Our study suggests that thyroxine replacement therapy in patients with suppressed thyroid stimulating hormone levels increases postmenopausal bone loss.
Two monophasic oral contraceptives containing gestodene (GTD, 75 micrograms) and ethinylestradiol (EE, 30 micrograms) or norgestimate (NGS, 250 micrograms) and EE (35 micrograms) were compared during the first six cycles of use. The subjects were randomly assigned to receive either type: 97 received GTD/EE and 92 NGS/EE. Six women in the GTD/EE group and nine in the NGS/EE group withdrew from the study; three (3%) and two (2%), respectively, withdrew because of adverse reactions. A total of 562 cycles for GTD/EE and 523 for NGS/EE were available. No woman became pregnant during the study. Overall, 94.4% of cycles in the GTD/EE group and 92.8% in the NGS/EE group were normal. A similar incidence of breakthrough bleeding (0.2% of cycles for GTD and 1.6% for NGS) and spotting (5.4% vs. 5.6%) was observed. Amenorrhea was never reported. Duration of withdrawal bleeding tended to be slightly longer in the NGS/EE group, significantly so for cycles 2 (0.5 days, p = 0.016), 4 (0.5 days, p = 0.031) and 5 (0.4 days, p = 0.045). Cycle 2 was significantly longer in the GTD/EE group (0.3 days, p = 0.027). Side-effects were reported by 12 (12%) women in the GTD/EE group and 13 (14%) in the NGS/EE group. The most common side-effects were headache (five cases (5%) in the GTD/EE group and two (2%) in the NGS/EE group) and breast pain (three (3%) and eight (9%) cases respectively). There were no statistically significant differences between the two groups with respect to change in body weight or changes in blood pressure and in laboratory data.(ABSTRACT TRUNCATED AT 250 WORDS)
The aim of the present study was to evaluate the efficacy and tolerability of the dopamine agonist drug dihydroergocryptine in the suppression of puerperal lactation. A single blind and placebo-controlled study was performed. A total of 90 postpartum women was acutely or repeatedly treated with dihydroergocryptine at different doses in order to investigate the efficacy of this drug in the suppression of puerperal lactation and to find the optimum dose for therapy. Prolactin levels, mammary symptomatology and rebound effects were monitored during the repeated treatment and also 1 and 8 days after drug discontinuation. With acute administration, dihydroergocryptine significantly reduced prolactin levels only at the dose of 10 mg and not at 5 mg. With repeated administration, a daily dose of 15 mg was more effective than 10 mg in reducing prolactin levels and in suppressing puerperal lactation. No side-effects occurred during the treatment. These results suggest that dihydroergocryptine might be considered an effective drug in the suppression of puerperal lactation.
We treated 18 infertile patients affected by histologically confirmed luteal phase deficiency with 75 IU of purified follicle-stimulating hormone (FSH) daily during the first 5 days of the cycle. Patients who were not pregnant after the first cycle of treatment underwent a second cycle. In the second cycle the daily doses of purified FSH were doubled if luteal phase deficiency had persisted during the first cycle. During the two cycles before treatment and during treatment, patients underwent an endometrial biopsy 1-3 days before the expected onset of menses. An assessment of progesterone serum concentrations was also performed on days 8, 6 and 4 before the expected onset of menses. Treatment was administered in a total of 33 cycles resulting in 30 ovulatory cycles. Six pregnancies were achieved. Among non-conception ovulatory cycles, 13 presented delayed endometrial dating and 11 normal endometrium. The mean +/- SD of the sum of the three progesterone determinations was 14.7 +/- 1.4 ng/ml in pretreatment cycles, 14.6 +/- 1.6 ng/ml in cycles with normalization of endometrial dating, 14.8 +/- 1.7 ng/ml in cycles with persistence of luteal phase deficiency and 30.4 +/- 3.0 ng/ml in conception cycles (P < 0.05 versus other groups). We conclude that purified FSH, if effective in the treatment of luteal phase deficiency, does not act through an increase in progesterone concentrations.
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