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. Sher,
My husband and I are fifty. He has a history of testicular cancer. We are in the process of having a second round of IVF. I have a problem with thin endometrial lining. In the previous IVF attempt, we achieved only 7mm. I disparately want to increase the possibility of having a more receptive lining with the use of vaginal Viagra. Can you please give me information on how to obtain this revolutionary product. Is it only available to your clients? I am willing to submit my data for any research that may advance knowledge in this area.
Thank in advance for your help.
Have your RE contact Robert Makhane at MDRX Pharmacy in Southern California for more information.
Geoff Sher
I have had a natural modified cycle. At the first consultation I was told I had an antral ovarian reserve of 6, a cyst on my left ovary and an AMH of 5.9. It was thought that I would have a poor response to stimulation due to my age 43. My second scan was a totally different outcome. I was told that I had a cyst on my right side, but not on the left and it was likely that my antral follicles were in fact ? Residue fluid filled sacs secondary to the cyst. On the left ovary was one follicle, which measured 16mm. I was told to start sc menapor 150mg and sc ceratide 0.25. On my third scan the follicle had grown to 19mm. Egg collection, which was horrendously painfull, yielded no egg. So was this in fact just another ovarian cyst? and why was it so painful? I have a follow up in 2 weeks, but as yet no explanation as to what happened. Where do I go from here. Does this mean that I have no ovarian reserve at all?
Hi Dr. Sher I have a couple of questions: First was dx at the age of 13 with PCOS I have all the hair growth and extremely high testosteron levels. In 2013 I was placed on ortho- tricycline after a few months of the cycles of pills I developed a blood clot in my leg, so of course I had to stop the birth control. My periods are absent. I went to see a specialist a couple and we did 3 rounds of clomid with no success after each round of Clomid I would have an ultrasound to see if there was any follicles, again there was no follicles present. I am currently not on anything and have not had a period for almost 2 months now. What would be your suggestions on the next step..
Thank you for your time and God bless
Hi Bethany,
I would like to help you but to attempt to do so would require access to much more information.
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 book,”In Vitro Fertilization, the ART of Making Babies” is now available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Geoffrey Sher MD
Hi Dr Sher,
I had one child fine and then had 3 first trimester miscarriages. I was told the miscarriages were due to antipaternal cytotoxic antibodies and had lymphocyte immune therapy. I did go on to have a gorgeous boy 9 months later but both myself and my son have never been well. My health declined 6 months into the pregnancy and has not recovered. My son has been similarly unwell. The main difficulties are extreme weakness and fatigue with an over reaction to foods, viruses, etc. It has led to a diagnosis of M.E.
Can I ask whether there are any known risks to the mother or baby for having LIT? Or whether the risks have been researched? And it is possible to reverse any effects from having LIT?
I am asking because it seems doctors I speak to have no knowledge or understanding of the treatment I had and so they cannot commit on any potential harms. Thank you so much for any help you can give.
It is not impossible that the LIT might have caused these problems…but it is not likely. Discuss with an immunologist!
Good luck!
Geoff Sher
Hi Dr Sher,
Thanks so much for this forum. You are a Godsend.
I have done two prior IVF cycles with Gonal f (300 and 325 units), collecting 15 and 17 eggs each time.
A high proportion successfully of these fertilised (ICSI was used). Some arrested. We also did PGT and about half where chromosomally normal. Several each time made it to Day 5 Blastocysts. Two were transferred during the first and three were transferred during the second cycle (fresh). During the second cycle, I was treated with 20mg Prednisone and had IVIG a week prior to the transfer, as I have a history of auto-immune conditions, and testsed positive for elevated NKCs in blood tests.
Neither of these cycles resulted in successful implantation. I have PCOS (I take metformin) and potential immune-related issues. For the current cycle I am doing freeze all and hopefully will do a transfer in two months time, in the hope that the endometrium will settle down and be more receptive.
I am currently on CD13 of a Gonal f cycle (Day 12 of Drugs). The FS reduced my level of Gonal f to 275, with a view to having a slightly later collection (on the previous cycles I was collected on about CD12). This appeared to not work, as my response was not as good. On Day 8 of meds, my dose was increased to 350, and on Day 10 my dose was increased to 400 (My E2 was 3000 on Day 10, and I had lots of follicles, max size 14mm).
Today on Day 12, my largest follicle is 16mm, with 10+ follicles on each ovary, ranging from about 6-16mm.
I had been hoping for a follicle at 18mm today, with a view to potentially doing a collection on Day 14 of Meds. Unfortunately as they don’t seem to be growing fast enough, I will either have to have a collection on Day 17 of Meds (CD 18) or they may cancel my cycle. (The darn hospital doesn’t do collections on the weekend, so CD16 and 17 are not available)
I don’t want to cancel the cycle obviously, but I don’t want the long stimulation cycle to damage the quality of the eggs?
Also, if this length of cycle is actually OK, I don’t want my FS to unnecessarily cancel the cycle, as I do have lots of follicles growing.
My questions:
Will my follicles be too large/old by CD 18 (Meds Day 17)?
(largest follicle would potentially be about 24-26mm by then)
Is there anything I can do to maximise the growth of the smaller follicles? (protein??)
I will try and discuss “coasting” with my specialist, but he doesn’t seem to be across many new approaches.
And one last question. I have sucessfully been triggered with 1. 10,000 units of hcg, and 2. a dose of Ovidrel, for my last two cycles respectively. This FS (a new one) seems to want to use Decapeptyl (which I believe is GNRHa). I’m not convinced that my pituitary responds well to my body telling it to release LH (from seeing what happens in my natural cycles), so I’m a bit scared that this would be a bad trigger for me to maximise maturation. Is this a legitimate fear??
Many thanks in advance for any guidance you can provide.
Thank you so much.
Kind Regards,
Renee.
1. Will my follicles be too large/old by CD 18 (Meds Day 17)?
(largest follicle would potentially be about 24-26mm by then)
A: Follicles larger than n22mm usually do not harbor good quality eggs.
2. Is there anything I can do to maximise the growth of the smaller follicles? (protein??)
I will try and discuss “coasting” with my specialist, but he doesn’t seem to be across many new approaches.
A: I am afraid nothing can selectively boos smaller follicles and, “coasting” has no value unless you are hyperstimulating.
3.I have sucessfully been triggered with 1. 10,000 units of hcg, and 2. a dose of Ovidrel, for my last two cycles respectively. This FS (a new one) seems to want to use Decapeptyl (which I believe is GNRHa). I’m not convinced that my pituitary responds well to my body telling it to release LH (from seeing what happens in my natural cycles), so I’m a bit scared that this would be a bad trigger for me to maximise maturation. Is this a legitimate fear??
A:
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 GnRH-agonist such as Lupron/Decapeptyl/Superfact, 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/Decapeptyl/Superfact) 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 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”.
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.