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Thread: Egg quality

  1. #1
    Join Date
    Dec 2008
    Posts
    2

    Unhappy Egg quality

    me 38 DH 31 been in treatment for 2+ years/unexplained fertility.

    IVF #1 cancel due to Lupron sensitivity (product 3 follicles).
    IVF #2 proceeded without Lupron protocol. Follistism (225 x 2 a day...). This cycle I as able to product 16 follicles via retrieval. 11 fertilized out of 16, 7 were good base on day 3 evaluation.
    4 grade 2 8 cells
    3 grade 3 and 5

    We transferred 3 grade 2 on day 3 and hope to have some left to freeze. Found out NONE of the leftover made it to blast grade A or B to freeze.

    Is this an indication that my egg quality is very poor since they can not make it to freeze especially one of them was grade 2 on day 3?

  2. #2
    Join Date
    Oct 2008
    Posts
    387

    Default Egg quality

    Tough to say on the Board. There are many issues we need to look at. Some that come to mind are:

    1) The exact quality of the embryos on and before day 3 (egg issues) vs. day 5 quality.
    2) Why was day 5 ET not attempted
    3) Sperm factor - SDI test - sperm DNA kicks in after day 3
    4) Uterine scar tissue - result of Fluid US or office hysteroscopy
    5) Immune issues - NK test and APLA testing at millenova.com
    6) ET technique
    7) Thickness of the uterine lining at ET (>9mm best)
    8) Type of protocol used - decerease amount of LH (repronex or menopure), decrease overall dose
    9) Appropriate coasting method.
    10) Check for insulin resistance - metformin only if elevated fasting insulin
    If you are local, might I recommend that you call Angie at 877-665-BABY and set up a free in-person consultation with me at SIRM-Dallas, located at 7777 Forest Lane, Suite C-638. If on the other hand you are from out of town, call to set up a free medical telephone consultation with me.

  3. #3
    Join Date
    Dec 2008
    Posts
    2

    Default

    First and most of all, I would like to thank you very much for sharing your thoughts and expert advice on this subject.


    Short background history:
    Being treated at reproductivegynecologyinc.com (Akron Ohio)


    Clomiphene Citrate Therapy/IUI 3 times. Break in between treatment due to cysts.

    Grandotropin/IUI. 3x. Break in between treatment due to cysts.
    Got pregnant on the first cycle via injectable but lost betw 6 to 8 wk. Had D&C and tissue analyzed and no abnormality shown. (no additonal test was done since this is the frist mc).


    First IVF attempt: Long Lupron Protocol
    10 units of Lupron for 14 days
    5 units of Lupron + Follistim Injection in the eve (300)
    Blood estradoil and vaginal ultrasound 5 days later. Ultrasound shown three folicles. Told to stop Lupron but continue Follistim and convert cycle to IUI.


    Note: I believe we have gone through all their preliminary tests for IVF procedure except further genetic test.


    1) The exact quality of the embryos on and before day 3 (egg issues) vs. day 5 quality.
    Was only told how many eggs fertilized and come in for a 3 ET.
    2) Why was day 5 ET not attempted

    Not sure
    3) Sperm factor - SDI test - sperm DNA kicks in after day 3

    Not sure
    4) Uterine scar tissue - result of Fluid US or office hysteroscopy

    Is sonohysterogram the same (it was done before starting IVF). Found nothing and looks nornal.
    5) Immune issues - NK test and APLA testing at millenova.com
    Do not know about this one either.
    6) ET technique
    Abdominal ultrasound to aid in correct placement of the embryo catheter.
    7) Thickness of the uterine lining at ET (>9mm best)

    I was told it looks good.
    8) Type of protocol used - decerease amount of LH (repronex or menopure), decrease overall dose

    Gonadotropin/Ganirelix Protocol
    Birth control pills for 2 months
    Blood work/Baseline Ultrasound on cycle day 3
    Begin Follistim morning and eve (225 x 2) continue for 8 days. 3 Ganirelix shots was added the last 3 days.
    HCG trigger shot and told to be back for egg retrieval at a specified time.

    9) Appropriate coasting method.

    Not knowledgeble enough on this subject.

    10) Check for insulin resistance - metformin only if elevated fasting insulin
    If you are local, might I recommend that you call Angie at 877-665-BABY and set up a free in-person consultation with me at SIRM-Dallas, located at 7777 Forest Lane, Suite C-638. If on the other hand you are from out of town, call to set up a free medical telephone consultation with me.
    ***************

  4. #4
    Join Date
    Oct 2008
    Posts
    387

    Default hopeless

    It looks like decreased ovarian reserve is the main issue. I would recommend an estrogen priming protocol with 750 IU and adding some LH (menopur). Not sure if it would work but worth trying before considering egg donation. Please see below:
    CONTROLLED OVARIAN HYPERSTIMULATION (COH) IN “POOR RESPONDERS”




    BACKGROUND:

    Women are born with all the eggs they will ever have, after menarche (the earliest onset of menstruation) a monthly process of using up numerous eggs continues until the number of eggs remaining in the woman’s ovaries falls below a certain critical threshold, at which time ovarian function starts to decline and the woman becomes relatively resistant to ovarian stimulation with fertility drugs... This phase of the woman’s reproductive life is referred to as the climacteric. The onset of the climacteric is heralded by gradually increasing blood concentrations of FSH and a decline in Inhibin B levels, as measured on the 3rd day of a spontaneous menstrual cycle and continue for a number of years (approximately 4-6 years) until virtually all remaining eggs have been used up. Reduced ovarian responsivity to fertility drugs is usually the direct consequence of a decline in ovarian function brought about by the onset of the climacteric and pending menopause.

    While the onset of the climacteric rarely commences prior to age 35yrs (usually after age 40yrs), it can occur at any age. It is characterized by a reduction of ovarian responsivity to fertility drugs as evidenced by rising blood levels of FSH and falling Inhibin B levels (on day 3) along with reduced responsivity to fertility drugs. Simply women who are in the climacteric recruit fewer eggs for each cycle and therefore produce fewer follicles/eggs even following the administration of relatively high doses of fertility drugs.

    While it is true that Lupron elicits a degree of resistance to FSH (fertility drugs included), the number of follicles a woman is capable of producing is limited by the number of eggs in her ovaries which progressively reduces throughout the reproductive years and then progressively declines at an ever increasing rate with the onset of the climacteric. The problem is that you need to inhibit premature LH release during the cycle in order to produce healthy eggs. Lupron is a preferred way of achieving this. Antagon can also be used, but it has no proven advantage over Lupron in this setting.

    Simply put, Lupron represents an essential component of stimulation in resistant women who otherwise frequently have a premature LH surge.

    It is possible to offset much of the FSH receptor-antagonistic effects of Lupron by priming the woman’s ovaries with estrogen for 7-10 days in advance of administering gonadotropins, by reducing the Lupron dosage to a bare minimum and by trying to use only pure FSH preparations such as Folistim and limiting LH containing products such as Pergonal, Repronex, and Humagon to a bare minimum. The last thing such women need is to have additional LH added by the doctor.

    We do not use “micro-flare protocols” for the same reason. With such protocols, Lupron is started virtually with the gonadotropins. This causes an immediate outpouring of both FSH & LH by the woman’s pituitary gland, While the FSH can improve ovarian response, the LH reduces egg quality and, indirectly (by ovaries), hinders endometrial growth in response to estrogen.

    So it is not as simple as it at first appears to be. Optimizing response requires a very individualized approach, not a “recipe approach”. The first stimulation attempt is based on the woman’s age, previous response to prior stimulation cycles, blood levels of FSH, E2, and Inhibin B and then “tweaking” the protocol based on response to the chosen dosage and stimulation regime…in subsequent stimulation cycles. Arbitrary addition or subtraction of ingredients is not in the patient’s best interest.

    It is common practice to administer gonadotropin releasing hormone agonists (GnRHa) such as lupreulide acetate (Lupron) and more recently, GnRH-antagonists such as Antagon or Cetrorelix, to prevent the release of LH with COH. GnRHa exert their LH-lowering effect. over a number of days. They act by causing an initial outpouring and then depletion of pituitary gonadotropins. This results in the LH level falling to within negligible concentrations, within 4-7 days, thereby establishing a relatively “LH-free environment”. GnRH antagonists, on the other hand, act by rapidly (within 48-72hrs) blocking pituitary LH release, so as to achieve the same effect.

    CONTROLLED OVARIAN HYPERSTIMULATION (COH):

    The most commonly prescribed protocol for Lupron/gonadotropin administration is the so-called “long protocol”. Here, Lupron is given, starting a week or so prior to menstruation. This precipitates an initial rise in FSH and LH level, which is rapidly followed by a precipitous fall to near zero. This is followed by uterine withdrawal bleeding (menstruation), whereupon gonadotropin treatment is initiated while daily lupron injections continue, to ensure an “LH-free” environment. Lupron can be supplanted by Antagon or Cetrotide (both are GnRH antagonists)

    Another approach to COH, is by way of so-called “flare protocols”. Here, gonadotropin and GnRHa therapy are is initiated simultaneously at the start of menstruation The intent is to deliberately allow lupron to effect an initial surge (“the flare effect”) in pituitary FSH release so as to augment ovarian response to the gonadotropin medication. Unfortunately, this approach represents “a double edged sword” as the desired increased release of FSH is inevitably accompanied by a comparable rise in blood LH levels that stimulates ovarian stromal androgen production which could potentially compromise egg quality and endometrial development, especially in certain categories of patients. We believe that in this way, “flare protocols” have the potential to compromise IVF outcome and reduce success rates. Accordingly, we do NOT advocate the use of “flare protocols” at all.

    “Estrogen priming” in women who are resistant to gonadotropins: Patients who have demonstrated reduced ovarian response to COH and those who by way of significantly raised FSH and reduced Inhibin B levels are also likely to be “poor responders”, are treated by way of a “modified” long protocol, using estrogen to prime ovarian FSH receptors to FSHprior to initiating gonadotropin therapy. Here, GnRH agonist is administered for a number of days prior to menstruation to effect pituitary down-regulation (as with the “long protocol). Upon menstruation and confirmation by ultrasound that blood estradiol concentration is below 70 picograms per milliliter, (i.e. that the ovaries have been adequately suppressed), the Lupron is switched to Antagon/Cetrotide (GnRH antagonists) at half the regular dosage (125mcg daily) or alternatively, the dosage of GnRH agonist (Lupron) is drastically lowered and the woman is givens twice-weekly injections of estradiol valerate for a period of 7-10 days. COH is then initiated using a relatively high dosage of FSH-dominant gonadotropins such as Folistim or Gonal F for a period of 7 days. The gonadotropin dosage is then substantively reduced. All along the daily administration of GnRH agonist is continued until the “HCG trigger” (or can be supplanted by Antagon or Cetrotide daily from the initiation of COH until hCG administration). By this approach we have been able to significantly improve ovarian response to gonadotropins in many of hitherto “highly resistant patients”.

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