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.
I started 10u lupron 7dpo when progesterone was 15 and estrogen was 145.
Today is 12dpo and my period is due tomorrow, but today’s bloods show progesterone is 14 and estrogen is 206.
I’ve been on lupron for 6 days and I usually get a period exactly 7 days after I start lupron, but it doesn’t look like I will get a period tomorrow with that progesterone level.
I know you’re not a fan of being on lupron for a long time as it can be suppressive.
Do my levels suggest a cyst or does it just look like a longer than usual luteal phase? Is it ok to be on lupron for another 5 or so days? I will be dropping lupron down to 5iu when I start a period but worried 10-12 days on lupron to down regulate is too long. Do you generally get your patients to cancel when it looks like they’re going to be on lupron for more than 7-10 days while down regulating?
I would do an US to look for an ovarian cyst and yes, if necessary, I would continue a few more days of Lupron.
Geoff Sher
Hello Dr. Sher,
I’m 29 yr married to a 36yr man for six years. We never have children and I never conceived. We’ve done all blood work and physical exams look nomal. I’m taking leveothyroxine for alomst 4 years now due to high borderline TSH (was 4 mlU/L first time checked). I have regular cycle 28-35 days. Husband SA ups and downs, count 3- 36 million, motility fine around 45-65% but not good morphology. His normal morphology between 2-4%. He was diagnosed with varcocele grade I &II but no surgery done. We’ve done two unsuccessful ivf and below are the details:
Ivf #1 On Jan 2017 when I was 28 yr old.
Protocol: gonal f, menopur, ganirelix, and HCG. I started taking contraceptive pills a month before the start day as part of the protocol.
Stim days are 13
First 3 days 225 gonal f, and 1 menopur, then douoled gonal f to 300 for 5 days and same dose of menopur. Then reduced gonal f to 200 for 3 days and same dose of menopur last two days reduced gonal f to 75 and doupled menopur to 4. 10,000 hcg given on day 13.
E2
14 eggs retrieved, 7 mature, 6 fertilized with icsi.
Husband’s sample on day of eggs retrieval: concentration was 9.5 million and motility was 63% but morphology was not documented.
No OHSS noted.
Day 6 update call: all 6 embryos arrested due to lots of fragmentation. No transfer.
Embryologist’s conclusion: All 6 embryos on days 6 were from 4 cells, 10 cells & 12 cells with fragmentation. ” Could be the protocol did not work well, E2 level was low, or could be egg quality and sperm quality together” he said.
Ivf #2: on March 2018,
Changed the clinic.
I responded very well and my E2 level was higher than expected.
Protocol: fostimon, centrotide, hcg, dexamethason, vitamin D, folic acid.
Stim days are 10 days
No contraceptive pills.
Started with Fostimon 300 for 3 days then reduced fostimon to 225 and added centrotide 0.25 for 7 days.
7500 hcg given on day 10.
My E2 level was as following: 150 pmol/L , 1382 pmol/L, 4909 pmol/L, 13702 pmol/L
25 Eggs retrieved, 20 mature, 13 fertilized with icsi.
Husband’s sample on day of egg retrieval: total count 24 million, concentration: 8 million, motility 65%, abnormal morphology 100%
Lab called me the next day and said they plan for day 5 transfer.
On day 5, my doctor came to me and said that they have only 5 embryos and they’ve not reached blastocyst stage yet. They were doing fine until day 3 then they started to slow growing thereafter. They have fragmentation too. He asked me if I want to put them back or give them more time in the lab and see if they will catch up. We decided to put the best three. 2 8 cells and 1 6 cells all grade 3. Now I’m in 2 ww but with not too much hope. The other 2 did not make it to blast stage.
Embryologist’s conclusion: eggs were highly fragile during icsi process and husband’s sample not good ( abnormal morphology 100%). ” The failure of this attempt is a combination of eggs quality and sperm quality” he said.
I’m not convinced that I have bad eggs quality since I’m young and all my hormones within normal limit and free from any medical, surgical and family condition.
FYI: We’ve never done sperm DNA fragmentation or karyotype before. But we did genetic diseases tests me and husband and all negative.
My questions are:
1- In your point of view, what are the causes of our failure? Is it egg quality or sperm quality or both?
2- Do you think protocol was not appropriate for me that’s why in both attempts I produced not good eggs and no blastocyst formed.
3- what is the protocol that can work for us?? What we can do to prevent this result in future?
3- Shoud we have done 50 ivf and 50 icsi for better result or it is not worth it since we have poor sperm morphology?
Sorry for long post but I really appreciate your response and advise.
Thank you.
Hi Dr Sher, for FET using lupron, is there a reason to prescribe a single shot depot lupron over the 2-week kit? Is the depot shot even advisable for FET? Thank you in advance.
It can be used!
Geoff Sher
When a hypothyroid woman gets pregnant, should her dose be raised? Is there some TSH level which would be good when pregnant?
It is advisable to regulate dosage of TH so as to maintain LSH between 1 and 3.5 MIU/ml.
Geoff Sher
Dr Dr. Sher,
Thank you so much for your incredibly informative blog. I’m doing my first IVF cycle (32 years old) in a week mostly due to MFI and have the following questions:
1. I was on 2 prior clomid cycles (first 50mg, second 100mg) and had my bloodwork done on CD21 during the 2nd clomid cycle. Would this affect my AMH and other levels? I had my baseline bloodwork done a year ago the AMH was 2.3 now it’s 3.2 on CD21 (same lab, though after taking 100mg Clomid CD2-7 this time). Then after stopping clomid, I had an ultrasound done on day 3, and the AFC was 19. Do you think AFC is more accurate for developing the right procedure vs. AMH and FSH?
2. My DHEA-S level is very high (469 ug/dl) but my Testosterone total is within the normal range (33.6 ng/mL) – thanks to my high SHBG level (195 nmol/L) my Free Testosterone index is low (0.61). This would make sense as I understand T binds tightly to SHBG while DHEA is only loosely bound to it. My protocol would be taking Menopur 75 + Follistim 150 then Cetrotide on day 6/7. I watched your video on how Menopur increased LH and wonder if with my elevated DHEA I would be more exposed to androgen? Or do you think for some reason the DHEA is not being converted to T in an elevated manner in my case and I would be ok with the Menopur exposure right at the start of stims?
Thank you so much and I look forward to hearing your opinion.
1.In my opinion, AMH is a far better metod (more reliable) than either basal FSH or AFC, regardless of when it is measured.
2. DHEA is in my opinion best omitted. Moreover the taking of DHEA could explain (at least in paret) your raised DHEAS level.
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.
Geoff Sher
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