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

Citation
Wk. Leung et al., Correlation between Helicobacter pylori infection, gastric inflammation and serum homocysteine concentration, HELICOBACT, 6(2), 2001, pp. 146-150
Citations number
19
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
HELICOBACTER
ISSN journal
10834389 → ACNP
Volume
6
Issue
2
Year of publication
2001
Pages
146 - 150
Database
ISI
SICI code
1083-4389(2001)6:2<146:CBHPIG>2.0.ZU;2-B
Abstract
Background. Epidemiological studies have suggested a link between chronic H elicobacter pylori infection and ischemic heart disease but the underlying mechanism remains elusive. We hypothesized that H. pylori-associated chroni c gastritis causes impairment of absorption of vitamin cofactors that are e ssential in the metabolism of homocysteine and results in hyperhomocysteine mia. Materials and Methods, Forty-nine dyspeptic patients were studied. H, pylor i infection was defined by rapid urease test and histology. Fasting serum h omocysteine level, which was measured by a validated commercial fluorescenc e polarization immunoassay, was correlated with H. pylori infection statuse s and gastric histology. H. pylori-infected patients were followed up for 2 4 weeks post eradication for changes in serum homocysteine concentration. Results. Univariate analyses showed that serum homocysteine level correlate d with increasing age (p <.001), male sex (p =.003) and smoking habit (p =. 025). There was no significant difference in serum homocysteine levels betw een H. pylori infected and uninfected subjects (median 10.5 vs. 10.2 <mu>mo l/l). After successful eradication of the bacterium, there was no significa nt reduction in homocysteine level. Moreover, there was no correlation betw een homocysteine level and gastric histology including H. pylori density, a ctivity and inflammation scores, presence of atrophy or intestinal metaplas ia. Conclusions. The postulated link between H. pylori infection and ischemic h eart disease, if it actually exists, is unlikely to be mediated through hyp erhomocysteinemia.