Helicobacter pylori–induced hypergastrinemia is accompanied by increased acid secretion in patients with duodenal ulcer (DU) but not in infected healthy volunteers. The aim of this study was to investigate the mechanism underlying this difference.

Thirty-four H. pylori–negative and 20 H. pylori–positive healthy volunteers and 15 H. pylori–positive patients with DU were studied. Maximal acid output and sensitivity to gastrin (gastrin concentration required to achieve 50% maximal acid output) were assessed by examining the dose response to gastrin 17. Inhibitory control was tested by comparing the maximal acid response to cholecystokinin octapeptide with that for gastrin 17.

Sensitivity to gastrin was similar in patients with DU (median, 69.5 ng · L⁻¹; range, 26.2-142) and H. pylori– negative healthy volunteers (median, 82.2 ng · L^minus;1; range, 17.7-410); H. pylori–positive healthy volunteers were less sensitive than either (164.5 ng · L^minus;1; range, 44.8 to >3360 ng · L⁻¹). Patients with DU had higher maximal acid output (51.2 mmol · h^minus;1; range, 30.8-73.7 mmol · h⁻¹) than either infected healthy volunteers (37.8 mmol · h⁻¹; range, 0.0-65.0 mmol · h⁻¹; P< 0.04) or uninfected healthy volunteers (35.3 mmol · h⁻¹; range, 21.3-67.3 mmol · h⁻¹; P < 0.002). The maximal acid output in both groups of healthy subjects was similar. The proportion of maximal acid output to gastrin 17 achieved by cholecystokinin was similar in patients with DU (36.6%; range, 21.5%-58.2%) and H. pylori–negative healthy volunteers (28.7%; range, 5.9%-85.8%).

A combination of decreased sensitivity to gastrin in infected healthy volunteers and increased maximal acid secretory capacity in patients with DU underlies their different acid response to H. pylori–induced hypergastrinemia. GASTROENTEROLOGY 1998;114:50-57