Association of the myeloperoxidase ^(468)G→K polymorphism with gastric inflammation and duodenal ulcer risk
Association of the myeloperoxidase ^(468)G→K polymorphism with gastric inflammation and duodenal ulcer risk作者机构：DivisionofGastroenterologyDepartmentofInternalMedicineKaohsiungVeteransGeneralHospitalNationalYang-MingUniversityKaohsiungTaiwanChina DepartmentofPathologyKaohsiungVeteransGeneralHospitalNationalYang-MingUniversityKaohsiungTaiwanChina AngelaChenInstituteofBiomedicalSciencesNationalSunYat-SenUniversityKaohsiungTaiwanChina DepartmentofInternalMedicineKaohsiungChangGungMemorialHospitalKaohsiungTaiwanChina DepartmentofInternalMedicineDankookUniversityHospitalSouthKorea DepartmentofHealthCareandHospitalAdministrationChia-NanUniversityofPharmacyandScienceTainanTaiwanChina
出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)
年 卷 期：2005年第11卷第18期
页 面：2796-2801页
核心收录：
学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学]
基 金：Supported by the grants from the Research Foundation of Kaohsiung Veterans General Hospital Kaohsiung Taiwan China VGHKS9274 and the National Science Council Taiwan China NSC-92-2314B-075B-006
主 题：Duodenal ulcer Helicobacter pylorr Myeloperoxidase Polymorphism
摘 要：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.
维普期刊数据库