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Anyone tried this for Poor Responders??
3 replies to this topic
Posted 29 January 2006 - 10:10 AM
I've been corresponding and am waiting on a telephone consult with a Dr at SIRM in USA. They have a lot of success with poor responders and this is their main protocol for them...
Has anyone tried anything like it here in Australia??
Agonist/Antagonist Conversion Protocol (A/ACP)
The GnRH Agonist/Antagonist Conversion Protocol (A/ACP) :
It is our position that some form of pituitary blockade, either in the form of a GnRH agonist (e.g. Lupron, Buserelin, Nafarelin, and Synarel. Decapeptyl) or a GnRH antagonist (e.g. Antagon, Cetrotide, Cetrorelix, and Ganarelix) is an essential component in ovarian stimulation of “poor responders” undergoing IVF. If this is not done, a progressive rise in LH –induced ovarian androgens (male hormones ….mainly testosterone) will inevitably affect follicle/ egg development, resulting in compromised embryo quality.
The follicles/ eggs of women on GnRH-agonist “flare protocols” are exposed to an exaggerated Lupron-induced LH release, (the “flare effect” while the follicles/eggs of women, who receive GnRH antagonists starting 6-8 days into the stimulation cycle are exposed to endogenous LH -induced ovarian androgens( especially testosterone). This might not be problematic in “normal responders” but could be decidedly prejudicial in “poor responders” and older women where endogenous basal LH levels are often raised and the ovaries may be inordinately sensitive to LH and where excessive exposure of follicles and eggs to testosterone could severely compromise egg development and thus embryo quality.
exhausted of its LH and residual minimal LH is present in the circulation by the time stimulation with gonadotropins begins, the above mentioned adverse testosterone-effect is largely negated. On the down side is the fact that prolonged administration of GnRH agonists such as Lupron (such as with the GnRH agonist down-regulation protocol could suppress subsequent ovarian response to ovarian stimulation with gonadotropins, by competitively binding with ovarian FSH receptors.
We introduced of our Agonist/Antagonist Conversion Protocol (A/ACP) more than a year ago in an effort to counter this effect.
With the A/ACP, low dose Antagon/Cetrotide is commenced at the onset of spontaneous menstruation or following bleeding that follows initiation of GnRH agonist (e.g. Lupron) therapy using a long-down-regulation protocol arrangement. We currently prescribe the A/ACP to most of our IVF patients regardless of whether they are “normal responders” or “poor responders”. Preliminary results suggest a significant improvement in egg number, egg/embryo quality as well as in implantation and viable IVF pregnancy rates. The A/ACP has however, proven to be most advantageous in “poor responders” where additional enhancement of ovarian response to gonadotropins may be achieved through incorporation of “estrogen priming”. We have reported on the fact that the addition of estradiol for about a week following the initiation of the A/ACP, prior to commencing FSH-dominant gonadotropin stimulation appears to further enhance ovarian response, presumably by up-regulating ovarian FSH-receptors.
There is one potential draw back to the use of the A/ACP, in that the sustained use of a GnRH antagonist ( e.g. Antagon/Cetrotide) throughout the stimulation phase of the cycle, appears to compromise the predictive value of serial plasma estradiol measurements as a measure of follicle growth and development in that the estradiol levels tend to be much lower in comparison to cases where agonist (Synarel, Lupron) alone is used or where a “ conventional” GnRH antagonist protocol is employed ( i.e. antagonist administration is commenced 6-8 days following initiation of gonadotropin stimulation). Rather than being due to reduced production of estradiol by the ovary(ies), the lower blood concentration of estradiol seen with prolonged exposure to GnRH-antagonist, could be the result of a subtle, agonist-induced alteration in the configuration of the estradiol molecule , such that currently available commercial kits used to measure estradiol levels are rendered much less sensitive/specific. Thus when the A/ACP is employed, we rely much more heavily on ultrasound growth of follicles along with observation of the trend in the rise of estradiol levels, than on absolute estradiol values. Thus we commonly refrain from prescribing the A/ACP in “high responders” who are predisposed to the development of severe ovarian hyperstimulation syndrome (OHSS) and accordingly where the accurate measurement of plasma estradiol plays a very important role in the safe management of their stimulation cycles.
It is remarkable, that while using the A/ACP + "estrogen priming " in “poor responders “ whose FSH levels were often well above threshold limits, the cycle cancellation has consistently been maintained below 10% ( i.e. much lower than expected). Many of these patients who had previously been told that they should give up on using their own eggs, and switch to ovum donation because of “poor ovarian reserve”, have subsequently achieved viable pregnancies at SIRM using the A/ACP with “estrogen priming”.
Posted 29 January 2006 - 10:20 AM
Very interesting indeed!!
Sound similar to what a few other people have mentioned to me previously (can't remember if that was called 'agonist protocol') but I have it on my list of things to discuss next time I visit my doc. Will print this off and ask him to read it.
Sounds 'right up my alley' - pls keep us informed.
Posted 29 January 2006 - 01:15 PM
I have read what you posted and am perhaps a little confused however I believe that this is what I did. I am a poor responder with my first ivf only getting one egg which did not make it over night. I was on Lucrin and Puregon. My 2nd ivf cycle I was on Cetrotide and Puregon and a short cycle. The whole cycle of injections only went for 13 days and then I had epu. On this protocol I got 4 eggs, 3 fertilised, 2 put back on day 5 and a successful singleton pregnancy was achieved (DD born 30/8/05).
If you would like to know more then please pm me. I know that cetrotide was not widely used and still a little "experimental" here in OZ when I had it and it was very expensive but truly worth it for us. We used SIVF in Canberra for our ivf and it was icsi as we also had a male motility problem as well.
Posted 29 January 2006 - 07:49 PM
I know that Antagonist cycles are done here but with Cetrotide starting about day 5 I think. I am with the same clinic as Robyn and my FS said there is some evidence from animal studies that Cetrotide damages primordial follicles and hence could affect fertility in FUTURE cycles. I have done a flare cycle and it didn't make any difference to my egg quantity and quality however I am not a poor responder numbers-wise by any stretch of the imagination.
lining up for IVF/ISCI#5 - perhaps, maybe???
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