Helicobacter pylori: A Belittled Cause of Immune Thrombocytopenic Purpura (ITP) and Role of Helicobacter pylori Eradication Therapy for Treating ITP

Abstract

Immune thrombocytopenic purpura (ITP) is an autoimmune disease characterized by production of auto antibodies against platelet surface antigens. ITP affects women more often than men and is more common in children than adults. ITP is a diagnosis of exclusion after other identifiable etiologies have been ruled out. After the first report by Gasbarrini et al. (1998) showing rising platelet counts in ITP patients following Helicobacter pylori (HP) eradication therapy, there is growing evidence that highlights the role of HP in triggering ITP. The H-pylori infection induced ITP is validated by many proposed mechanisms such as molecular mimicry due to production of auto antibodies against H-pylori surface virulent factors (CagA) and cross reactivity of these antibodies with platelet surface antigens (GP IIb/IIIa, GP Ib/IX, and GP Ia/IIa), phagocytic perturbation due to enhanced phagocytic activity of monocytes, enhanced dendritic cell numbers and response, platelets aggregation due to presence of anti- H-pylori IgG and von Willebrand factor (vWf) and finally host immune response against H-pylori virulent factors CagA and VacA leading to ITP. Eradication of Helicobacter pylori infection has been variably associated with a platelet response in patients with immune thrombocytopenic purpura (ITP). Eradication therapy is simple and inexpensive, with limited toxicity and the advantage of avoiding long-term immunosuppressive treatment for those who respond. Although the evidence and follow-up are limited, it appears reasonable to routinely screen patients with ITP for H pylori, particularly in those populations with a high background prevalence of H pylori infection.