Effects of Helicobacter pylori infection on Zollinger-Ellison syndrome

Abstract

Both Zollinger-Ellison syndrome (ZES) and Helicobacter pylori infection are major etiologic factors for peptic ulcer. The aim of this study was to investigate the effect of H. pylori infection on ZES with special reference to acid secretion. Sixteen patients with ZES were selected (median age, 59 years; range, 39-66 years; M/F, 9/7), and H. pylori status, ulcer location, gastric acid secretion, serum pepsinogen (PG) I and II concentrations, and PG I/II ratio were determined. The seroprevalence of H. pylori infection was 50%, whereas active H. pylori infection was seen in only 25% of the patients. Thirteen patients had duodenal ulcer (DU), 1 had gastric ulcer (GU), and 2 had both GU and DU. DU was seen in both H. pylori-positive and H. pylori-negative patients, whereas GU was found only in H. pylori-positive patients. Both basal and maximal acid outputs were significantly lower in H. pylori-positive patients than in H. pylori-negative patients (P< 0.05). Moreover, both serum PG I and the PG I/II ratio were significantly lower in H. pylori-positive patients than in H. pylori-negative patients. These results indicate that ZES is an independent risk factor for DU, but H. pylori infection may play some role in the development of GU in ZES. In patients with ZES, H. pylori infection may reduce both hypersecretion from parietal cells and PG I secretion from chief cells, and hyperacidity of the stomach in ZES may have eradicated H. pylori in some patients.

What is the role of Helicobacter pylori infection in ZES-associated peptic ulcer?

“…As in several previous reports on ZES, Watanabe et al 5 have shown acid secretion to be lower in H. pyloripositive patients than in H. pylori-negative patients. They suggested two possible mechanisms for gastric acid secretion in H. pylori-positive patients; i.e., H. pylori-induced atrophic gastritis and a direct inhibitory action of H. pylori on parietal cells.…”

“…Current views are that H. pylori infection is often acquired in childhood, but that age at onset of ZES is under 20 years in fewer than 10% of the patients. 5,7,13 The similar seroprevalence of H. pylori in patients with ZES and in the general population also points to this factor. Watanabe et al 5 reported no difference in gastric acid secretion between seropositive and seronegative patients with H. pylori-negative ZES, but they found that serum pepsinogen I levels were significantly higher in the seronegative than in the seropositive patients.…”

“…Kishimoto et al 8 reported a frequency of 31.8% (50/157 patients) in patients with ZES in Japan between 1965 and 1991. In the report of Watanabe et al 5 the frequency of gastric ulcer in patients with ZES was relatively low; 3 of 16 patients with ZES (18.8%). This may reflect the declining incidence of H. pylori infection in Japan.…”

“…The most interesting finding reported by Watanabe et al 5 is that gastric ulcer in ZES patients occurred solely in those with H. pylori infection, although the number of patients with gastric ulcer was not large enough to conclude that H. pylori infection is pivotal for gastric ulceration in ZES. The prevalence of gastric ulcer in patients with ZES seems to reflect the prevalence of H. pylori infection in the general population.…”

“…In this issue of the Journal, Watanabe et al 5 report the effect of H. pylori infection on ZES. Their study suggests that the hypersecretion of hydrochloric acid is an independent risk factor for duodenal ulcer in patients with ZES, but that H. pylori infection is necessary for the associated gastric ulceration.…”