The pathological role of Helicobacter pylori is largely unproven in our region of high incidence of infection but very low incidence of serious gastroduodenal lesions. The aim of this study was to investigate the effect of H. pylori infection on gastric acid secretion. One week after gastroduodenoscopy, basal and pentagastrin (8 micrograms/kg) stimulated gastric acid secretion were measured in 39 dyspeptic Nigerians. H. pylori status was determined using urease test, culture, histology and serology, while gastritis was assessed using the Sydney system criteria. The median maximal acid output (MAO) and peak acid output (PAO) in mmol/h were significantly higher in H. pylori positive (29.3, range 7.4-81.6 and 34.4, range 7.6-144.0) than in H. pylori negative (16.6, range 4.2-44.1 and 22.4, range 5.6-48.6) patients, p = 0.019 and p = 0.029, respectively. Stimulated gastric acid secretion was significantly higher in patients with duodenal ulcer (n = 8) than in H. pylori negative (n = 11) patients, but was similar in non-ulcer dyspeptics (n = 20) and H. pylori negative patients. The median basal acid output was not significantly different between the groups of patients. Our patients (median age 32 years) had normal mucosa (12.1%), pangastritis with corpus predominance (12.1%), antrum-only gastritis (24.3%) and pangastritis with antral predominance (51.5%). In the subset of H. pylori positive patients (n = 28, 71.8%), there were no significant correlations between grade of antral chronic inflammation, gastritis index score, anti-H. pylori IgG titre and gastric acid secretion, p > 0.05. H. pylori infection increases MAO and PAO in our relatively young patients with antral predominant chronic gastritis.