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©2005 Baishideng Publishing Group Inc. All rights reserved.
Association of the myeloperoxidase-468G→A polymorphism with gastric inflammation and duodenal ulcer risk
Ping-I Hsu, Jyh-Jen Jwo, Hui-Hwa Tseng, Kwok-Hung Lai, Gin-Ho Lo, Ching-Chu Lo, Chung-Jen Wu, Seng-Kee Chuah, Il-Ran Hwang, Jin-Liang Chen, Yu-Shan Chen, Angela Chen
Ping-I Hsu, Kwok-Hung Lai, Gin-Ho Lo, Ching-Chu Lo, Chung-Jen Wu, Yu-Shan Chen, Division of Gastroenterology, Department of Internal Medicine, Kaohsiung Veterans General Hospital, National Yang-Ming University, Kaohsiung, Taiwan, China
Hui-Hwa Tseng, Department of Pathology, Kaohsiung Veterans General Hospital, National Yang-Ming University, Kaohsiung, Taiwan, China
Seng-Kee Chuah, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan, China
Il-Ran Hwang, Department of Internal Medicine, Dankook University Hospital, South Korea
Jin-Liang Chen, Department of Health Care and Hospital Administration, Chia-Nan University of Pharmacy and Science, Tainan, Taiwan, China
Jyh-Jen Jwo, Angela Chen, Institute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan, China
Author contributions: All authors contributed equally to the work.
Supported by the grants from the Research Foundation of Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, China VGHKS92-74 and the National Science Council, Taiwan, China NSC-92-2314-B-075B-006
Correspondence to: Angela Chen, PhD, Institute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung 80424, Taiwan, China. achen@mail.nsysu.edu.tw
Telephone: +886-7-5255815 Fax: +886-7-5255816
Received: November 2, 2004
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.
