4 research outputs found

    Predictors of IVF/ICSI success following treatment of endometriosis as the cause of primary infertility

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    Objectives: Treatment of endometriosis prior to IVF/ICSI could be followed by the significant reduction of ovarian reserve. The aim is to identify potential markers of the IVF/ICSI outcome in patients with endometriosis associated infertility and to evaluate their clinical significance. Material and methods: The prospective cohort study included 73 patients with primary infertility caused by endometriosis that were subjected to 77 IVF/ICSI cycles. Patients were classified into two groups. In the first group some type of treatment had previously been applied, and in the second group patients were immediately subjected to the IVF/ICSI procedures. Results: When pregnancy was achieved, there were significantly more patients under 35 years of age, more patients with primary infertility duration up to 3 years, and more patients with endometriosis that was previously treated (77.4%) (p < 0.039). In the cases of the successful outcome Endometriosis Fertility Index > 7, lower basal FSH and FSH/LH ratio were found, as well as significantly higher basal E2, basal P4 and AMH. Significantly lower doses of gonadotropins were needed in cases of the successful outcome, and long protocol with agonists was more frequently used. Multivariate logistic regres­sion analysis showed that previous therapy of endometriosis, P4 ≥ 0.7 ng/mL, AMH ≥ 0.9 ng/mL, A class of embryos, and the use of long protocol with agonists were predictors of the successful IVF/ICSI outcome. Conclusions: Therapy for endometriosis, AMH and P4 levels appeared to be predictors for the successful IVF/ICSI outcome and the use of long protocol with agonists could be advised in these cycles

    Effect of sodium valproate on luteinizing hormone secretion in pre- and postmenopausal women and its modulation by naloxone infusion.

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    The synchronized activity of the GnRH neurons can be modulated through both excitatory and inhibitory circuits: one such inhibitory modulator is gamma-aminobutyric acid (GABA), but this has been little studied in humans. The aim of this study was to examine whether acute or chronic modulation of the GABA-ergic system with the drug sodium valproate (VPA) affects gonadotropin secretory frequency and/or amplitude in a steroid-dependent manner, and whether any such modulation might interact with endogenous opioids. Sixty postmenopausal women (age range 50-60 yr, group I), 50 postmenopausal women who had been on estrogen replacement therapy (group II), and 30 women in the luteal phase of their regular menstrual cycle (age range 25-40 yr, group III) were studied. VPA was administered acutely using doses of 300, 600, and 1200 mg orally. Samples for serum gonadotropins were taken at intervals over 24 h. Each dose of VPA caused significant LH suppression in group I. The maximum degree of suppressibility was the same with the three doses of VPA (14-20%). However, no dose had any effect on gonadotropin levels in group II. In group III, the single high dose of 1200 mg VPA significantly suppressed serum LH levels. The efficacy of chronic VPA administration in the three groups studied was assessed by measuring LH pulsatility (10-min samples) over 6 h, before and after 1 month's treatment with VPA. No change in either mean basal LH or in the LH pulsatility parameters was found. Naloxone infusion (1.6 mg/h for 6 h) had no effect on LH pulsatility in group I. When 1200 mg of VPA was administered before naloxone infusion, the level of LH suppression was 18% and was associated with a significant decrease in LH pulse frequency (P < 0.01). Naloxone infusion alone significantly increased mean serum LH and LH pulse frequency in group II patients (P < 0.01), and this elevation was antagonized by VPA pretreatment. Naloxone infusion alone significantly increased mean LH levels and LH pulse frequency in patients in group III, and this was also blocked by VPA pretreatment. These results suggest that an acute increase in GABA-ergic tone may inhibit gonadotropin secretion in the estrogen-deprived state, or when endogenous opioid inhibition is blocked in postmenopausal women on estrogens, as well as during the luteal phase of the menstrual cycle. It is possible that GABA-ergic pathways interact with opioids in the inhibitory modulation of gonadotropins in the human female
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