Excessive egg consumption, xanthomatosis, and hypercholesterolaemia.

methyldopa given for two to six weeks causes a rise in serum prolactin concentrations in hypertensive patients. Our studies have confirmed that patients on long-term treatment with methyldopa have raised serum prolactin concentrations. Furthermore, we have shown that even a single oral dose of methyldopa will increase serum prolactin concentrations. Basal serum prolactin levels varied considerably in the seven patients who received a single dose of methyldopa, but they did not correlate with the level of blood pressure. That the rise in prolactin produced by methyldopa was not merely a result of hypotension is suggested by the results in two patients given bethanidine (which lowers blood pressure by a peripheral adrenergic neurone blocking effect); there was no change in serum prolactin concentrations in spite of a considerable fall in blood pressure. It is difficult to assess the importance of these drug-induced changes in serum prolactin concentrations. There are considerable species differences in the effects of prolactin itself on blood pressure,1' 14 and its effect in man is unknown. Whether prolactin is a mediator of the sodium retention produced by methyldopa is also open to question.15 Finally, galactorrhoea is seen in a few patients on methyldopa, but the relation of this to the magnitude of the prolactin response is not clear. The control of GH secretion is relatively more complex than that of prolactin. GH secretion is modulated by catecholamines, and in man there is evidence that alpha-adrenergic stimulation increases and beta-adrenergic stimulation decreases circulating concentrations.16 Furthermore, administration of levodopa, the precursor of dopamine, has been reported to increase circulating GH.17 When GH secretion was measured over 24 hours in a group of Parkinsonian patients given levodopa, however, 79 , of the time GH concentrations failed to rise.18 Using insulin hypo-glycaemia as the stimulus for GH secretion, the difference between patients on short-term and long-term methyldopa therapy may be explicable in terms of the time course of substitution of endogenous catecholamines with metabolites of methyldopa within the brain. There may be a similar explanation for the greater effect of methyldopa on serum prolactin levels in patients on prolonged methyldopa treatment, since, unlike GH, prolactin secretion is inhibited by catecholamines."1 These data suggest a novel aspect of the effects of long-term hypotensive therapy. As new, more potent, centrally acting antihypertensive drugs become available, hormonally mediated effects may become of considerable importance. We are grateful to Dr Ruth Haslam and her colleagues in …