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Objective: To use gonadotropin-releasing hormone agonist (GnRH-a) instead of human chorionic gonadotropin (hCG) to induce oocyte maturation for in vitro fertilization (IVF)., Design: Pituitary and ovarian responses to GnRH-a and the outcome of IVF were studied prospectively. Data from patients injected with hCG were analyzed retrospectively., Setting: Program of IVF at the Rambam (Governmental) Hospital, Haifa, Israel., Patients and Interventions: One or two doses of buserelin acetate 250 to 500 micrograms were administered to six patients with moderate response (Estradiol [E2], 1,494 +/- 422 [+/- SD] pg/mL) and 8 patients with exaggerated response (E2, 7,673 +/- 3,028 pg/mL) to gonadotropin stimulation. Progesterone (P) and E2 were administered for luteal support., Main Outcome Measures: Gonadotropin-releasing hormone agonist effectively triggered luteinizing hormone (LH)/follicle-stimulating hormone (FSH) surge. Mature oocytes were recovered in all patients. Luteal E2 and P were lower than in patients injected with hCG. No signs of ovarian hyperstimulation syndrome were observed., Results: Serum LH and FSH rose over 4 and 12 hours, respectively, and were significantly (P less than 0.05) elevated for 24 hours. Of all mature oocytes, 67% fertilized and 82% cleaved. Four pregnancies were obtained., Conclusions: A bolus of GnRH-a is able to trigger an adequate midcycle LH/FSH surge, resulting in oocyte maturation and pregnancy. Our preliminary results also suggest that it allows a more accurate control of ovarian steroid levels during the luteal phase and may prevent the clinical manifestation of ovarian hyperstimulation syndrome.

Eighteen postmenopausal women with severe hot flashes had continuous recordings of finger temperature and skin resistance as objective indexes of flushing episodes, and serial measurements of anterior pituitary hormones as indirect indexes of hypothalamic neurotransmitter activity. Significant increases of growth hormone, adrenocorticotropic hormone (ACTH), and luteinizing hormone (LH) occurred with maximal concentrations at 30, five, and 15 minutes, respectively, after the onset of the skin temperature rises. No significant fluctuations of prolactin (PRL), thyroid-stimulating hormone (TSH), or follicle-stimulating hormone (FSH) were observed. The mean serum cortisol concentration increased 15 minutes after the hot flash, presumably consequent to the preceding elevation of ACTH. Pituitary ACTH release may be secondary to hypothalamic cooling, whereas increased growth hormone and LH output and the thermoregulatory adjustments comprising the flushing episodes are all consistent with cyclic episodes of increased hypothalamic norepinephrine activity.

To avoid the risks of oestrogen therapy in post-menopausal women, we have examined the effects of a progestin, megestrol acetate (MA), on hot flushes and bone metabolism. Ten normal post-menopausal women were studied before and after the oral administration of 20, 40 and 80 mg of MA daily for 4 wk at each dose level. Finger temperature and skin resistance were recorded for 8 h as objective indices of flushing and perspiration, respectively. The fasting ratios of urinary calcium: creatinine (Ca/Cr) and hydroxyproline: creatinine (OHPr/Cr) were used as indices of bone resorption. A reduction (P less than 0.01) of flushing episodes was noted on all dose levels of MA, with 56, 11, 6 and 1 flushes occurring on 0, 20, 40 and 80 mg of medication. A decrease (P less than 0.05) of Ca/Cr was noted only with 80 mg of MA, whereas OHPr/Cr remained unchanged. We conclude that progestin therapy may provide an alternative mode of treatment for post-menopausal hot flushes. Definitive demonstration of an effect on post-menopausal bone resorption will require a long-term study of bone density.

The effectiveness of clonidine in suppressing the occurrence of postmenopausal hot flashes was examined using a dose-response study design and objective recordings of hot flashes. Patients with frequent flashes were studied before and after oral administration of placebo and 0.1, 0.2, and 0.4 mg of clonidine daily for 2 weeks at each dose level. Finger temperature and skin resistance were recorded as indices of hot flash episodes. Four of 10 subjects beginning the study withdrew because of drug-related side effects. Clonidine was found to reduce significantly the frequency of hot flashes as compared with baseline (P less than .005) and with effects of the placebo (P less than .05). At the maximum dosage the mean rate of hot flash occurrence decreased 46%. It was concluded that clonidine does reduce the frequency of postmenopausal flashes.

A method for selective termination of multiple pregnancy by means of transvaginal ultrasonography-guided aspiration of gestational sacs is described. This technique was applied successfully in two women in whom the number of embryos was reduced from four to two at 7 weeks' gestation.

A study was conducted of 2 young adult women with pituitary insufficiency and complaints of hot flushes. Both underwent continuous recordings of skin temperature of the finger and skin resistance over the sternum as objective indices of flushing episodes. Frequent blood samples were also obtained during the recordings for the measurement of serum LH and FSH levels. During the 10 h of recording, 12 subjective hot flushes occurred and each was associated with a rise of finger temperature of greater than 1 C. Eighty-five percent of the temperature rises were associated with measurable decreases in skin resistance. The mean interval between flushes, the magnitude of the skin temperature and resistance changes, and the relationship of these changes to the onset of subjective flushes were identical to those observed in symptomatic postmenopausal women. Circulating gonadotropin levels were in the low to low normal range in comparison to values observed in premenopausal women and showed minimal pulsatile release. There were no significant correlations between finger temperature changes and LH levels in either subject. These results suggest that the previously described association of pulsatile LH release and the occurrence of hot flushes in postmenopausal women cannot be attributed to augmented LH secretion per se and, therefore, may be due to hypothalamic factors responsible for pulsatile LH release.

Following menopause, some women are troubled by hot flashes (episodes of flushing and perspiration), whereas others do not experience the symptom. To determine whether the extent of estrogen deficiency influences the occurrence of the disturbance, the authors measured the levels of estradiol (E2), estrone (E1), and sex-hormone binding globulin (SHBG), and the percent and total non-SHBG-bound E2 in 24 women with frequent hot flashes and 24 women who had never experienced the symptom. Significantly lower levels of E2 (P less than .002), E1 (P less than .05), percent non-SHBG E2 (P less than .05), and total non-SHBG-bound E2 (P less than .01) were found in the symptomatic women. Similar differences were confirmed in 18 subject pairs matched for age, years since menopause, and presence or absence of ovaries. The finding of a significantly (P less than .05) lower percent ideal body weight in the women with hot flashes suggests that the known effects of body weight on the rate of extraglandular estrogen production and the level of SHBG in postmenopausal women may be important variables determining the occurrence of hot flashes.