1994 Volume 173 Issue 2 Pages 199-208
NAKAMURA, T., TAKEBE, K., IMAMURA, K., MIYAZAWA, T., ISHII, M., KUDOH, K., TERADA, A., MACHIDA, K., KIKUCHI, H., KASAI, F., TANDOH, Y., ARAI, Y. and YAMADA, N. Decreased Gastric Secretory Functions in Diabetic Patients with Autonomic Neuropathy. Tohoku J. Exp. Med., 1994, 173 (2), 199-208-A total of 37 subjects consisted of 10 healthy subjects (Group III), 15 diabetic patients without autonomic neuropathy (Group II), and 12 diabetic patients with autnomic neuropathy including gastroparesis in 6 cases (Group I). All three groups were comparable in age. In order to clarify the gastric function in diabetic patients with autonomic neuropathy, secretion of serum gastrin, gastric secretory function, endoscopic Congo red test of fundic glands, and coefciency of variance of electrocardiographic beat-to-beat intervals (C.V.R-R) were examined. In Group I, 5 patients had hypergastrinemia, but its elevation was inhibited when an acid solution was injected into the stomach. Gastric secretion and C.V.R-R were markedly lower in Group I, compared with Groups II and III. In Group I, the area of fundic glands (parietal cells) was reduced considerably. The C.V.R-R was significantly correlated with fasting serum gastrin concentration and with maximal acid output. From these results, in diabetic patients with autonomic neuropathy (vagal neuropathy), gastric acid secretion in response to tetragastrin stimulation was lowered with a reduction in area of fundic gland distribution. Hypergastrinemia may reflect a negative feedback mechanism responding to decreased acidity of gastric content in the antrum.