Published online May 14, 2005. doi: 10.3748/wjg.v11.i18.2796
Revised: November 3, 2004
Accepted: November 23, 2004
Published online: May 14, 2005
AIM: To elucidate the relations between the myeloperoxidase-468G→A polymorphism and the development of duodenal ulcer (DU), and to investigate the impacts of this host genetic polymorphism on the histopathological features of Helicobacter pylori (H pylori)-related gastritis.
METHODS: In a case-control study of 115 consecutive DU patients and 182 controls, the myeloperoxidase-468G→A polymorphism was genotyped. Additionally, gastric mucosal changes were examined according to the updated Sydney System.
RESULTS: The two study groups differed in the distributions of myeloperoxidase genotypes (P = 0.008). All six individuals carrying myeloperoxidase A/A genotypes were in the DU group. The carriage of myeloperoxidase allele A and H pylori infection were associated with an increased risk of DU with odds ratios (OR) of 2.3 and 5.8, respectively. The combined risk of the carriage of myeloperoxidase allele A and H pylori infection for DU was 8.7 (95% CI, 3.5-21.8). In the H pylori-infected individuals, allele A carriers displayed higher bacterial density scores (P = 0.04) in the antrum than did non-carriers.
CONCLUSION: This work verifies for the first time the association of myeloperoxidase-468G→A polymorphism with antral H pylori density and DU disease. The mechanisms underlying this genetic polymorphism in developing DU disease merit further investigations.