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  4. The interleukin-I RN polymorphism and Helicobacter pylori infection in the development of duodenal ulcer
 
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The interleukin-I RN polymorphism and Helicobacter pylori infection in the development of duodenal ulcer

Journal
Helicobacter
Journal Volume
9
Journal Issue
6
Pages
605-613
Date Issued
2004
Author(s)
Ping-I Hsu
Chin-Ni Li
Hui-Hwa Tseng
Kwok-Hung Lai
PING-NING HSU  
Gin-Ho Lo
Ching-Chu Lo
Jeng-Jung Yeh
Luo-Ping Ger
Michael Hsiao
Yoshio Yamaoka
Il-Ran Hwang
Angela Chen
DOI
10.1111/j.1083-4389.2004.00277.x
URI
https://www.scopus.com/inward/record.uri?eid=2-s2.0-19944378060&doi=10.1111%2fj.1083-4389.2004.00277.x&partnerID=40&md5=91ab8cac75c989dcf64165fcb2ca5749
https://scholars.lib.ntu.edu.tw/handle/123456789/545345
https://pubmed.ncbi.nlm.nih.gov/15610073/
Abstract
Background. The host genetic factors that determine the clinical outcomes for Helicobacter pylori-infected individuals remain unclear. Aims. To elucidate the relations among interleukin-1 locus polymorphisms, and H. pylori infection in the development of duodenal ulcers. Materials and methods. In a case-control study involving 168 control subjects and 147 patients with duodenal ulcer, biallelic polymorphisms of two interleukin-1 loci, IL-1B-511 and IL-1B+3954, as well as the penta-allelic variable number of tandem repeats of interleukin-1 receptor antagonist IL-1RN, were genotyped, and the H. pylori states of controls and patients were examined. Results. Helicobacter pylori infection, male gender and the carriage of IL-1RN*2 independently increased the risk of duodenal ulcer with odds ratios of 6.4 (95% confidence interval, 3.7-11.0), 1.9 (95% confidence interval, 1.1-3.4) and 2.7 (95% confidence interval, 1.1-6.8), respectively. Statistical analysis revealed an interaction between IL-1RN*2 and H. pylon infection with the duodenal ulcer risk conferred by the H. pylori infection substantially increased (odds ratios, 22.6; 95% confidence interval, 5.9-86.5) by the carriage of IL-1RN*2. In addition, a synergistic interaction between IL-1RN*2 and blood group O existed. The combined risk of H. pylori infection, the carriage of IL-1RN*2 and blood group O for duodenal ulcer was 27.5 (95% confidence interval, 3.1-243.6). Conclusions. This work is the first to verify IL-1RN*2 as an independent factor that governs the development of duodenal ulcers. Our data indicate that H. pylori infection and IL-1RN*2 synergistically determine susceptibility to duodenal ulcer. The blood group phenotype is possibly a crucial determinant for the outcome of the impact of an interleukin-1 locus polymorphism on H. pylori-infected individuals.
Subjects
Duodenal ulcer; Helicobacter pylori; IL-1RN; Interleukin-1 receptor antagonist; Interleukin-1β; Polymorphism
SDGs

[SDGs]SDG3

Other Subjects
interleukin 1 receptor blocking agent; interleukin 1beta; IL1RN protein, human; interleukin 1; interleukin 1 receptor blocking agent; sialoglycoprotein; adult; aged; article; case control study; controlled study; duodenum ulcer; female; gene; gene locus; genetic polymorphism; genetic susceptibility; Gram negative infection; Helicobacter pylori; host susceptibility; human; il 1rn gene; major clinical study; male; priority journal; allele; blood group ABO system; duodenum ulcer; genetic polymorphism; genetic predisposition; genetics; genotype; Helicobacter infection; Helicobacter pylori; microbiology; middle aged; risk factor; Taiwan; Helicobacter; Helicobacter pylori; Negibacteria; ABO Blood-Group System; Adult; Alleles; Case-Control Studies; Duodenal Ulcer; Female; Genetic Predisposition to Disease; Genotype; Helicobacter Infections; Helicobacter pylori; Humans; Interleukin 1 Receptor Antagonist Protein; Interleukin-1; Male; Middle Aged; Polymorphism, Genetic; Risk Factors; Sialoglycoproteins; Taiwan
Type
journal article

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