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THE ROLE OF DOPAMINERGIC DEPLETION IN THE PATHOGENESIS OF CUSHING'S DISEASE AND THE POSSIBLE CONSEQUENCES FOR MEDICAL THERAPY

In four patients suffering from pituitary dependent Cushing's syndrome plasma ACTH and cortisol were lowered after a single dose of 2.5 mg bromocriptine, but ACTH and cortisol responses to hypoglycaemia remained absent after bromocriptine administration. In contrast, in three of these patients a growth hormone response which had previously been absent appeared to return 3 h after bromocriptine. While untreated, basal prolactin levels were at the upper limit of normal and a subnormal response was seen after hypoglycaemia. With bromocriptine therapy, basal prolactin levels were depressed and no reaction to hypoglycaemia was seen. In three patients 400 μg TRH did not elicit an increase of TSH and growth hormone while a normal increase of prolactin was induced. In one patient a dose of 2.5 mg bromocriptine caused an attack of nausea and hypotension possibly complicated by relative adrenocortical insufficiency. Four patients were studied during treatment with a daily dose of 5–20 mg bromocriptine for 1–20 weeks. In one patient, pituitary‐adrenocortical function escaped three times from the effect of bromocriptine treatment. One patient showed an increase of urinary 17‐OHCS during treatment lasting 7 days. Two other patients responded well to bromocriptine therapy, In one patient the treatment had to be stopped after 7 days because of complaints of extreme muscle weakness, while urinary 17‐OHCS had become low‐normal; in another patient Cortisol Secretion Rate was normalized throughout bromocriptine treatment lasting 20 weeks.