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 Doctor Sher,
I’ve got a question about a trigger shot. I read in your book that you don’t see any benefits of a half-dose hcg shot and I’d like to ask your advice on my case.
I’ve done a long protocol and after 11 days of stims I have 11 follicles from 13 to 21 mm. My estradiol level is 2100 pg/ml and progesteron 2.3 ng/ml. My dr told me to trigger with 5,00 iui of Pregnyl tonight. I told him I was a bit concerned about the low dose and he said I can use 10,000 iui if I’m worried. Do you think 10,000 iui will work fine? Are there any special circumstances which would require a 5,000 iui dose? Many thanks.
Not only do I not see any benefit in 5000U hCG, I think it compromises egg maturation and is a bad idea!
Geoff Sher
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Addendum:
“Triggering” Egg Maturation in IVF: Comparing urine-derived hCG, Recombinant DNA-hCG and GnRH-agonist:
Geoffrey Sher MD
Ideal egg development sets the scene for optimal egg maturation that occurs 36-42h prior to ovulation or egg retrieval. Without prior optimal egg development (ovogenesis), egg maturation will be dysfunctional and most eggs will be rendered “incompetent” and unable upon fertilization to propagate viable embryos. In IVF, optimal ovogenesis requires the selection and implementation of an individualized approach to controlled ovaria stimulation (COS). Thereupon, at the ideal time, maturational division of the egg’s chromosomes (i.e. meiosis) is “triggered” through the administration of hCG or an agonist such as Lupron, which induces an LH surge. The, dosage and timing of the “trigger shot” profoundly affects the efficiency of meiosis, the potential to yield “competent (euploid) mature (M2) eggs, and as such represents a rate limiting step in the IVF process .
“Triggering meiosis with Urine-derived hCG (Pregnyl/Profasi/Novarel) versus recombinant hCG (Ovidrel): Until quite recently, the standard method used to “trigger” egg maturation was through the administration of 10,000 units of hCGu. Subsequently,, a DNA recombinant form of hCGr (Ovidrel)was introduced and marketed in 250 mcg doses. But clinical experience strongly suggests that 250 mcg of Ovidrel is most likely not equivalent in biological potency to 10,000 units of hCG. It probably only has 50%-70%of the potency of a 10,000U dose of hCGu and as such might not be sufficient to fully promote meiosis, especially in cases where the woman has numerous follicles. For this reason, I firmly believe that when hCGr is selected as the “trigger shot” the dosage should best be doubled to 500 mcg at which dosage it will probably have an equivalent effect on promoting meiosis as would 10,000 units of hCGu. Failure to “trigger” with 10,000U hCGu or 500mcg hCGr, will in my opinion increase the likelihood of disorderly meiosis, “incompetent (aneuploid) eggs” and the risk of follicles not yielding eggs at egg retrieval (“empty follicles”). Having said this, it is my personal opinion that it is unnecessary to supplant hCGu with hCGr since the latter is considerably more expensive and is probably no more biopotent than the latter.
Some clinicians, when faced with a risk of OHSS developing will deliberately elect to reduce the dosage of hCG administered as a trigger in the hope that by doing so the risk of critical OHSS developing will be lowered. It is my opinion, that such an approach is not optimal because a low dose of hCG (e.g., 5000 units, hCGu or 25omcg hCGr) is likely inadequate to optimize the efficiency of meiosis particularly when it comes to cases such as this where there are numerous follicles. It has been suggested that the preferential use of an “agonist (Lupron) trigger” in women at risk of developing severe ovarian hyperstimulation syndrome could potentially reduce the risk of the condition becoming critical and thereby placing the woman at risk of developing life-endangering complications. It is with this in mind that many RE’s prefer to trigger meiosis by way of an “agonist (Lupron) trigger rather than through the use of hCG. The agonist promptly causes the woman’s pituitary gland to expunge a large amount of LH over a short period of time and it is this LH “surge” that triggers meiosis. The problem with using this approach, in my opinion, is that it is hard to predict how much LH will be released in by the pituitary gland. For this reason, I personally prefer to use hCGu for the trigger, even in cases of ovarian hyperstimulation hyperstimulated, with one important proviso…that being that is she underwent “prolonged coasting” in order to reduce the risk of critical OHSS, prior to the 10,000 unit hCGu “ trigger”.
The timing of the “trigger shot “to initiate meiosis: This should coincide with the majority of ovarian follicles being >15 mm in mean diameter with several follicles having reached 18-22 mm. Follicles of larger than 22 mm will usually harbor overdeveloped eggs which in turn will usually fail to produce good quality eggs. Conversely, follicles less than 15 mm will usually harbor underdeveloped eggs that are more likely to be aneuploid and incompetent following the “trigger”.
Dr. Sher, I am 35 years old and have a 21-month old daughter from IVF in 2015. That cycle I produced only 4 follicles, 2 retrieved and fertilized and both transferred on day 3. Most recently, I have done 2 min-IVF cycles and a protocol that is the same as the one used to conceive my daughter and have produced only 1 follicle each time. I have low AMH and am a pretty poor responder. The protocol used for the latest A/A protocol used is 225 Gonal-F and 225 Menopur with a half-dose Ganirelix per day until HCG trigger. Went to retrieval with this last cycle…but, my estrogen was lower (138 day of trigger) than it was even with the 2 mini-IVF cycles (191 and 210, respectively) so I wasn’t super confident in it working but went ahead anyways. Previous abdominal surgeries have left me with a lot of scar tissue but most recent HSG has showed them to be open, apparently. I’ve read some of your posts about Mini-IVF not being ideal for those in my situation but that is what my Dr. has recommended I do if I do want to try again (and not use donor eggs or embryos) because I am only producing one follicle anyways. I am not ready to give up on my eggs yet and I am looking for another opinion or protocol that I may have success with? I am also not looking to keep traveling down this road fruitlessly either though…so, your input and honesty is much appreciated.
Hello!
I am 34 with hypothalamic ammenorhea and Crohns Disease. Very low LH, day 3 FSH around 5, AMH of 2.27, thin lining. I have a son from an IUI cycle using Menopur, but have had 2 chemical pregnancies from IUIs since. (Total of 4 IUIs – 1st successful, 2nd chemical, 3rd negative, 4th chemical). I have also done 3 IVF cycles in between the 1st and 2nd IUIs but my embryos never made it to blasts. Always had a great response to stims, almost perfect fertilization, but by day 3 things always looked bad and by day 5 we were left with nothing. (Did antagonist protocol, and also tried micro dose lupron.). Seems like I have better luck w IUIs. ????
My question is… moving forward, do you feel its smarter to continue with IUIs or do we try another cycle of IVF ?? and possibly do genetic testing, if we have any blasts to test. I have never had immune testing done, however I am taking low dose prednisone already to help control my Crohns. I also take 6mp, an immunomodulator for Crohns maintenance.
Any advice would be greatly appreciated, as I dont know what to do moving forward. I am getting pregnant, just not getting the right egg…. 🙁
I would favor IVF, but the protocol used for ovarian stimulation needs to be critically reviewed. In addition, you may need treatment with vaginal Viagra to try and improve endometrial thickening.
Whenever a patient fails to achieve a viable pregnancy following embryo transfer (ET), the first question asked is why! Was it simply due to, bad luck?, How likely is the failure to recur in future attempts and what can be done differently, to avoid it happening next time?.
It is an indisputable fact that any IVF procedure is at least as likely to fail as it is to succeed. Thus when it comes to outcome, luck is an undeniable factor. Notwithstanding, it is incumbent upon the treating physician to carefully consider and address the causes of IVF failure before proceeding to another attempt:
1.Age: The chance of a woman under 35Y of age having a baby per embryo transfer is about 35-40%. From there it declines progressively to under 5% by the time she reaches her mid-forties. This is largely due to declining chromosomal integrity of the eggs with advancing age…”a wear and tear effect” on eggs that are in the ovaries from birth.
2.Embryo Quality/”competency (capable of propagating a viable pregnancy)”. As stated, the woman’s age plays a big role in determining egg/embryo quality/”competency”. This having been said, aside from age the protocol used for controlled ovarian stimulation (COS) is the next most important factor. It is especially important when it comes to older women, and women with diminished ovarian reserve (DOR) where it becomes essential to be aggressive, and to customize and individualize the ovarian stimulation protocol.
We used to believe that the uterine environment is more beneficial to embryo development than is the incubator/petri dish and that accordingly, the earlier on in development that embryos are transferred to the uterus, the better. To achieve this goal, we used to select embryos for transfer based upon their day two or microscopic appearance (“grade”). But we have since learned that the further an embryo has advanced in its development, the more likely it is to be “competent” and that embryos failing to reach the expanded blastocyst stage within 5-6 days of being fertilized are almost invariably “incompetent” and are unworthy of being transferred. Moreover, the introduction into clinical practice about a decade ago, (by Levent Keskintepe PhD and myself) of Preimplantation Genetic Sampling (PGS), which assesses for the presence of all the embryos chromosomes (complete chromosomal karyotyping), provides another tool by which to select the most “competent” embryos for transfer. This methodology has selective benefit when it comes to older women, women with DOR, cases of unexplained repeated IVF failure and women who experience recurrent pregnancy loss (RPL).
3.The number of the embryos transferred: Most patients believe that the more embryos transferred the greater the chance of success. To some extent this might be true, but if the problem lies with the use of a suboptimal COS protocol, transferring more embryos at a time won’t improve the chance of success. Nor will the transfer of a greater number of embryos solve an underlying embryo implantation dysfunction (anatomical molecular or immunologic).Moreover, the transfer of multiple embryos, should they implant, can and all too often does result in triplets or greater (high order multiples) which increases the incidence of maternal pregnancy-induced complications and of premature delivery with its serious risks to the newborn. It is for this reason that I rarely recommend the transfer of more than 2 embryos at a time and am moving in the direction of advising single embryo transfers …especially when it comes to transferring embryos derived through the fertilization of eggs from young women.
4.Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:
a.A“ thin uterine lining”
b.A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
c.Immunologic implantation dysfunction (IID)
d.Endocrine/molecular endometrial receptivity issues
Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).
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.
•Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
•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?
•Blastocyst Embryo Transfers should be the Standard of Care in IVF
•IVF: How Many Attempts should be considered before Stopping?
•“Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
•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)
•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!
•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:
•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
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
Hi Dr. Sher,
I went for my 6 week two day ultrasound today. We saw and heard a heartbeat of 116. There was a gestational sac that measured normally. My RE didn’t see the yolk sac. He said it must be hidden. Is that normal and should I be worried?
Dr Sher,
I am 16dp5dt of a good quality blast. I got a positive beta on 9dp5dt of 241 and it perfectly doubled on 11dp5dt to 483. My RE did not want to test further after good results; however after having a MMC at 8 weeks after seeing a heartbeat with my last FET, I wanted to check the beta again for reassurance. We repeated yesterday at 15dp5dt and it was 1363, a 68% increase and 64 hour doubling from Monday. So now instead of comfort I am more anxious. My RE and nurse reassure me that the rise is normal and are still optimistic for a good outcome; but I can’t help feeling worried. Do you agree with them that a viable pregnancy is still a strong possibility? Would repeating beta be helpful or just more confusing since it tends to start slowing soon? Thank you so much for your help.
It is hard to be sure. Needless to say one anticipates the beta hCG level to double every 48 hours or so. But sometimes it does not do so and the pregnancy still continues unabated. This is at times due to starting of with 2 embryos implanting whereupon one succumbs while the other survives causing a dip in the hCG level. Of course it can sometimes mean the pregnancy is failing. Only time will tell. Another beta hCG test 48h after the last one would offer more insight. It should double up.
Good luck and G-d bless!
Please keep me in the loop[!
Geoff Sher
I have severe to moderate ohss and spent a couple of weeks at the hospital. I got taped 3 times to drain fluid via my abdomen, twice with a pigtail drain that stayed in for a couple of days – with draining 4 l per day max. It was scary and exhausting to stay at the hospital. Now I’m at home with regular check ups at the hospital.
The last time I got drained was 4 days ago with 4 l being drained. I could go home afterwards. But it seems according to ultrasound I still have 3-4 l in me. I’m week 11+5 pregnant now. The hospital says my blood count from this week monday is good and the OHSS is not visible in it anymore.
I was wondering how the fluid in my stomach is going to go away and if at all. Does my body resolve the water by itself or do I need to get it drained one last time? When do the symptoms go away and when can I start having an “ordinary” pregnancy? Thanks so much. All the best, Ada
It will resolve and go away. This is a time limiting condition that in the 1st trimester is aggravated by the rising hCG of pregnancy.
Congratulations on your pregnancy. Sorry you had to go through this ordeal.