The association between tumour necrosis factor-α gene polymorphism and the susceptibility to rugal hyperplastic gastritis and gastric carcinoma

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Abstract

Objectives

Some subjects infected by Helicobacter pylori have enlarged folds in the gastric body, the precise mechanism of which remains obscure. The aim of this study was to clarify the association of tumour necrosis factor-α (TNFA) gene polymorphism with susceptibility to hyper-rugosity. We also examined the association of TNFA polymorphism with gastric carcinoma.

Subjects and methods

Four hundred and seventy-two subjects (male/female = 351/121, aged 26–81 years) without gastric carcinoma (control group), and 300 patients (male/female = 218/82, aged 32–91 years) with gastric carcinoma. Barium meal roentgenograms were performed in 396 subjects in the control group and fold width was measured at the greater curvature of the middle portion of the gastric body. Fasting plasma anti-H. pylori IgG titres, pepsinogens (PGs) I and II were analysed, and TNFA −857 promoter polymorphism was distinguished by the 5′ nuclease polymerase chain reaction assay and polymerase chain reaction restriction fragment length polymorphism using HincII in both groups.

Results

Adjusted odds ratios of TNFA −857 T/T genotype and H. pylori seropositivity for hyper-rugosity (fold width = 6.0 mm) were 6.7 (95% confidence interval (CI) 1.5–28, P< 0.01) and 18.2 (95% CI 4.2–78, P< 0.0001), respectively. There were no significant differences in any genotype or allele frequencies between the control and total gastric carcinoma group. In a subgroup of gastric carcinoma patients who were negative for the PG assay, however, the odds ratio of the T allele was 1.4 (95% CI 1.0–2.0, P< 0.05).

Conclusion

The TNFA −857 T/T genotype and H. pylori infection were strongly associated with rugal hyperplastic gastritis. The TNFA −857 T allele may promote gastric carcinoma without severe atrophy.

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