To study the effects of different types of progestogens on lipoprotein metabolism, we treated three groups of postmenopausal women (six subjects each) for three weeks with estradiol valerate, 2 mg per day, and continued the treatment with different sequential estradiol-progestogen regimens as follows: Group A received norethindrone acetate, 10 mg per day, from Day 15 to Day 24 of the cycle; Group B, medroxyprogesterone acetate, 10 mg per day; and Group C, norgestrel, 0.5 mg per day. These regimens were followed by two consecutive cycles. Total cholesterol decreased in all groups by 10 to 18 per cent from the base-line values (P < 0.05). High-density-lipoprotein (HDL) cholesterol decreased by 20 per cent from the base-line level during treatment with both the estradiol-norethindrone acetate (P < 0.05) and estradiol-norgestrel (P < 0.01) regimens, whereas estradiol with medroxyprogesterone acetate was not associated with a significant change in HDL cholesterol. Our results suggest that the androgenic progestogens of the 19-nortestosterone series reverse the beneficial effect of postmenopausal estrogen treatment on HDL cholesterol, whereas the hydroxyprogesterone derivative medroxyprogesterone acetate has no such effect.

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Prolactin (PRL) and thyrotropin (TSH) responses to a 200 mug intravenous thyrotropin-releasing hormone (TRH) bolus were measured by radioimmunoassay in 11 women with hyperprolactinemic amenorrhea and 9 with normoprolactinemic amenorrhea. In all cases, the tests were carried out under basal conditions and repeated during bromocriptine treatment. In women whose basal PRL level was normal; TRH caused a maximal PRL increment of 85 +/- 25.2 mug/l (mean +/- SE), while those women whose basal PRL level was raised showed a smaller increase (5.2 +/- 11.9 mug/l) (P=0.02). The peak levels were not significantly different in these two groups (95.0 +/- 26.7 and 134.6 +/- 35.9 mug/l) (P is greater than 0.1). During bromocriptine treatment, the raised PRL levels decreased in all cases, but levels over 30 mug/l remained in 3 patients, one of whom turned out to have a pituitary tumor. Prolactin responses to TRH were markedly inhibited in normoprolactinemic patients by the dose of bromocriptine used. The mean maximal net increase of PRL was 2.0 +/- 0.9 mug/l in normoprolactinemic patients and 11.0 +/- 8.1 mug/l in hyperprolactinemic patients taking bromocriptine. After TRH stimulation during bromocriptine, the peak PRL levels in hyperprolactinemic patients were higher (32.7 +/- 10.5 mug/l) than in normoprolactinemic patients (7.2 +/- 1.5 mug/l). Unlike what has been described for hypothyroid patients, the basal TSH level in euthyroid amenorrhea patients was not affected by bromocriptine, and we found that bromocriptine has no effect on the TRH-TSH response.

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