Patients with anorexia nervosa frequently manifest impaired glucose tolerance. However, alterations in pancreatic glucagon secretion have also been associated with alterations in diabetes mellitus. For this reason, pancreatic alpha- and beta-cell responses to glucose load were measured in 25 anorexic patients both before and after treatment. The baseline glucose challenge failed to suppress plasma glucagon levels in the patients. However, in the control subjects and patients after treatment, glucagon levels were suppressed after glucose ingestion. Plasma glucose levels during the baseline challenge were significantly higher than those of the control subjects; however, after treatment glucose responses were nearly normal. Finally, insulin responses at baseline and after treatment were lower in the patients than in control subjects. These results suggest that the impaired glucose tolerance manifested by anorexic patients may be attributable to significant alterations in both pancreatic alpha- and beta-cell secretions and in pancreatic alpha-cell and glucose interrelationships.

In order to clarify the role played by pancreatic \g=a\-celldysfunction in the impaired glucose recovery from hypoglycemia in patients with anorexia nervosa, the response of pancreatic \g=a\-cells to insulin-induced hypoglycemia was investigated in 16 patients with anorexia nervosa before and after treatment. The results were compared with those obtained after loading with arginine. Before treatment, despite comparable falls in plasma glucose levels, glucagon secretion was significantly reduced in the anorectic patients compared with control subjects. In addition, glucose recovery from hypoglycemia in the patients was attenuated. However, after treatment, both glucagon secretory activity and plasma glucose recovery following insulin-induced hypoglycemia were restored to normal. Plasma glucagon responses to arginine infusion were not significantly different in the untreated anorectic patients and control subjects. However, the plasma insulin response in the patients was significantly lower than in the control group. These results suggest that the impaired recovery of plasma glucose levels from insulin-induced hypoglycemia in patients with anorexia nervosa is primarily attributable to impaired pancreatic \g=a\-secretorycapability. In addition, this abnormality in pancreatic \g=a\-cellfunction is reversible with treatment leading to improved nutrition and weight gain.

Studies were performed in 120 patients with simple goitre, defined as relatively soft diffuse goitre. All were clinically and biochemically euthyroid and their antithyroid antibodies were negative. The TRH test was performed in 115, and a T3 suppression test was performed in 99 after the TRH test, while satisfactory biopsies of the thyroid were obtained in 37. The results showed that 28 of the 115 cases (24%) had an abnormal response to TRH; 8 (7%) were hyporesponders and 20 (17%) were hyperresponders. The T3 suppression test showed that 3 of 99 cases (3%) were non-suppressible. As determined by histological examination of the needle biopsy specimen, 17 of the 37 cases (46%) had normal follicles without lymphocytic infiltration, 10 (27%) had diffuse chronic thyroiditis, 5 (14%) had focal thyroiditis and 4 (11%) had diffuse epithelial hyperplastic change, and 1 (3%) had an adenomatous goitre. It is suggested that simple goitre defined as above includes various thyroid diseases and that the results of TRH tests, antithyroid antibody estimations and histological findings do not correlate in many patients.

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