Fcγ receptor IIB gene polymorphism in adult Japanese patients with primary immune thrombocytopenia.

Several studies have indicated that platelet recovery occurs in a subgroup of immune thrombocytopenia (ITP) patients after successful Helicobacter pylori (H pylori) eradication. Interestingly, a higher response rate to H pylori eradication therapy has been reported in Japan and Italy than in the United States and European countries other than Italy, suggesting that the efficacy of H pylori eradication is influenced by ethnicity, probably through genetic and environmental factors. In addition, Asahi et al observed that monocytes from H pylori–infected ITP patients demonstrated low levels of inhibitory FcgRIIB and enhanced platelet phagocytosis, both of which were reversed after successful H pylori eradication. The FcgRIIB 232I/T (Ile/Thr) polymorphism (rs1050501) has been identified as a genetic factor associated with susceptibility to various autoimmune diseases. The FcgRIIB 232T cannot inhibit activating receptors because it is not present in lipid rafts, resulting in decreased FcgRIIB-mediated inhibition of macrophage and B-cell responses. We analyzed the FcgRIIB 232I/T polymorphisms by restrictionfragment-length polymorphism polymerase chain reaction in 206 adult Japanese patients with primary ITP and in 193 healthy controls (supplementalMethods, available on the Bloodwebsite). The FcgRIIB 232T carriers were more frequently detected in ITP patients than in healthy controls (P5 .003; odds ratio [OR]5 1.87; 95% confidence interval [CI], 1.24-2.82) (Table 1). Our results differed from those described by Breunis et al using 44 adult Dutch patients with ITP and Xu et al using 178 adult Chinese patients with ITP. This discrepancy might be explained by study design factors including sample size and ethnic differences. Interestingly, the distribution of the FcgRIIB 232T carriers is more common in Asians than in Caucasians. This distribution is similar to the regional differences observed for the effect of H pylori eradication therapy in ITP patients. We compared the distribution of FcgRIIB 232I/T polymorphisms between H pylori–infected ITP patients and healthy controls or Hpylori–uninfected ITP patients and healthy controls (Table 1). The frequency of the FcgRIIB 232T carriers was significantly higher in H pylori–infected ITP patients than in healthy controls (49.0% vs 30.6%; P5 .002; OR5 2.18; 95% CI, 1.33-3.59).H pylori infection plays a role in ITP pathogenesis by altering the FcgR balance of monocytes in favor of activating FcgR, through downregulation of inhibitory FcgRIIB. Furthermore, our data suggest that the functionally impaired FcgRIIB 232T carriers may contribute to disease pathogenesis in a subgroup of H pylori–infected ITP patients. We further evaluated associations between FcgRIIB 232I/T polymorphisms and therapeutic response rates to H pylori eradication in