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Infusion of growth-hormone release inhibiting hormone (G.H.-R.I.H.) in four fasting subjects reduced plasma glucagon and insulin concentrations to undetectable levels and this was associated with a highly significant decline in plasma-glucose (28±S.E.M. 3 mg. per 100 ml. in 1 hour, p

The administration of the long-acting dopaminergic agonist bromocriptine to five healthy volunteers inhibited the rise in plasma-aldosterone that normally follows the administration of frusemide. This inhibition was not due to a lowering of plasma-renin activity. It is suggested that dopamine may modulate the normal secretion of aldosterone either directly, or indirectly, possibly by inhibition of prolactin secretion.

Growth hormone release inhibiting hormone (GHRIH) was administered by constant infusion over 75 minutes to eight acromegalic patients at different doses. 100 to 1,000 mug were equally effective in reducing circulating growth hormone (GH) levels; 25 mug lowered GH levels in only five patients, and at this dose the extent of the fall was smaller than from doses of 100 mug or more. 10 mug was ineffective. Injection of single doses of 500 mug by intravenous, subcutaneous, and intramuscular routes caused only small and transient reductions in GH levels, though the effect was improved by injecting the hormone intramuscularly in 2 ml of 16% gelatin. Injection of a suspension of 4 mg GHRIH in 1 ml of arachis oil lowered growth hormone levels for between three and four hours.In four acromegalic patients an oral 50-g glucose tolerance test was performed during a continuous infusion of either saline or 1,000 mug GHRIH. The "paradoxical" rise in growth hormone seen in these patients during the saline infusion was suppressed by GHRIH. The blood glucose responses were, moreover, modified by GHRIH in that the peak was delayed and occurred at the end of the infusion in each case. A "normal" glucose tolerance curve was converted to a "diabetic" type of response in two patients. This effect could be accounted for by the inhibition of insulin secretion known to occur with large doses of GHRIH.We speculate that acromegaly may be primarily a hypothalmic disease due to deficiency of GHRIH resulting in excessive secretion of growth hormone from the pituitary and adenoma formation due to inappropriate and prolonged stimulation of the pituitary.

A new long-acting repeatable injectable form of bromocriptine, (Parlodel LAR, Sandoz, Basle, Switzerland) has recently been developed. We studied the clinical, hormonal and radiological changes in six female patients with microprolactinomas and eight (3 female and 5 male) with macroprolactinomas receiving monthly injections of Parlodel LAR 50 to 100 mg for 6 months. Five patients with microadenomas and 4 with macroadenomas had normal prolactin (PRL) levels with Parlodel LAR 50 mg after one (5 patients), two (2 patients), or five (2 patients) injections; two patients with macroadenomas had normal or near normal PRL levels only after 4 monthly injections of 100 mg. Clinical improvement paralleled the changes in serum PRL. A complete normalization of a visual field defect occurred in one patient after 5 months of therapy. Marked shrinkage of the adenoma was shown by magnetic resonance and/or computed tomographical imaging in three patients with macroadenomas after 1 week. Side-effects were mild and usually transient. Parlodel LAR represents a novel treatment of hyperprolactinemic states which is both effective and well tolerated, and appears to be a useful alternative to oral therapy for long-term treatment.

Elevated plasma and urinary corticosteroid levels, a disturbed diurnal rhythm, and adrenocortical resistance to dexamethasone suppression were seen in three patients with severe depression. These abnormalities of pituitary-adrenal function are similar to those observed in Cushing's syndrome, but they disappeared with successful treatment of the depression. Diagnostic confusion could arise in a patient with depression and suspected Cushing's syndrome.

The contributions of changes in the rate of gastric emptying and insulin response to the abnormalities of oral glucose tolerance found in thyroid disease have been studied in 12 thyrotoxic and 9 hypothyroid patients. In thyrotoxicosis, rapid gastric emptying was associated with elevated peak blood-glucose and insulin levels, but there was evidence suggesting some impairment of insulin response. However, in the fasting state, despite normal blood-sugar concentrations plasma-insulin levels were elevated. 2 patients were prediabetic, with diabetic glucose-tolerance curves and markedly impaired insulin release when thyrotoxic; although their glucose tolerance reverted to normal with treatment of the thyrotoxicosis, their insulin responses remained subnormal. In hypothyroidism gastric emptying was prolonged; blood-glucose concentrations were depressed both fasting and after glucose loading, while insulin levels were unchanged. With the exception of hyperinsulinaemia at the end of the glucose-tolerance tests in the hypothyroid patients, all the abnormalities were reversed by treatment.