Gastric Secretion in Chronic Pancreatitis

Abstract

The isolation of a gastrin like secretagogue from patients with non-beta cell tumors of the pancreas suggested that other pancreatic disease should be studied for gastric hypersecretion. Animal studies have revealed hypersecretion in experimentally induced pancreatitis and atrophy and similar claims have been made for humans Gastric secretion was studied by the augmented histamine test in 19 male alcoholics with documented chronic pancreatits. The mean B. A. O. was 1. 28 mEq/hr. and the mean T. A. O. was 16. 2 mEq/hr; both of these values are below the normal means and not in accord with the animal studies. The mechanism responsible for hypersecretion in the experimental situations is not defined, but either a gastric secretagogue is produced by the atrophic pancreas or the normal pancreas secretes a gastric inhibitory susbtance. The evidence for both of these views is discussed. An explanation for the present results is that some residual pancreatic flow might still be present in humans to prevent hypersecretion. A gastrin like secretagogue may have been present in these subjects but gastrin may have an inhibitory as well as a stimulating effect and the former may have been the more significant one here. Biopsies of the gastric mucosa excluded end-organ failure. Gastritis was present in 53% of the subjects and advanced in only 20% indicating that the mucosa was capable of responding to a stimulus in the majority of patients.