Helicobacter pylori-associated immune thrombocytopenia: clinical features and pathogenic mechanisms

Abstract

Immune thrombocytopenia (ITP) is an autoimmune disease mediated by anti-platelet autoantibodies. There is growing evidence that the eradication of Helicobacter pylori (H. pylori) effectively increases platelet count in a considerable proportion of ITP patients infected with this bacterium. In the majority of ITP patients responding to H. pylori eradication therapy, the anti-platelet autoantibody response is completely resolved with no relapse for more than 7 years, indicating that the disease is cured. Therefore, adult patients with suspected ITP should be examined for H. pylori infection, and eradication therapy is recommended if the infection is present. Notably, however, the efficacy of H. pylori eradication therapy in ITP patients varies widely among countries, with a higher response rate in Japan compared with the United States and European countries other than Italy. The pathogenesis of H. pylori-associated ITP is still uncertain, although the mechanisms are known to involve multiple factors. H. pylori may modulate the Fcγ-receptor balance of monocytes/macrophages in favor of activating Fcγ receptors, and H. pylori components may mimic the molecular makeup of platelet antigens. Further studies of the pathogenic process of H. pylori-associated ITP may be useful for the development of new therapeutic strategies for ITP.

Keywords: Autoantibody; Childhood; Fcγ receptor; Helicobacter pylori; Idiopathic thrombocytopenic purpura; Immune thrombocytopenia; Systemic lupus erythematosus.

Figure 1

Changes in platelet count and in anti-GPIIb/IIIa antibody-producing circulating B cells before and 3 mo after an Helicobacter pylori eradication regimen in Helicobacter pylori-positive immune thrombocytopenia patients with no additional disease, or with systemic lupus erythematosus or liver cirrhosis. Changes in absolute values were compared by paired t test. ^aP < 0.05. A dotted line indicates the cut-off for circulating anti-GPIIb/IIIa antibody-producing B cells, which was 2/10⁵ peripheral blood mononuclear cells (PBMCs). ITP: Immune thrombocytopenia; SLE: Systemic lupus erythematosus.