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 Dr .Sher
Because of microadenoma my prolactin level is high . I took
Carbergoline for 3 years.And my prolactin level is between 60 to 100 ng / ml Can I start the IVF cycle with this level of prolactin
You really need to see your neurologist. The prolactin level is quite high and perhaps the prolactinoma needs to be surgically addressed first.
Geoff Sher
Hi Dr Sher
I have been in touch with you before but have some further questions since having a review with my fertility clinic after my unsuccessful IVF cycle. I’m 43 years old and I had 4 follicles, one was a large cyst, and had 1 egg collected after 7 days of 350IU/L Gonal F injections. The egg fertilised (not via ICSI) and made it to blastocyst stage but I got a negative hcg test 10 days after a 5 day transfer. My clinic want to stay with this same protocol for my next cycle which is due to commence soon.
Having read the information you’ve provided here I want some things to change with my upcoming cycle and would appreciate your thoughts Dr Sher.
I took DHEA 75mg daily supplements for 3 months, before and during my IVF cycle, might this have negatively impacted my stimulation reaction and success? Should I stop taking DHEA altogether (I have dropped my dosage to 25mg daily since my unsuccessful cycle)? Should I have a test done to see if I need DHEA supplementation?
Would changing to ICSI be of benefit to me? My partner is also in his 40’s and all sperm analysis tests have come back great. This would be an extra cost as my clinic do not do ICSI as standard.
Should I take the higher dose of Ovitrelle for my trigger shot before egg collection? 500 instead of 250. I feel this would be beneficial for me and my clinic would be supportive of this change, even though they feel it’s unnecessary
My clinic gave me another shot of 250 Ovitrelle on the day of Embryo Transfer, and I had no other hormonal support during my 2 week wait. Should I opt for progesterone support during this time as well as or instead of the Ovitrelle?
I also took Norethisterone as my down regulation in my last cycle. I have short cycles, ranging from 16 to 27days with no consistency. My clinic started me on Norethisterone on Day 16 of my cycle rather than the normal Day 21, could this have negatively impacted my cycle or does it not really matter when this drug is started? Should my ovulation be monitored for my next cycle so Norethisterone can be started 7 days after ovulation?
I also had low blood pressure at my Egg Retrieval appointment, and also fainted 6 days after embryo transfer. Since my cycle ended my own doctor has noted low BP also. Is this something that needs special consideration for my next cycle?
I am feeling disappointed that my clinic haven’t suggested any changes, and so I would like to change some things to help me feel more positively about this upcoming cycle
Many thanks for any advice
A
1. I took DHEA 75mg daily supplements for 3 months, before and during my IVF cycle, might this have negatively impacted my stimulation reaction and success? Should I stop taking DHEA altogether (I have dropped my dosage to 25mg daily since my unsuccessful cycle)? Should I have a test done to see if I need DHEA supplementation?
A: Dehydroepiandrosterone (DHEA), is steroid hormone produced by the adrenal glands and ovary. It is involved in producing the male hormones, androstenedione testosterone and also estrogen. DHEA blood levels tend to decline naturally with age.
Under the effect if luteinizing hormone (LH), DHEA is metabolized to testosterone in ovarian connective tissue (theca/stroma). Thereupon the testosterone is transported to the granulosa cells that form the innermost layer of the ovarian follicles where, under the influence of follicle stimulating hormone (FSH)-induced desmolase and aromatase enzymatic activity the testosterone is converted to estradiol. As this happens, granulosa cells multiply, follicle fluid volume increases along with estrogen output and egg development is promoted.
It is recognition of the essential/indispensable role that male hormones (mainly testosterone) play in follicle and egg development that prompted the belief that by giving DHEA and boosting ovarian testosterone production might benefit follicle/egg development. This belief was given some credence by an Israeli study that in 2010 reported on improved fertility when a group of infertile women were given the administration of 75mg of oral DHEA for 5 months. However, this study was seriously flawed by the fact that it did not separate out women who had diminished ovarian reserve, older women and those with PCOS, all of whom have increased LH-induced production of testosterone. In fact, we recently completed a study (currently being processed for publication) where we conclusively showed that when follicular fluid testosterone levels exceeded a certain threshold, egg quality was seriously prejudiced as evidenced by a marked increase in the incidence of egg chromosomal defects (aneuploidy).
Consider the following: Ovarian testosterone is needed for follicular development. However, the amount required is small. Too much ovarian testosterone spills over into the follicular fluid and has a deleterious effect on egg/follicle development. Some women (women with diminished ovarian reserve –DOR, older women and those with polycystic ovarian syndrome-PCOS) who tend to have increased LH biological activity, already over-produce testosterone. To such women, the administration of DHEA to such women, by “adding fuel to the fire” can be decidedly prejudicial, in my opinion. Young women with normal ovarian reserve do not over produce LH-induced ovarian testosterone, and are thus probably not at significant risk from DHEA supplementation. It is noteworthy that to date, none of the studies that suggest a benefit from DHEA therapy have differentiated between young healthy normal women with normal ovarian reserve on the one hand and older women, those with DOR and women with PCOS on the other hand.
In Some countries DHEA treatment requires a medical prescription and medical supervision. Not so in the U.S.A where it can be bought over the counter. Since DHEA is involved in sex hormone production, including testosterone and estrogen, individuals with malignant conditions that may be hormone dependent (certain types of breast cancer or testicular cancer) should not receive DHEA supplementation. Also, if overdosed with DHEA some “sensitive women” might so increase their blood concentrations of testosterone that they develop increased aggressive tendencies or male characteristics such as hirsuites (increased hair growth) and a deepening voice. DHEA can also interact other medications, such as barbiturates, corticosteroids, insulin and with other oral diabetic medications.
BUT the strongest argument against the use of routine DHEA supplementation is the potential risk of compromising egg quality in certain categories of women and since there is presently no convincing evidence of any benefit, why take the risk in using it on anyone.
Finally, for those who in spite of the above, still feel compelled to take DHEA, the best advice I can give is to consult their health care providers before starting the process.
Addendum: One potential advantage of DHEA therapy if used appropriately came from a study conducted by Washington University School of Medicine in St. Louis, MI and reported in the November 2004 issue of the “Journal of the American Medical Association” which showed that judicious (selective) administration of 50mg DHEA daily for 6 months resulted in a significant reduction of abdominal fat and blood insulin in elderly women.
2. Would changing to ICSI be of benefit to me? My partner is also in his 40’s and all sperm analysis tests have come back great. This would be an extra cost as my clinic do not do ICSI as standard.
A: I think that is a good idea
C. Should I take the higher dose of Ovitrelle for my trigger shot before egg collection? 500 instead of 250. I feel this would be beneficial for me and my clinic would be supportive of this change, even though they feel it’s unnecessary
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 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 (hCGu-Pregnyl/Profasi/Novarel) versus recombinant hCG-(hCGr-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 250mcg 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”.
4. My clinic gave me another shot of 250 Ovitrelle on the day of Embryo Transfer, and I had no other hormonal support during my 2 week wait. Should I opt for progesterone support during this time as well as or instead of the Ovitrelle?
A: I would not use hCGr (Ovitrelle) at this stage. IT confounds the ability to detect implantation through hCG testing…early on and in my opinion ios of no benefit.
5. I also took Norethisterone as my down regulation in my last cycle. I have short cycles, ranging from 16 to 27days with no consistency. My clinic started me on Norethisterone on Day 16 of my cycle rather than the normal Day 21, could this have negatively impacted my cycle or does it not really matter when this drug is started? Should my ovulation be monitored for my next cycle so Norethisterone can be started 7 days after ovulation?
A. Northisterone is a nor-testosterone progestin,. I do not prescribe it
6. I also had low blood pressure at my Egg Retrieval appointment, and also fainted 6 days after embryo transfer. Since my cycle ended my own doctor has noted low BP also. Is this something that needs special consideration for my next cycle?
A: No
Good luck!
Geoff Sher (702-533-2691)
Hi Dr. Sher,
I am going to try a timed intercourse taking 225 menopur and a 10,0000 gonassi trigger.
I have two questions:
Is the trigger necessary? If I am not taking anything to suppress ovulation, could I not just take the menopur until my body releases the eggs on its own?
I’m 39…with a string of failed ivfs. How many dominant follicles would you proceed with for a woman my age who has failed over six cycles? My doctor said he would advise cancelling if I get over 3 dominant follicles. I don’t understand why as the likelihood of any of them progressing at my age and with my ivf history is low.
1. Is the trigger necessary? If I am not taking anything to suppress ovulation, could I not just take the menopur until my body releases the eggs on its own?
A: The trigger is very necessary or you probably won’t ovulate.
2. I’m 39…with a string of failed ivfs. How many dominant follicles would you proceed with for a woman my age who has failed over six cycles? My doctor said he would advise cancelling if I get over 3 dominant follicles. I don’t understand why as the likelihood of any of them progressing at my age and with my ivf history is low.
A: Sorry, but I do not understand this reasoning.
Geoff Sher
According to lmp I should be 5 weeks 3 days.
At 3w6d my hcg was 86
4w1d it was 190
At 5w it was 800. So it slowed down. Then on 5w2d it was 975.
5w3d it was 956. They told me that I will be having a miscarriage. I am still having all pregnancy symptoms. No cramping or bleeding at all. My progesterone was “great” according to them. I’m so confused.
Wait a week and do an ultrasound.
Geoff Sher
Is Lupron necessary for Frozen embryo transplant? What alternatives?
It is advisable but not essential.
Geoff Sher