AbstractSerum gastrin levels were measured radioimmunologically in 123 patients with various gastrointestinal diseases to study the pathophysiological role in the diseases.1)In winter diarrhea, mean fasting gastrin level tended to be slightly higher in the severer patients but the difference from the control level were not statistically significant. After test meal, however, mean serum gastrin level increased rapidly and reached a peak by after 10 minutes followed by levelling off for 20 minutes. This result may suggest that a feedback mechanism between the secretion of gastrin and secretin is disturbed in the disease.2)In bacillary dysentery, mean fasting serum gastrin levels in the acute stage did not differ from that of controls.3)Mean fasting serum gastrin levels in neonatal hepatitis and chronic hepatitis of school children were significantly lower but the level in congenital biliary atresia was not different as compared to those of age‐matched controls. Further investigation of gastrin metabolism in liver may be needed.4)In duodenal ulcer, mean fasting serum gastrin level was not different statistically from the control value but mean gastrin response to feeding was significantly greater and longer than that of controls. This abnormality of gastrin release in children with duodenal ulcer may have a significant role in the pathogenesis of the disease.5)In superior mesenteric artery syndrome, mean fasting gastrin level was significantly lower than that of controls and mean serum gastrin responses to test meal both in sitting and prone positions were significantly lower than those of controls. No statistical difference was found when the response were compared between in a sitting and prone positions. The hypogastrinemic response to meal in patients with this order was probably considered to be due to impaired function of G‐cells which was caused by dilatation of the stomach and/or duodenum resulting in the mucosal damage.6)The increment of gastrin secretion following glucocorticoid administration was found in children with anaphylactoid purpura and the effect was confirmed in rats. This results suggest that the so‐called steroid ulcer may partly be caused by steroid induced gastrin hypersecr