Five women with hypothalamic amenorrhea were treated with LH-RH (10-15 microg i.v. at 90 min intervals for 17-20 days). In all women this chronic intermittent LH-RH administration resulted in a normalization of serum gonadotropin levels. Four women exhibited preovulatory estradiol serum levels with subsequent LH peaks. In three women the LH peaks were followed by normal luteal phase serum progesterone levels. One woman with hyperprolactinemic amenorrhea was also treated with the same therapeutic regimen which induced ovulation as judged from normal luteal phase serum progesterone levels. The results indicate that normal pituitary-ovarian function can be established in hypothalamic amenorrhea by chronic intermittent administration of LH-RH. They also suggest that in the human female hypothalamic LH-RH function may be only permissive in that the cyclicity of endocrine events during the menstrual cycle is regulated on pituitary and ovarian levels. Hyperproactinemic amenorrhea appears to be associated with insufficient endogenous LH-RH secretion which can be substituted by exogenous chronic intermittent administration of LH-RH. Elevated prolactin levels per se do not interfere with the pituitary positive feedback mechanisms nor with the gonadotropin action on the ovarian level.

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Placental transfer of radioactive C 14 -digitoxin was investigated in four pregnant women. The concentration of the labeled drug and its metabolic products in the various fetal organs was determined. Less than 1 per cent of the administered glycoside was detected in the fetus as unchanged digitoxin and less than 3.5 per cent as its metabolites. The fetal heart and kidney of 11 to 12 weeks gestation had the highest concentrations. However, at near term the fetal liver, gallbladder and intestine had somewhat similar concentrations. Metabolic conversion of the cardiac glycoside by fetal liver as well as biliary excretion is indicated from the tissue distribution data.

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