Patterns of prolactin (PRL) secretion were studied in a group of 18 hyperprolactinaemic patients with galactorrhoea and menstrual disorders and in a control group of thirty-two women in the early puerperium (24 h after a normal delivery) following provocative (TRH and Chlorpromazine) and suppressive (L-Dopa and bromocriptine) stimuli. Five out of the eighteen hyperprolactinaemic patients tested had radiological evidence of a pituitary tumour, and two were treated surgically. The early puerperium patients with elevated basal PRL levels (100--700 ng/ml) demonstrated a significant PRL response to the various treatments. On the other hand, in the hyperprolactinaemic group, an impaired PRL response to TRH, Chlorpromazine and L-Dopa was noted in patients with basal PRL levels higher than 30 ng/ml, whereas bromocriptine suppressed effectively PRL levels in all the hyperprolactinaemic patients tested irrespective of their basal PRL concentrations. The ratio between the fall in PRL concentrations (as percent of the baseline) after L-Dopa administration (delta%L) versus the PRL decrement after bromocriptine treatment (delta%B) was calculated. In the early puerperium group with normal pituitary prolactin secreting cells this ratio was equal to 0.8. In the hyperprolactinaemic group, the five patients with radiological evidence of a pituitary tumour had significantly lower ratios ranging from 0.2 to 0.57. These data suggest that in terms of prolactin release, prolactin producing tumour cells are intrinsically refractory to hypo thalamic dopaminergic signals. The calculation of individual delta%L/delta%B ratios may serve, therefore, as a valuable indicator for early detection of autonomous pituitary prolactin secreting cells and for evaluation of the extent of the pituitary lesion.

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Administration of clomiphene citrate (150 mg/day) for 5 days to twenty-four ovariectomized patients and seven normal female patients evoked a significant release of FSH and LH in the normal control group and suppressed the gonadotrophin secretion in the castrated patients. A similar suppressive effect on gonadotrophin secretion was noted in eight ovariectomized patients treated for 10 days with low doses (50 microgram/day) of ethinyl oestradiol. It is suggested that in the ovariectomized hypoestrogenic patients, clomiphene acted as an oestrogen, suppressing by a negative feedback action gonadotrophin release in a way similar to ethinyl oestradiol. In the normal control group with an adequate steroid environment, clomiphene acted (probably at the hypothalamic level) as an oestrogen antagonist and stimulated gonadotrophin secretion. In view of our findings, it seems as if the ability of anovulatory patients to respond to clomiphene treatment by increased gonadotrophin secretion depends upon the absolute concentration of the compound in the different organs and by the quantitative relation of clomiphene to the endogenous oestrogens.

The acute effect of pethidine administration on cAMP levels and ornithine decarboxylase (ODC) activity of fetal human brain from mid trimester abortion was studied. Both activities remained at the low level up to 9 h after intravenous injection of the drug to the pregnant mother. Our data suggest that pethidine causes at least temporary alterations in the cAMP levels and ODC activity of the fetal developing brain.

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