Abstract

Inconsistency of reported associations of the G/A polymorphism (rs2301756) in the PTPN11 gene and gastric atrophy prompted us to undertake a meta-analysis. We searched PubMed for published literature up to July 2013. Individual data from studies with case-control design were evaluated for the PTPN11 G/A polymorphism in Helicobacter pylori (-) (seronegative) and (+) (seropositive) subjects (four studies each, totaling 3,597 cases and 4,865 controls). Associations of PTPN11 polymorphism with gastric atrophy in H. pylori (-) and (+) subjects are more readily interpreted in the homozygous and recessive models given that the dominant codominant effects skirted null associations. Thus, homozygous and recessive effects indicated reduced risk [odds ratio (OR) 0.92-0.96, p = 0.51-0.74], which is significant among H. pylori (+) subjects (OR 0.66-0.68, p = 0.04-0.05). Confined to the Japanese, reduced risk effects were unaltered in both groups, less protective among seronegative subjects (OR 0.85-0.86, p = 0.71-0.73) than seropositive subjects with significance in the recessive model (OR 0.67, p = 0.05). Sensitivity analysis demonstrated robustness of the seropositive findings, but probably not the seronegative results where homozygous and recessive pooled ORs were altered from protection to increased risk. Evidence of overall and subgroup decreased risks, strong in seropositive subjects, demonstrates protective effects of the PTPN11 G/A polymorphism from gastric atrophy.

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