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. 1 month after a failed ivf cycle my day 3 hormon levels are
e2 133,5
fsh 7,27
lh 2,22
i am 40 years old. are they good ?
e2 is high , is it due to ivf cycle.how can i lower e2 level ?
thenks
It sounds like you could have an ovarian functional cyst. Have an US done to see!
Geoff Sher
I would like some advice. I have had treatment in London in clinics with very good success rates. I have had 1st cycle ending in miscarriage at 8 week (on heparin and aspirin empirically), then FET negative test. Then I had a further cycle and tested all embryos remaining from 1st and the second cycle (12 blastocysts) and got 3 PGS tested normal good quality embryos. 3 x FET negative. Clinic success for my age using PGS 50%.
The had an ERA showing not receptive but receptive after a further day of progesterone.
now 44. Egg donation cycles with frozen eggs. fresh embryo transfer and 2 x frozen embryos negative. clinic success 70%
Thrombophilia screen negative.
Sperm high DNA fragmentation at 35-64% and andrologist is recommending sperm extraction to get fresher sperm.
Clinic recommending surrogate or donor sperm as next step.
I am cautious about immune treatment as limited evidence. I am a doctor.
I have had a 1 cm submucosal fibroid removed and a few polyps removed with a hysteroscopy on an annual basis before cycles checking for polyps.
Another clinic has just recommended going to them and blames out clinic standards though I think there is more to it that this. Is it a uterus or sperm?
Hi Dr.Sher,
I had an IVF cycle last year when I was 29. Surprisingly all the blastocysts came back abnormal (2 complex abnormal and 6 mosaic). My doctor suggested me not transferring any but to start another cycle for obtaining absolutely normal embryos. Since I reside abroad and the cost to start another cycle in the US is high so I didn’t take his advice. In February this year, I conceived naturally for the first time, however miscarried at 8 weeks. We did a chromosome test for the fetus and it was 45X. Both my husband and I were tested chromosomely normal and we just couldn’t figure out why we kept getting mosaic or abnormal embryos. After hearing more and more cases where mosaic embryos been transferred turning into healthy babies, I would also like to give my mosaic embryos a shot. I hope to hear about your opinion and to know which embryo has the highest priority for transfer.
1. mosaic partial trisomy 8q22.1-qter
2.mosaic monosomy 18
3.mosaic monosomy 3, mosaic monosomy 19
4.mosaic monosomy6, mosaic partial trisomy 21pter-q21.1
5.mosaic partial monosomy 1p34.3-qter
6.mosaic monosomy 2
Thank you.
I would use #s 1,2,5 &6.
Human embryo development occurs through a process that encompasses reprogramming, sequential cleavage divisions and mitotic chromosome segregation and embryonic genome activation. Chromosomal abnormalities may arise during germ cell and/or pre-implantation embryo development, and represents a major cause of early pregnancy loss. About a decade ago, I and an associate, Levent Keskintepe Ph.D were the first to introduce full embryo karyotyping (identification of all 46 chromosomes) through preimplantation genetic sampling (PGS) as a method by which to selectively transfer only euploid embryos (i.e. those that have a full component of chromosomes) to the uterus. We subsequently reported on a 2-3 fold improvement in implantation and birth rates as well as a significant reduction in early pregnancy loss, following IVF. Since then PGS has grown dramatically in popularity such that it is now widely used throughout the world.
Most IVF programs that offer PGS services, require that all participating patients consent to all their aneuploid embryos (i.e. those with an irregular quota of chromosomes) be disposed of. However, there is now growing evidence to suggest that following embryo transfer, some aneuploid embryos will in the process of ongoing development, convert to the euploid state (i.e. “autocorrection”) and then go on to develop into chromosomally normal offspring. In fact, I am personally aware of several such cases occurring within our IVF network. So clearly , summarily discarding all aneuploid embryos as a matter of routine we are sometimes destroying some embryos that might otherwise have “autocorrected” and gone on to develop into normal offspring.
Thus by discarding aneuploid embryos the possibility exists that we could be denying some women the opportunity of having a baby. This creates a major ethical and moral dilemma for those of us that provide the option of PGS to our patients. On the one hand, we strive “to avoid knowingly doing harm” (the Hippocratic Oath) and as such would prefer to avoid or minimize the risk of miscarriage and/or chromosomal birth defects and on the other hand we would not wish to deny patients with aneuploid embryos, the opportunity to have a baby.
The basis for such embryo “autocorrection” lies in the fact that some embryos found through PGS-karyotyping to harbor one or more aneuploid cells (blastomeres) will often also harbor chromosomally normal (euploid) cells (blastomeres). The coexistence of both aneuploid and euploid cells coexisting in the same embryo is referred to as “mosaicism.” As stated, some mosaic embryos will In the process of subsequent cell replication convert to the normal euploid state (i.e. autocorrect)
It is against this background, that an ever increasing number of IVF practitioners, rather than summarily discard PGS-identified aneuploid embryos are now choosing to cryobanking (freeze-store) certain of them, to leave open the possibility of ultimately transferring them to the uterus. In order to best understand the complexity of the factors involved in such decision making, it is essential to understand the causes of embryo aneuploidy of which there are two varieties:
1.Meiotic aneuploidy” results from aberrations in chromosomal numerical configuration that originate in either the egg (most commonly) and/or in sperm, during preconceptual maturational division (meiosis). Since meiosis occurs in the pre-fertilized egg or in and sperm, it follows that when aneuploidy occurs due to defective meiosis, all subsequent cells in the developing embryo/blastocyst/conceptus inevitably will be aneuploid, precluding subsequent “autocorrection”. Meiotic aneuploidy will thus invariably be perpetuated in all the cells of the embryo as they replicate. It is a permanent phenomenon and is irreversible. All embryos so affected are thus fatally damaged. Most will fail to implant and those that do implant will either be lost in early pregnancy or develop into chromosomally defective offspring (e.g. Down syndrome, Edward syndrome, Turner syndrome).
2.“Mitotic aneuploidy” occurs when following fertilization and subsequent cell replication (cleavage), some cells (blastomeres) of a meiotically euploid early embryo mutate and become aneuploid. This is referred to as mosaicism. Thereupon, with continued subsequent cell replication (mitosis) the chromosomal make-up (karyotype) of the embryo might either comprise of predominantly aneuploid cells or euploid cells. The subsequent viability or competency of the conceptus will thereupon depend on whether euploid or aneuploid cells predominate. If in such mosaic embryos aneuploid cells predominate, the embryo will be “incompetent”). If (as is frequently the case) euploid cells prevail, the mosaic embryo will be “competent” and capable of propagating a normal conceptus.
Since some mitotically aneuploid (“mosaic”) embryos can, and indeed do “autocorrect’ while meiotically aneuploid embryos cannot, it follows that an ability to differentiate between these two varieties of aneuploidy would be of considerable clinical value. And would provide a strong argument in favor of preserving certain aneuploid embryos for future dispensation.
Aneuploidy, involves the addition (trisomy) or subtraction (monosomy) of one chromosome in a given pair. As previously stated, some aneuploidies are meiotic in origin while others are mitotic “mosaics”. Certain aneuploidies involve only a single, chromosome pair (simple aneuploidy) while others involve more than a single pair (i.e. complex aneuploidy). Aside from monosomy involving absence of the y-sex chromosome (i.e. XO) which can resulting in a live birth (Turner syndrome) all monosomies involving autosomes (non-sex chromosomes) are lethal and will not result in viable offspring). Some autosomal meiotic aneuploidies, especially trisomies 13, 18, 21, can progress to viable, but severely chromosomally defective babies. All other meiotic autosomal trisomies will almost invariably, either not attach to the uterine lining or upon attachment, will soon be rejected. All forms of meiotic aneuploidy are irreversible while mitotic aneuploidy (“mosaicism) often autocorrects in the uterus. Most complex aneuploidies are meiotic in origin and will almost invariably fail to propagate viable pregnancies.
There is presently no microscopic or genetic test that can reliable differentiate between meiotic and mitotic aneuploidy. Notwithstanding this, the fact that some “mosaic” embryos can autocorrect in the uterus, makes a strong argument in favor of transferring aneuploid of embryos in the hope that the one(s) transferred might be “mosaic” and might propagate viable healthy pregnancies. On the other hand, it is the fear that embryo aneuploidy might result in a chromosomally abnormal baby that has led many IVF physicians to strongly oppose the transfer of any aneuploid embryos to the uterus.
While certain meiotic aneuploid trisomies (e.g. trisomies 13, 18, & 21) can and sometimes do result in chromosomally defective babies, no other meiotic autosomal trisomies can do so. Thus the transfer of trisomic embryos in the hope that one or more might be mosaic, should exclude the use of embryos with trisomies 13, 18 or 21. Conversely, no autosomal monosomic embryos are believed to be capable of resulting in viable pregnancies, thereby making the transfer of autosomally monosomic embryos, in the hope that they are “mosaic”, a far less risky proposition. Needless to say, if such action is being contemplated, it is absolutely essential to make full disclosure to the patient (s) , and to insure the completion of a detailed informed consent agreement which would include a commitment by the patient (s) to undergo prenatal genetic testing aimed at excluding a chromosomal defect in the developing baby and/or a willingness to terminate the pregnancy should a serious bith defect be diagnosed.
Good luck!
Geoff Sher
Hi Dr. Sher,
I am 40 years old, and I have had successful pregnancies. However, since having my son at 38, I have had three miscarriages. The most recent being a result of my fist round of IVF. Testing showed that my FSH is 8, my AHM is 1.03, and my AFC was 14. My husband has no issues. We did the estrogen priming patch protocol for our first round of IVF. I used 400 of Gonal F and 150 of Luveris daily, and certrotide to prevent ovulation until trigger. At retrieval, we only got 3 eggs; all were mature and two fertilized, resulting in 8 cell, grade 3 embryos. We transferred both, and I got pregnant, but had a chemical pregnancy shortly after. Our RE recommended against PGS testing, and when we met with her today, she recommended that we do the same protocol for our next round, but with increasing the Gonal F to 450. I mentioned the MDL protocol, and she said it could work, but given that the patch antagonist protocol got us two good embryos, we should try that again. I would like to get more embryos so we have some left to freeze. At my age, I am concerned that the majority of eggs will be abnormal, and would rather have the option of doing a FET if need be. Do you think that we should stick to this same protocol? Thank you so much for your time.
Hi Dr. Sher on a freeze all cycle for ngs is it ok to start transfer meds on the first bleed as long as all levels are back to normal? Thanks
In my opinion, yes…
Geoff Sher