Timing of initiation and dose schedule of leuprolide influence the time course of ovarian suppression.

Suppression of the ovary using a gonadotropin releasing-hormone agonist prior to stimulation for oocyte retrieval*

The study was designed to investigate the source of progesterone secretion during pituitary suppression and ovarian stimulation. It involved 416 women undergoing in-vitro fertilization (IVF) who were treated with gonadotrophin-releasing hormone agonist (GnRHa) and human menopausal gonadotrophin (HMG) (group I), 139 women undergoing ovulation induction with HMG only (group II) and nine women who were diagnosed previously as late-onset adrenal hyperplasia and treated continuously with dexamethasone, in addition to ovulation induction (group III). During HMG treatment, serum oestradiol and progesterone were measured every 1-2 days. If progesterone concentration exceeded 3.0 nmol/l, at least 36 h before human chorionic gonadotrophin (HCG) administration, the patients were prospectively randomized to treatment with dexamethasone or not and the hormones concentrations were measured again 12 h later. Mean age and pretreatment serum concentrations of dehydroepiandrosterone sulphate, androstenedione, testosterone and luteinizing hormone/follicle stimulating hormone (LH/FSH) ratio, were not significantly different in the patients with and without progesterone elevation. Pituitary down-regulation did not reduce the incidence of progesterone elevation (13.9 and 12.2% in groups I and II respectively), while in group III, progesterone concentrations did not increase. After dexamethasone administration a significant decrease in serum progesterone concentration was demonstrated (mean +/- SD, -2.1 +/- 1.4 and -1.6 +/- 1.2 in groups I and II respectively, while in the untreated patients it increased (+1.9 +/- 1.9 and +4.2 +/- 4.8). The increase in serum progesterone concentrations was not accompanied by an increase in cortisol and 11-deoxycortisol but by an increase in LH. After dexamethasone administration the concentrations of cortisol, 11-deoxycortisol and LH significantly decreased. Progesterone concentration was positively correlated with both oestradiol concentration (r = 0.290; P < 0.05) and the number of oocytes retrieved (r = 0.207; P < 0.05). We conclude that at least a part of serum follicular-phase progesterone appears to be of adrenal origin. High oestrogen concentrations (or other ovarian factors) may cause changes in the hypothalamic-pituitary-adrenal axis and in adrenal enzyme activity as a part of the complex 'cross-talk' between the hypothalamic-pituitary-ovarian and the hypothalamic-pituitary-adrenal axes.

/pdf/the-origin-of-serum-progesterone-during-the-follicular-phase-46m1cw47jw.pdf

The origin of serum progesterone during the follicular phase of menotropin-stimulated cycles.

Long-term suppression of ovarian function by a luteinizing-hormone releasing hormone agonist implant in patients with endometriosis

R.H.Mehta1 and T.C.Anand Kumar cysts remains unclear. Three hypotheses have been proposed to explain this phenomenon: Hope Infertility Clinic, Reproductive Health Clinic And Research Centre, 12 Aga Abbas Ali Road, Bangalore 560 042, India Hypothesis I 1To whom correspondence should be addressed Commencement of GnRH agonist, either as a single dose of This debate was previously published on Webtrack 96, the long-acting form or as daily s.c. doses, results in an initial December 1, 1999 transient ‘flare-up effect’ on the pituitary leading to a surge of circulating gonadotrophins. It is postulated that this surge Pituitary desensitization with gonadotrophin-releasing hortriggers the growth of the primordial follicles. The absence of mone (GnRH) agonists prior to ovarian stimulation is now a a subsequent luteinizing hormone (LH) surge prevents the routine part of most in-vitro fertilization (IVF) and intracytorupture or luteinization of the follicles which then get converted plasmic sperm injection (ICSI) procedures. The two criteria into cystic structures. This hypothesis was first proposed to which are used to determine whether pituitary desensitization explain the presence of ovarian cysts after GnRH agonist has occurred are: (i) serum oestradiol concentrations of 50 administration (Feldberg et al., 1989) and then later by most pg/ml and (ii) the absence of any ovarian cysts with a diameter other investigators reporting on the presence of ovarian cysts 15–20 mm(Ron-El et al., 1989; Sampaio et al., 1991; Jenkins after administration of GnRH agonists ( Herman et al., 1990; et al., 1993; Tarlatzis et al., 1994; Keltz et al., 1995). It takes Ron-El et al., 1990; Stewart et al., 1992; Jenkins et al., 1993; ~10–15 days for this effect of GnRH agonist to manifest on Tarlatzis et al., 1994). the ovary, irrespective of the phase of the cycle (early follicular The incidence of ovarian cyst formation following GnRH phase or mid-luteal phase) in which the GnRH agonist is agonist treatment in IVF cycles is related to the serum started, the type of GnRH agonist used (long-acting triptorelin progesterone concentrations on the day of GnRH agonist or short-acting buserelin or leuprolide acetate) and the mode treatment initiation (Marqalioth et al., 1991) and is lower when of administration (nasal spray, i.m. administration of longprogesterone is administered prior to starting GnRH agonist acting preparations or s.c. administration) (Sampaio et al. treatment (Aston et al., 1995). This is attributed to the ability 1991; Parinaud et al., 1992; Jenkins et al., 1993). of progesterone to decrease gonadotrophin release in response There have been several reports on the presence of ovarian to GnRH agonist (Araki et al., 1985), therefore the initial cysts while the women are still undergoing treatment with transient ‘flare-up effect’ of GnRH agonist becomes subdued GnRH agonists (Feldberg et al., 1989; Ron-El et al., 1989; and subsequently the formation of cysts. This hypothesis Sampaio et al., 1991; Jenkins et al., 1992; Parinaud et al., explains the presence or formation of ovarian cysts after GnRH 1992; Stewart et al., 1992; Jenkins et al., 1993; Tarlatzis et al., agonist administration, but fails to explain how these ‘cysts’ 1994; Keltz et al., 1995; Weissman et al., 1998). The elevated continue growing and secreting oestradiol in the absence of concentrations of serum oestradiol and the high concentration any endogenous or exogenous gonadotrophin stimulation for of oestradiol in the fluids aspirated from these cysts indicate a prolonged period of time. that these cysts originate from the ovarian follicles and have Several authors (Ron-El et al., 1989; Herman et al., 1990) been termed as ‘functional follicular cysts’ (Jenkins et al., have clearly demonstrated that there is a sharp rise in the 1993). Some of these cysts may also be endometriomata serum FSH and LH concentrations within the first 48 h of (Yanushpolsky et al., 1998). GnRH agonist administration with a concomitant rise in The incidence of formation of such cysts is reported to be oestradiol concentrations. Daily administration of buserelin or 2–40% (Feldberg et al., 1989; Ron-El et al., 1989; Parinaud leuprolide acetate for 4 days after the administration of longet al., 1992; Jenkins et al., 1993; Tarlatzis et al., 1994). There acting GnRH agonist results in a decrease in both serum are some reports that the incidence is higher in older women gonadotrophin and oestradiol values. In cases where these (Keltz et al., 1995); in those in whom GnRH agonists have cysts have been observed, the gonadotrophin concentrations been started in the follicular phase, compared with those in decrease but the diameter of the cysts and circulating oestradiol whom it is started in the mid-luteal phase (Ben-Rafael et al., concentrations are maintained or increase (Herman et al., 1990). 1990); and in those having higher basal (day 2) values of According to this hypothesis, if it is the ‘flare-up’ effect of follicle stimulating hormone (FSH) in the pre-treatment cycle (Keltz et al., 1995). The reasons for the formation of such the GnRH agonist which triggers the rise in gonadotrophin

Can GnRH agonists act directly on the ovary and contribute to cyst formation

The present study was designed to elucidate gonadal steroid influences on gonadotropin release and subsequent pituitary desensitization to GnRH. Sixteen women, 10 of whom were normal and 6 of whom had hypogonadism, were infused with GnRH at rates ranging from 0.313–10 eg/h via an indwelling iv catheter for 66 h. Blood samples obtained throughout the GnRH infusion were analyzed for LH, FSH, estradiol, and progesterone. A prompt and substantial release of gonadotropin occurred in women with ovarian failure or during the luteal phase in normal women compared with that during the follicular phaseof the menstrual cycle. Thereafter, a gradual decrease in gonadotropin secretion occurred due to pituitary desensitization, which was slower in the follicular phase than in other groups. A dose-related increase in integrated LH release occurred during GnRH infusion, but this response tapered off with administration of large doses of GnRH to women with ovarian failure or during the luteal phase. In contrast, it increas...

Reduction in pituitary desensitization and prolongation of gonadotropin release by estrogen during continuous administration of gonadotropin-releasing hormone in women: its antagonism by progesterone.

The present study was designed to elucidate gonadal steroid influences on gonadotropin release and subsequent pituitary desensitization to GnRH Sixteen women, 10 of whom were normal and 6 of whom had hypogonadism, were infused with GnRH at rates ranging from 0313–10 eg/h via an indwelling iv catheter for 66 h Blood samples obtained throughout the GnRH infusion were analyzed for LH, FSH, estradiol, and progesterone A prompt and substantial release of gonadotropin occurred in women with ovarian failure or during the luteal phase in normal women compared with that during the follicular phaseof the menstrual cycle Thereafter, a gradual decrease in gonadotropin secretion occurred due to pituitary desensitization, which was slower in the follicular phase than in other groups A dose-related increase in integrated LH release occurred during GnRH infusion, but this response tapered off with administration of large doses of GnRH to women with ovarian failure or during the luteal phase In contrast, it increas

Reduction in Pituitary Desensitization and Prolongation of Gonadotropin Release by Estrogen during Continuous Administration of Gonadotropin-Releasing Hormone in Women: Its Antagonism by Progesterone

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Reduction in pituitary desensitization and prolongation of gonadotropin release by estrogen during continuous administration of gonadotropin-releasing hormone in women: its antagonism by progesterone.

Reduction in Pituitary Desensitization and Prolongation of Gonadotropin Release by Estrogen during Continuous Administration of Gonadotropin-Releasing Hormone in Women: Its Antagonism by Progesterone