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 have had 3 CS operations. My IVF cycle failed after transfer. `My Dr noted fluid in my uterus during stims, but it cleared up once i started progesterone. i read that fluids in uterus can drastically reduce chances of implantation even if the fluid cleared up before transfer. I am getting ready for an FET with my one and only PGS normal embryo and i am scared of getting fluids again.
Please what can i do to avoid fluid collecting in my uterus this time? I really need your advice!
As long as the fluid is gone by the day of transfer…all should be fine. There is probably nothing to be done to avoid this from happening again. You could however do a hysterosonogram or hysteroscopy to exclude surface lesions in the cavity.
Geoff Sher
You have a embryo that returned with the following result.
1. Is it possible for 1 embryo to have so many trisomies?
2. Could this have been a lab error?
3. Is it advisable to retest?
Sorry! I did not see the karyotype report you referred to.
Geoff Sher
Sorry so the test results were on one embryo +2 +3 +4 +5 +13
Dear dr. Sher,
can you tell me if there is any relation between an empty follicle syndrome and an anembryonic pregnancy?
After stopping OCP’s I started to have an irregulair (but ovulatoiry) cycle. When we didn’t conceive after 2 years we went to the GP and found out my husband had severe oligoastenospermia and I was diagnosed with PCOS. We started our first round of ICSI, I used menopur. Respons was well with 225 IE, and at the time of the punction there were about 10 follicles > 16 mm. Unfortunately only 2 oocytes were retrieved and both of them were immature and the weren’t able to fertilise them. For our second ICSI we used bemfola, and with 150 IE 6 follicles of appropriate size developed. From these 6 follicles 5 oocytes were retrieved, and (after some severe searching for sperm because they couldn’t find anything) they were able to fertilise all 5. 1 embryo was transfered after the punction and 3 other embryo’s were transfered as cryo’s. Unfortunately, we didn’t get pregnant with these attempts.
When deciding our further treatment plan we discovered the oligoastenospermia turned into a non-obstructive azoospermia and we decided to start using a sperm donor. After the second IUI we found out I’m pregnant and we were trilled! After the first ultrasound at 6+2 weeks unfortunately only a small gestational sac was visible and no yolk sac, fetal pole or heart beat. Tomorrow (at 6+6 weeks) we have our next ultrasound to see if there is any devolpment, but they already consulted us it would be likely this pregnancy would end in a miscarriage.
Thank you in advance for answering!
Yes…in my opinion, there cold be such a relationship between EFS and and anembryonic pregnancy (blighted ovum). The reason (as explained below) is that EFS , in my opinion, could well be related to abnormal egg development and that is associated abnormal embryonic development (including an anembryonic pregnancy).
Frequently, when following vigorous and often repeated flushing of follicles at egg retrieval they fail to yield eggs, it is ascribed to “Empty Follicle Syndrome.” This is a gross misnomer, because all follicles contain eggs. So why were no eggs retrieved from the follicles? Most likely it was because they would/could not yield the eggs they harbored.
This situation is most commonly seen in older women, women who have severely diminished ovarian reserve, and in women with polycystic ovarian syndrome (PCOS). In my opinion it is often preventable when an optimal, individualized and strategic protocol for controlled ovarian stimulation (COS) is employed and the correct timing and dosage is applied to the “hCG trigger shot.”
Normally, following optimal ovarian stimulation, the hCG “trigger shot” is given for the purpose of it triggering meiosis (reproductive division) that is intended to halve the number of chromosomes from 46 to 23 within 32-36 hours. The hCG trigger also enables the egg to signal the “cumulus cells” that bind it firmly to the inner wall of the follicle (through enzymatic activity), to loosen or disperse, so that the egg can detach and readily be captured at egg retrieval (ER).
Ordinarily, normal eggs (and even those with only one or two chromosomal irregularities) will readily detach and be captured with the very first attempt to empty a follicle. Eggs that have several chromosomal numerical abnormalities (i.e., are “complex aneuploid”) are often unable to facilitate this process. This explains why when the egg is complex aneuploid, its follicle will not yield an egg…and why, when it requires repeated flushing of a follicle to harvest an egg, it is highly suggestive of it being aneuploid and thus “incompetent” (i.e., incapable of subsequently propagating a normal embryo).
Older women, women with diminished ovarian reserve, and those with polycystic ovarian syndrome, tend to have more biologically active LH in circulation. LH causes production of male hormone (androgens, predominantly testosterone), by ovarian connective tissue (stroma/theca). A little testosterone is needed for optimal follicle development and for FSH-induced ovogenesis (egg development). Too much LH activity compromises the latter, and eggs so affected are far more likely to be aneuploid following meiosis.
Women with the above conditions have increased LH activity and are thus more likely to produce excessive ovarian testosterone. It follows that sustained, premature elevations in LH or premature luteinization (often referred to as a “premature LH surge”) will prejudice egg development. Such compromised eggs are much more likely to end up being complex aneuploid following the administration of the hCG trigger, leading to fruitless attempts at retrieval and the so called “empty follicle syndrome.”
The developing eggs of women who have increased LH activity (older women, women with diminished ovarian reserve, and those with PCOS) are inordinately vulnerable to the effects of protracted exposure to LH-induced ovarian testosterone. Because of this, the administration of medications that provoke further pituitary LH release (e.g., clomiphene and Letrozole), drugs that contain LH or hCG (e.g., Menopur), or protocols of ovarian stimulation that provoke increased exposure to the woman’s own pituitary LH (e.g., “flare-agonist protocols”) and the use of “late pituitary blockade” (antagonist) protocols can be prejudicial.
The importance of individualizing COS protocol selection, precision with regard to the dosage and type of hCG trigger used, and the timing of its administration in such cases cannot be overstated. The ideal dosage of urinary-derived hCG (hCG-u) such as Novarel, Pregnyl and Profasi is 10,000U. When recombinant DNA-derived hCG (hCG-r) such as Ovidrel is used, the optimal dosage is 500mcg. A lower dosage of hCG can, by compromising meiosis, increase the risk of egg aneuploidy, and thus of IVF outcome.
There is in my opinion no such condition as “Empty Follicle Syndrome.” All follicles contain eggs. Failure to access those eggs at ER can often be a result of the protocol used for controlled ovarian stimulation.
Geoff Sher
Hi, I just finished an unsuccessful IVF cycle. I’m 38 yrs old, with low AMH of 0.448 ng/mL and FSH of 5.5 IU/L. Prior to this IVF cycle I had 1 miscarriage at 10 weeks, 1 ectopic pregnancy and 3 chemical pregnancies that registered only 6 to 11 HCG. For 3 months prior to the IVF cycle, I took 75 DHEA, 300 Ubiquinol, Vit D, folate, pre-natal daily. My IVF protocol was Antagonist with Estrace priming for 9 days prior, then daily injections of Menopur 225 and Puregon 225 (for 12 days) and Saizen 0.66mg (for 10 days). On Day 6, I started Orgalutran. My trigger was Pregnyl 10,000 IU. I had 9 eggs retrieved, 7 were mature and 5 fertilized via ICSI. All 5 were still growing at Day 5, but very slowly, so none were yet at Blastocyst stage. By Day 6, all 5 had arrested. My doctor has noted that my egg quality is very poor and I should now consider donor eggs. My question is if you would agree with this prognosis or is there any hope that I might be successful with a different protocol? Thank you.
Hi Dr Sher,
I’m 39, have had 3 mc’s (incl. one ectopic resulting in removal of Fallopian tube). I’m grateful to say we have a lovely 5 year old daughter .
I have just completed my first (and unsuccessful) round of ivf.
I’ve been taking 50mg/ day DHEA for approx 6 months at the advice of my fertility specialist.
Your article regarding DHEA got my attention as you mentioned that for some women this supplement can cause aggression. This is definitely the case with me. My fertility specialist had me taking 75/day initially but then we reduced it to 50/day. Even with the dose split across the day (2 x 25mg) I still feel aggressive. Thankfully no extra body hair or manly voice though!
Do you think the DHEA could be detrimental to my egg development due to my sensitivity to it?
Thank you in advance for your input,
Kind Regards,
Zoe