AIM: To elucidate the relations between the myeloperoxidase ~(-468)G→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 py/ori)-related gastritis. METHODS: In a case-control study of 115 consecutive DU patients and 182 controls, the myeloperoxidase ~(-468)G→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 ~(-468)G→A polymorphism with antral H pylori density and DU disease. The mechanisms underlying this genetic polymorphism in developing DU disease merit further investigations. AIM: To elucidate the relations between the myeloperoxidase ~ (-468) G → 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 py / ori ) -related gastritis. METHODS: In a case-control study of 115 consecutive DU patients and 182 controls, the myeloperoxidase ~ (-468) G → 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-infec ted 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 ~ (-468) G → A polymorphism with antral H pylori density and DU disease. The mechanism underlying this genetic polymorphism in developing DU disease merit further investigations.