Abstract

Immune thrombocytopenia (ITP) is an acquired bleeding disorder of autoimmune pathophysiology. The causes of ITP could be related to other pathology (viral, bacterial, or systemic), or ITP could develop without any apparent reason. While the immune system dysregulation mechanisms in ITP were described, its etiology remains unclear. Moreover, all existing treatment approaches are not specific for ITP, and its action is highly patient- specific. Here we describe recent findings in the origins and development of ITP and discuss novel experimental and theoretical approaches to diagnosing ITP and predicting therapy effects.

Highlights

  • Immune thrombocytopenia (ITP) is an acquired bleeding disorder of autoimmune pathophysiology

  • The first therapy line consists of injections of glucocorticosteroids (GCS) or intravenous immunoglobulins (IVIGs) [19]

  • The treatment of ITP is aimed at suppressing the immune system function, increasing platelet production or decreasing platelet consumption by splenectomy, but there is no treatment aimed at the origin of the decease

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Summary

Introduction

Immune thrombocytopenia (ITP) is an acquired bleeding disorder of autoimmune pathophysiology. There is no consistent treatment strategies for ITP, there are several recommended lines of therapy, based on the assumption that ITP was developed due to the presence of antiplatelet antibodies or platelet-targeted T-cells [1,18]. Systems biology approach might prove useful to develop diagnostic and predictive criteria for manifestation and progression of ITP and to evaluate the efficacy of the therapy options based on the phenotype of the patient. Though the starting point of acute ITP is uncertain, the mechanisms of autoimmune response were widely studied in chronic patients.

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