Duodenal ulcer with unexplained marked basal gastric acid hypersecretion

Abstract

Out of 1012 gastric analyses performed in 6 yr, 40 persons had basal acid output ≥ 15 mmol/hr. Of these, 8 had known causes for hypersecretion (6 had Zollinger-Ellison syndrome and 2 systemic mastocytosis); 1 died before further study, leaving 31 with unexplained basal acid hypersecretion (19.5 ± 0.60 mmol/hr) and peptic ulcer (30 duodenal ulcer and 1 gastric ulcer). All were male compared with the 72:28 M : F ratio in the duodenal ulcer population from which these were drawn. From among the same 1012 patients 29 male controls with duodenal ulcer and basal acid output < 6 mmol/hr (2.7 ± 0.31 mmol/hr) were matched for age, sex, and length of follow-up (3–81 mo). The hypersecretion group had higher fasting residual volume (154 ± 14 vs. 76 ± 8 ml, P < 0.01) and peak acid output (53 ± 3 vs. 33 ± 3 mmol/hr, P < 0.01). In 17 of the 31 subjects repeat testing of basal secretion (r = 0.64) was not significantly different (P > 0.1). In controls basal acid output was related to body weight (r = 0.65) but in the hypersecretors it was not (r = 0.11). In the hypersecretors, however, basal acid output was related to length of ulcer history (r = 0.71), but in the controls it was not (r = 0.06). A significant cholinergic contribution to the hypersecretion was inferred from >90% reduction by either atropine (15 μg/kg) or vagotomy in all 12 of the 31 hypersecretion subjects who were so studied. The clinical course of the two groups was not different as regards number of hospitalizations, episodes of bleeding, number of operations, number of perforations or obstruction, and the same proportion (9/31 vs. 8/29) remained free of complications during the average 12.5-yr period of total ulcer history. The finding of massive basal acid hypersecretion does not necessarily imply a Zollinger-Ellison syndrome nor call for unusually extensive surgery for peptic ulcer, vagotomy being sufficient to correct the hypersecretion.