Helicobacter pylori induced Immune Thrombocytopenic Purpura and perspective role of Helicobacter pylori eradication therapy for treating Immune Thrombocytopenic Purpura

Abstract

<abstract> <p>Immune thrombocytopenic purpura (ITP) is an autoimmune disease characterised by production of autoantibodies against platelet surface antigens. Recent studies have demonstrated a paramount association of ITP and <italic>Helicobacter pylori (H-pylori)</italic> infection with significant rise in platelet count following <italic>H-pylori</italic> eradication therapy. The <italic>H-pylori</italic> infection induced ITP is validated by many proposed mechanisms such as molecular mimicry due to production of autoantibodies against <italic>H-pylori</italic> 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- <italic>H-pylori</italic> IgG and von Willebrand factor (vWf) and finally host immune response against <italic>H-pylori</italic> virulent factors CagA and VacA leading to ITP. The effectiveness of <italic>H-pylori</italic> eradication therapy has also been demonstrated with platelet count being used as a predictive factor for assessment of treatment efficacy. Out of 201 patients 118 were responding to the triple therapy and remaining 83 patients were non-responders, showing the response rate of 58.7%. Out of 118 responders 69 patients were showing complete response (CR) and 49 were showing partial response (PR) to the <italic>H-pylori</italic> eradication therapy. However, more studies are required to elucidate this association and treatment efficacy.</p> </abstract>