Somatostatin, a recently synthesized hypothalamic growth hormone release-inhibiting factor (GIF), was used in the cyclic and linear form. In all subjects studied, the cyclic GIF inhibited gastrin secretion during basal conditions as well as during a standard food stimulus, with immediate rebound after the infusion was stopped. Similar responses were observed in a hypophysectomized patient, indicating that this effect of GIF was independent of suppression of growth hormone secretion. Cyclic and linear GIF, when administered in normal subjects during an infusion of synthetic human gastrin I, almost totally suppressed gastric secretion. The results indicate that GIF is a potent inhibitor of gastric secretion and gastrin release.

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1. Prostaglandin A-, prostaglandin E- and prostaglandin F-like substances were determined radioimmunologically in antral biopsy material obtained by endoscopy. 2. In patients with gastritis, the concentrations of prostaglandin (E+A)-like substances were six times as high and of prostaglandin F-like substances twice as high as in normal subjects. In chronic atrophic gastritis, the concentrations of prostaglandin (E+A)-like material was four times as high as in normal subjects whereas prostaglandin-F like material remained unchanged. In acute gastric ulcer, prostaglandin (E+A)-like material reached concentrations four times times higher than in normal subjects, accompanied by a fivefold increase of prostglandin F-like substances. After healing of the gastric ulcer, prostaglandins returned to normal values. 3. There was no correlation between gastrin and prostaglandins in all biopsy specimens.

To elucidate further the pathogenesis of steroid-induced ulceration, plasma gastrin levels, both basal and after a test meal, were studied in normal volunteers and patients treated with glucocorticoids or corticotropin. In normal subjects the acute intravenous administration of 100 mg prednisolone had no effect on plasma gastrin levels. After oral administration of prednisolone (40 mg daily, for four days) a significant increase of the basal, the reactive, and the over 90-min integrated gastrin release was observed. In this group, the glucocorticoid treatment had a slight, but significant influence on gastric acid and pepsin secretion, while acidity and pepsin output stimulated by pentagastrin was not affected. In patients treated with prednisolone for more than 24 weeks, the oral administration of this hormone failed to alter basal gastrin values but affected significantly secretion after the test meal. In patients with multiple sclerosis, after intramuscular administration of corticotropin (60 IU daily, for 12 days), an increase of the basal, the reactive, and the integrated gastrin release also was found. Glucocorticoid-induced hypergastrinemia provides information on the pathogenesis of steroid-induced ulceration.

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