Advice needed
3 Replies
ttc#2carrie - September 12

Hi Dr. Smith, I have posted a few questions to you before and really appreciated your comments.

All ICSI's
Here is some history...
1st conceived son

2nd IVF retrieved 10 eggs and 7 were mature and only 1 fertilized (based upon your comments about egg maturation, they weren't actually mature) -BFN I triggered come to find out when my E2 was WAY too low.

3rd IVF FSH/LH protocol, retrieved 6 eggs, 5 fertilized.
3 xfered -2 were 4+/5 and 1 4/5 I know the grading doesnt mean that much since all labs grade differently but they were multy celled and good quality. but none implanted!

SO my question is is there any suggestions as to what we can do next. PGD? or any embryo testing? It is known that I am considered a poor responder, but I am 32 and have good quality eggs, or so I thought. I am not sure what I am asking but just confused as to why these "good" embryos didnt work!!

Thanks so much!


Dr Smith - September 13

It is possible to answer most of the embryo questions by taking the embryos to the blastocyst stage prior to transfer. The vast majority of genetically abnormal are weeded out beteen the 4 and 8 cell stage of development. Embryos that arrest at the 4-8 cell stage are abnormal. Genetic problems would be unusual at 32. I would not recommend PGD for your situation. Its expensive, not as accurate as claimed, limited in the number of chomosomes that can be tested and may be harmful to the embryo, particularly if the biopsy is performed at the 4-cell stage.

I don't know why ICSI was performed in your case, but if your husband is severely oligoasthenoteratozoospermic (What a mouthful! it means low concentration, low motility and poor morphology), then there may be addional genetic problems as well. If that's the case, the sperm may be a contributing factor. If there are enough sperm to test, I would also suggest the Sperm Chromatin Structure Assay available from to rule this out. Damaged chromatin (DNA) can also cause embryoinc arrest at an early stage.

If the sperm are "normal", that leaves us with possibility of implantation problems. There is a panel of tests available through Millenova Laboratories in Chicago that will address implantation issues. For more information, see Even women who have had a successful pregnancy can aquire Natural Killer Cell problems.


ttc#2carrie - September 14

Thanks Dr. Smith, I am going to look into both.
My husbands sperm is borderline, he does have some issues, nothing major, but enough that it seems we are here. I have never been diagnosed with anything. I know I dont have PCOS, endometriosis is possible, but unlikely-have no symptoms. I do have a very slight hypothyrod issue, so many NK testing would work.
Do you recommend the Sperm Chromatin Structure Assay without "severely oligoasthenoteratozoospermic"? -(I had to cut and paste that from your post, no way I can say or pronounce that)
Also, I know this may be slightly out of your direct area, but I am sure you must know, what protocol do you think has worked best with poor responders?

I have had 3 opinions and no one has made any other suggestions or recommendations for testing me. I have never done a post coital, a clomid challendge test -do you recommend any of these??

I appreciate your suggestions, as no one has come with any answers, it's a lot easier to have a diagnosis, rather than just guessing!!

Thanks so much!


Dr Smith - September 15

Andrology lesson:

oligo = low number/concentraion
astheno = slow moving/immotile
terato = malformed (morphology)
zoo = cell (any cell)
spermia = something to do with sperm

oligoasthenoteratozoosperm - see, simple. Now you try. Yeah, right...

The SCSA is a good idea after a failed cycle that had a contributing male factor. A better idea before a cycle if the sperm issues are known.

The most common protocol for "poor responders" (which is actually a misnomer because the number of follicles that begin to develop on a given cycle is not related to the dose of stimulation medication - hence the patient is not a "poor responder", they just have fewer follicles at the begining of the cycle than the norm), is the flare protocol which uses your own homones (FSH and LH) as well as the ones you take by injection. Another protocol is also gaing favor. It uses a GnRH antagonist (Centrotide, Antagon) to prevent premature ovulation, thus elimination the potentially negative effect of Lupron (a GnRH agonist). I'm not going to go into the pro's and con's of each protocol here, but you can discuss their relative merits with your RE.

More gobbilygook:

GnRH = Gonadotropin Releasing Hormone a hormone found in the pituitary gland that stimulates the release of FSH and LH.
Agonist = supresses FSH/LH
Antagonist = stimulates FSH/LH



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