guidance. The success of this approach depends on precise timing of the initiation and conclusion of “prolonged coasting”. If started too early, follicle growth will arrest and the cycle will be lost. If commenced too late, too many follicles will be post-mature/cystic (>22mm) and as such will usually harbor abnormal or dysmature eggs. Use of “Coasting” almost always prevents the development of severe OHSS, optimizes egg/embryo quality and avoids unnecessary cycle cancellation. If correctly implemented, the worst you will encounter is moderate OHSS and this too is relatively uncommon.
2. MULTIPLE FOLLICLE ASPIRATION: In some cases, in spite of best effort, you inadvertently find mean follicle size to exceed 16mm, thereby leaving too little time to implement “coasting”. On other occasions, “coasting” fails to effectively lower the [E2} below 2,500pg/ml within 3 days. In such case the number of developing follicles can effectively and drastically reduced (culled) through selective transvaginal aspiration prior to initiating the “trigger” with
10,000U hCG. This will almost invariably be accompanied by a rapid and significant drop in the plasma estradiol concentration along with a drastic reduction in the risk of OHSS occurring without significantly compromising egg/embryo quality. Upon completing surgical follicular reduction, the surviving follicles can be allowed to continue their full development, at which point the hCG “trigger” can be implemented. The drawback associated with this approach is that it unfortunately interjects an additional surgical intervention into an already complex and stressful situation.
3. EMBRYO FREEZING AND DEFERMENT OF EMBRYO TRANSFEDR (ET): OHSS is always a self-limiting condition. In the absence of continued exposure to hCG, symptoms and signs as well as the risk of severe complications will ultimately abate. Thus, in the absence of pregnancy, all symptoms, signs and risks associated with OHSS will disappear within about 10-14 days of the hCG trigger. Conversely, since early pregnancy is always accompanied by a rapid and progressive rise in hCG , the severity of OHSS will increase until about the 9th or tenth gestational week whereupon a transition from ovarian to placental hormonal dominance occurs, the severity of OHSS rapidly diminishes and the patient will be out of risk. Accordingly, in cases where in spite of best effort to prevent OHSS, the woman develops symptoms and signs of progressive overstimulation prior to planned ET, all the blastocysts should be vitrified and cryostored for FET in a subsequent hormone replacement cycle. In this way women with OHSS can be spared the risk of the condition spiraling out of control.
4. TRIGGERING WITH LOW DOISAGE hCG; Because of the fact that hCG augments the development of OHSS, many RE’s prefer to use a reduced 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) in the hope that by doing so the risk of critical OHSS developing will be lowered. While this indeed might be true, it is my opinion, that the reduced dosage is usually insufficient to optimize the efficiency of egg meiosis, especially when there are so many follicles present. Thus, while the use of a reduced “trigger” dosage of hCG might well reduce the risk and occurrence of OHSS-related life-endangering complications, the price to be paid is reduced egg quality/”competency”.
5. “TRIGGERING” WITH A GnRH AGONIST (E.G. “LUPRON/BUSERELIN): More recently, an increasing number of RE’s are triggering egg maturation by way of injecting an agonist (Lupron/Buserelin/Superfact) to initiate the patient’s own pituitary gland to release a large amount of LH. 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.
In my opinion the best way to approach ovarian stimulation for IVF in women with PCOS, is through the use of a low dosage, FSH-dominant Long ovarian down-regulation protocol, done in readiness for “prolonged coasting” (see below) and “triggering” egg maturation with a full 10,00U dosage of hCG or (no less than) 500mcg of recombinant hCG (Ovidrel)….see below is If this is implemented appropriately, with proper timing, egg/embryo quality can be optimized.
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.
· Egg Maturation in IVF: How Egg “Immaturity”, “Post-maturity” and “Dysmaturity” Influence IVF Outcome:
· Commonly Asked Question in IVF: “Why Did so Few of my Eggs Fertilize and, so Many Fail to Reach Blastocyst?”
· 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?
· Taking A Fresh Look at Ovarian Hyperstimulation Syndrome (OHSS), its Presentation, Prevention and Management
· Preventing Severe Ovarian Hyperstimulation Syndrome (OHSS) with “Prolonged Coasting”
· 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?
If you are interested in seeking my advice or services, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com You can also apply online at http://www.SherIVF.com .
*FYI
The 4th edition of my newest book ,”In Vitro Fertilization, the ART of Making Babies” is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Geoffrey Sher MD