Endocrine abnormalities in patients undergoing long-term hemodialysis. The role of prolactin

The possible role of hyperprolactinemia in the sexual and thyroid abnormalities of patients with end-stage renal failure was studied in 56 patients undergoing long-term hemodialysis. Seventy-three per cent of the women and 25 per cent of the men receiving no prolactin (PRL)-enhancing drugs had elevated PRL levels (25 to 200 ng/ml, normal <20 ng/ml), and all those patients who were receiving α-methyldopa treatment (13 patients) had even higher PRL levels (30 to 1,107 ng/ml). The response of PRL to the administration of thyrotropin-releasing hormone (TRH) was blunted and prolonged, suggesting that hyperprolactinemia was in part due to prolonged plasma half-life of the hormones; this was confirmed by the insufficient PRL lowering effect of a single dose of bromocriptine in a short-term test, whereas a longer trial of six weeks demonstrated the PRL-suppressive effect of the drug.Amenorrhea or oligomenorrhea was a constant feature in women, four of whom also showed galactorrhea; during bromocriptine treatment, recurrence of menses was observed in some of the hyperprolactinemic amenorrheic women. Men with impotence had higher PRL levels than men with normal potency. Lack of appropriate elevation of luteinizing hormone (LH) levels despite low estradiol or testosterone levels was observed in approximately one third of the hyperprolactinemic subjects of both sexes, but also in a similar proportion of normoprolactinemic ones. However, treatment with bromocriptine resulted in an increase in basal LH in 13 of 16 patients with hyperprolactinemia. These data demonstrate that PRL measured in patients with advanced renal failure is biologically active and that hyperprolactinemia is one of the major factors in the hypogonadism of these patients. In addition, integrated circulating LH after the injection of exogenous luteinizing hormone-releasing hormone (LHRH) was normal, despite prolonged plasma half-life, suggesting that pituitary response was in fact impaired. Unrelated to PRL levels, 47 per cent of the patients had slightly elevated thyroid-stimulating hormone (TSH) levels, with normal total and free thyroxine (T4). Although triiodothyronine (T3) tended to cluster in the low-normal area, reverse-T3 levels were not consistent with preferential deiodination of T4 to reverse-T3. Elevation of the basal TSH levels was, at least in part, due to prolonged plasma half-life of the hormone. These biochemical changes were not related to clinically detectable dysfunction of the thyroid.