cqvip:Background &Aims: Proinflammatory interleukin (IL)-1 gene polymorphisms asso ciated with high levels of IL-1βactivity increase the risk for hypochlorhydria and distal gastric carcinoma. The aim of this study was to evaluate whether car riers of these polymorphic genes are protected against gastroesophageal reflux d isease (GERD). TNFA-308 polymorphisms were also studied. Methods: We prospectiv ely evaluated 385 patients without gastric cancer and peptic ulcer. Of these pat ients,383 (98 with GERD and 285 controls) were successfully genotyped for all cy tokines studied. The cagA status of Helicobacter pylori isolates was determined by polymerase chain reaction (PCR). IL1B-511/-31, IL1RN, and TNFA-308 polymor phisms were genotyped by PCR, PCR/restriction fragment length polymorphism, or PCR/confronting 2-pair primers. Histologic g astritis was assessed according to the updated Sydney system. The role of the pr oinflammatory cytokine genotypes in the genesis of GERD was evaluated before and after stratification by H. pylori status in logistic regression models controll ing for confounding factors. Results: IL1B-31 (a near-complete linkage disequi librium between polymorphism at -31 and -511 was found) and IL1RN*2 allele po lymorphisms were associated with GERD. After stratification, in the group of H. pylori-positive patients, cagA-positive status,IL1B-31 polymorphic alleles, I L1RN*2 alleles, and the degree of corpus gastritis were negatively associated w ith GERD. In the H. pylori-negative group, IL1B-31C/C genotype was inversely a ssociated with GERD even after adjustment for age and sex. Conclusions: This stu dy provides evidence supporting the independent protective role of cagA-positiv e H.pylori status and IL1B and ILRN allele polymorphisms against GERD.
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