© 2001 Journal of Clinical Pathology
Association between TNF-
promoter polymorphism and Helicobacter pylori cagA subtype infection
The Paik-Inje Memorial Institute for Biomedical Science, Inje University, Pusan 614735, Korea
Department of Pathology, College of Medicine, Inje University, Paik Hospital, Pusan 614735, Korea
Department of Internal Medicine, College of Medicine, Inje University, Paik Hospital, Pusan 614735, Korea
Correspondence to:
Dr Yang pathyang{at}ijnc.inje.ac.kr
AimsTo assess the importance of tumour necrosis factor
(TNF-
) promoter polymorphism in relation to infection with the cytotoxin associated gene A (cagA) subtype of Helicobacter pylori within a dyspeptic Korean population.
MethodsEighty three patients with gastric disease and 113 healthy controls were studied. The DNA from gastric biopsy specimens was analysed by H pylori specific and cagA specific polymerase chain reaction (PCR). To characterise TNF-
polymorphism at positions -308 and -238, PCR based restriction fragment length polymorphism analysis was performed.
ResultsHelicobacter pylori infection was closely correlated with G to A transition at position -308 of the TNF-
promoter when compared with healthy controls (odds ratio (OR), 2.912; 95% confidence interval (CI), 1.082 to 7.836; p = 0.034). Although TNF-
-308 polymorphism in patients with H pylori was not significantly different from that in patients without H pylori, the -308A polymorphism was strongly associated with H pylori cagA subtype infection when compared with the polymorphism in cagA negative H pylori infection (OR, 8.757; 95% CI, 1.413 to 54.262; p = 0.019) and healthy controls (OR, 3.683; 95% CI, 1.343 to 10.101; p = 0.011). G to A genetic change at position -238 of the TNF-
gene was not significantly associated with H pylori cagA subtype infection. In addition, genetic polymorphisms at both sites of the TNF-
promoter in patients with H pylori infection did not correlate with the severity of disease.
ConclusionTNF-
-308A polymorphism was significantly related to infection with the H pylori cagA subtype in Korean patients with gastric disease.
Key Words:
Helicobacter pylori cagA tumour necrosis factor
polymorphism
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