Gastroduodenal Changes Two Years After Eradication of Helicobacter pylori in a Population-Based Cohort

BACKGROUND: The main cause of chronic gastritis is Helicobacter pylori (H. pylori) infection. Some individuals with H. pylori-related chronic gastritis develop atrophy of the gastric mucosa, a risk factor for gastric neoplasia. When H. pylori-associated gastritis is encountered, it is important to be aware of its natural history and reversibility of associated histopathological and hormonal changes. METHODS: A sample of 501 volunteers from the general population in the municipality of Linkoping, Sweden, was examined with esophago-gastro-duodenoscopy (EGD) with biopsy. Blood samples were collected in the fasting state and the subjects answered a questionnaire concerning lifestyle factors, medications and disease history. At a primary follow-up examination, after 8 years, 314 participants were re-examined and those infected with H. pylori received eradication. Two years after successful eradication therapy, 82 participants attended re-examination with EGD and blood sampling, as in the previous examinations. RESULTS: In this prospective cohort study of a sample of volunteers from the general population, all of the 82 participants had chronic gastritis with at least one positive H. pylori test before eradication therapy. During follow-up, non-steroid-inflammatory-drug (NSAID) use had decreased significantly (P = 0.007, McNemar). The H. pylori serology was still positive in 79/82 subjects (P = 0.007, McNemar). The basal gastrin and cholecystokinin (CCK) concentrations both had decreased (P < 0.001 for both, Wilcoxon), whereas the P-somatostatin had increased (P < 0.001, Wilcoxon). Symptoms included in the self-administered symptom questionnaire concerned the last 3 months showed no big difference at all. The inflammation had decreased in both antrum (before 2/38/42/0 and after 60/22/0/0, P < 0.0001) and corpus (before 3/54/22/3 and after 58/23/1/0, P < 0.0001). Changes in the inflammatory activity had decreased significantly in both the antrum (P < 0.001) and the corpus (P < 0.001). Intestinal metaplasia was without changes. Regarding the duodenal bulb, the inflammation decreased. CONCLUSIONS: Being aware of the natural history of chronic gastritis, even beyond eradication of H. pylori, is important because of the associations to gastric neoplasia and ulcer disease. The blood mirror of gastroduodenal parameters showed decreased values, except for somatostatin that increased and a symptomatology with no significant changes although, morphologically determined, both inflammation and atrophy had decreased.