Correlation between Helicobacter pylori infection, gastric inflammation and serum homocysteine concentration.

Abstract

Epidemiological studies have suggested a link between chronic Helicobacter pylori infection and ischemic heart disease but the underlying mechanism remains elusive. We hypothesized that H. pylori-associated chronic gastritis causes impairment of absorption of vitamin cofactors that are essential in the metabolism of homocysteine and results in hyperhomocysteinemia. Forty-nine dyspeptic patients were studied. H. pylori infection was defined by rapid urease test and histology. Fasting serum homocysteine level, which was measured by a validated commercial fluorescence polarization immunoassay, was correlated with H. pylori infection statuses and gastric histology. H. pylori-infected patients were followed up for 24 weeks post eradication for changes in serum homocysteine concentration. Univariate analyses showed that serum homocysteine level correlated with increasing age (p <.001), male sex (p =.003) and smoking habit (p =.025). There was no significant difference in serum homocysteine levels between H. pylori infected and uninfected subjects (median 10.5 vs. 10.2 micromol/l). After successful eradication of the bacterium, there was no significant reduction in homocysteine level. Moreover, there was no correlation between homocysteine level and gastric histology including H. pylori density, activity and inflammation scores, presence of atrophy or intestinal metaplasia. The postulated link between H. pylori infection and ischemic heart disease, if it actually exists, is unlikely to be mediated through hyperhomocysteinemia.