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 pylori)-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 pylori)-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.
Authors: N J Peng; K H Lai; R S Liu; S C Lee; D G Tsay; C C Lo; H H Tseng; W K Huang; G H Lo; P I Hsu Journal: Dig Liver Dis Date: 2003-02 Impact factor: 4.088
Authors: M Plebani; D Basso; M Cassaro; L Brigato; M Scrigner; A Toma; F Di Mario; M Rugge Journal: Am J Gastroenterol Date: 1996-05 Impact factor: 10.864