Helicobacter pylori-induced damage to the gastric mucosa is not modulated by previous vagotomy or medical treatment of peptic ulcer disease: a comparative study of vagotomized patients, medically treated peptic ulcer patients and community control subjects.

BACKGROUND: An increase in the prevalence of precancerous lesions and atrophic changes in the gastric mucosa has been reported as long-term consequences of vagotomy-induced acid suppression. This study was designed to describe the long-term changes in the gastric mucosa caused by vagotomy and Helicobacter pylori infection.
METHODS: Seventy-nine patients with vagotomized peptic ulcers, 70 nonoperated patients with peptic ulcers, and 85 matched community control subjects were randomly selected to participate in an upper endoscopic study. Biopsy specimens were taken from predestined locations of the gastric mucosa.
RESULTS: Mean follow-up time for the vagotomized patients was 17.3 (range, 6-28) years and 12.7 (range, 10-17) years for the medically treated peptic ulcer patients. In H. pylori-positive subjects, severe atrophic changes in the distal gastric mucosa (prepylorus and angulus) was found in 30% (95% confidence interval (CI), 19-43) of the vagotomized patients and in 43% (95% CI, 29-58) of medically treated patients with peptic ulcers, and in 32% (95% CI, 20-46) of the community control subjects. Severe intestinal metaplasia was not found more frequently in vagotomized peptic ulcer patients compared with medically treated patients with peptic ulcers (p = 0.5). The histological picture of the age-matched community control subjects did not differ significantly from the patients with peptic ulcers when corrected for presence of H. pylori infection.
CONCLUSIONS: This study lends no support to theories of increased premalignant changes in the gastric mucosa of vagotomized patients. H. pylori infection rather than long-term acid suppression seems to be the explanation of the gastric mucosal changes seen after vagotomy.