Impact of Helicobacter pylori on the development of vitamin B12 deficiency in the absence of gastric atrophy.

Abstract

Cobalamin (vitamin B12) deficiency is associated with Helicobacter pylori infection. This study examined how serum vitamin B12 levels relate to gastric mucosa H. pylori density and histology, and to hematological findings in patients with minimal or no gastric atrophy. A second aim was to confirm that H. pylori eradication therapy increases serum B12. Biopsies of the gastric mucosa from a population of dyspeptic patients were graded for level of chronic inflammation, neutrophil activity, atrophy, and H. pylori density. A total of 145 H. pylori-infected patients with minimal or no atrophy were included in the study. Serum cobalamin level, hemoglobin level, and mean corpuscular volume were measured in the 145 patients before eradication therapy, and in 65 of the subjects after treatment. The hematologic findings before and after eradication therapy and correlations between serum vitamin B12 level and histologic parameters, hematologic findings, and patient age were statistically analyzed. There was no significant correlation between serum cobalamin level and patient age. Before treatment all the histopathological scores were inversely correlated with serum vitamin B12 level (p <.01) on univariate analysis. Only H. pylori density was significantly associated with B12 level on multivariate analysis. Serum hemoglobin and cobalamin levels were significantly increased after treatment, regardless of H. pylori eradication status (p <.001). The findings provide strong evidence that H. pylori infection is associated with cobalamin deficiency, and show that this is true even in patients with non-ulcer dyspepsia and minimal or no gastric atrophy.