Hyperglycemia in AMI is associated with poor outcome even among patients without known diabetes. This finding underlines the need for aggressive glucose management in this setting and may support a more vigorous screening strategy for early recognition of diabetes.

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Basal prolactin concentrations in 357 patients with renal disease of defined pathology have been compared with those in 210 control subjects. Elevated prolactin concentrations were found in 113 renal patients (32%) including 53 patients in whom elevated concentrations were possibly attributable to drug therapy. In the remaining 60 patients who had hyperprolactinaemia not attributable to drugs, elevated concentrations (P less than 0.005) were found exclusively in patients with impaired renal function. A significant correlation was observed between prolactin and creatinine concentrations in these patients (r = 0.45 P less than 0.005) and prolactin reverted towards normal after successful renal transplantation. A significant arteriovenous prolactin concentration difference across the kidney (mean 16% range 8-29% P less than 0.02) was found in seven patients with non-renal non-endocrine disease. It is concluded that the hyperprolactinaemia found commonly in patients with impaired renal function is only partly attributable to drug therapy. The positive correlation between prolactin and creatinine reversion of prolactin towards normal after successful transplantation and arteriovenous hormone concentration differences across the normal kidney suggests that the kidney has a important role in prolactin metabolism. Abnormal regulation of prolactin secretion in renal failure may also be involved.

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SUMMARYThe laboratory assessment of prolactin status was evaluated by detailed study of 921 subjects (587 normal subjects and 334 patients with pathological conditions). The effect on serum prolactin levels of age, sex, circadian rhythm, pulsatility of secretion, stress, drug ingestion, and pregnancy was defined in normal subjects. The normal prolactin responses to stimulation (TRH, metoclopramide) and suppression (t-dopa, bromocriptine) were also determined. Basal prolactin levels were measured in patients with defined pathological conditions including prolactinoma, idiopathic hyperprolactinaemia, acromegaly, Cushing's disease, chronic renal failure, primary hypothyroidism, pituitary ablation, Kallman's syndrome, Nelson's syndrome, growth hormone deficiency, gonadotrophin deficiency, craniopharyngioma, panhypopituitarism, and chronic progressive arthropathy. Based on these data, a strategy for the routine laboratory assessment of prolactin status is outlined. NORMAL SUBJECTS

In a study of 221 patients with progressive uraemia and after successful renal transplantation, all patients had normal levels of plasma 11-hydroxycorticosteroids and sex hormone binding globulin (SHBG). Concentrations of T4 and Ts fell significantly (P < 0.005) with progressive uraemia whilst TSH remained normal. Levels of gonadal steroids also fell significantly (P < 0.0005) and in some patients there was gonadal failure with LH and FSH > 50 U/l; in the remainder, there was a modest increase in LH and minor increase in FSH as renal function deteriorated. Elevated Prl concentrations (P < 0.005) occurred even in moderate chronic renal failure and levels rose with progressive uraemia. In patients on maintenance haemodialysis, TSH response to thyrotrophin releasing hormone (TRH) was signifi¬ cantly blunted (P < 0.01) at 20 min but showed a late rise at 60 min; basal levels of GH were elevated in 27% and there was a heterogeneous GH response to TRH; LH response to gonadotrophin releasing hormone (GnRH) was normal whilst response of FSH was significantly blunted (P < 0.01). Irrespective of basal Prl level, there was a grossly blunted Prl response to TRH and metoclopramide (MCP) and no suppression of Prl after acute administration of i.-dopa or bromocriptine. Following successful renal transplantation, endocrine status was entirely normal.It is concluded that gross biochemical endocrine abnor¬ malities arise with progressive uraemia, which are not ameliorated by maintenance haemodialysis but are abolished by successful transplantation. There is evi¬ dence of both hypothalamic and pituitary dysfunction contributing to these anomalies, which may be sensitive indices of non urea and creatinine related uraemic toxicity, and whose significance requires further evaluation.

Specific binding of 125I-labelled ovine prolactin iodinated by a lactoperoxidase method was demonstrated in crude membrane preparations of kidneys and adrenals of male Sprague-Dawley rats and livers from female rats. Membrane preparations derived from the 100,000 g fractions of tissue homogenates contained most of the specific prolactin binding. Kinetic and affinity characteristics of prolactin binding to kidney membranes were examined in detail. Maximal specific binding occurred after incubation for 30 h at room temperature. Scatchard analysis indicated that prolactin binding to kidney membranes was of high affinity (dissociation constant = 1.4 x 10(-10) mol/l) and similar to that for liver membranes, although kidney membranes from male rats bound approximately sixfold less prolactin/mg membrane protein than did liver membranes from female rats. Specific prolactin binding was demonstrated in both renal medulla and cortex. Autoradiography showed maximal prolactin binding activity in the epithelial cells of the proximal tubule and faint activity in the tubular cells throughout the nephron. Specificity of uptake by proximal tubular cells was indicated by the gross reduction in prolactin activity when excess ovine prolactin was administered simultaneously. The demonstration of specific binding sites for prolactin localized primarily in the proximal tubules was consistent with renal action of prolactin, predominantly on sodium metabolism.