Abstract
Immune thrombocytopenia (ITP) is an acquired autoimmune hemorrhagic disease involving increased platelet destruction and insufficient platelet production, leading to thrombocytopenia, with or without clinical manifestations of bleeding. Although thrombocytopenia may cause coagulation dysfunction and hemorrhagic complications, the bleeding severity is not certainly proportional to the number of platelets. In some cases, there is no significant bleeding symptom even the platelet count is extremely low, which suggests there are additional compensatory mechanisms to control or ameliorate the bleeding complications in ITP patients. The present article aims to review recent investigations on the compensatory mechanisms of coagulation function in the patients with ITP. Key words: Thrombocytopenia; Microsomes; Phosphatidylserines; Thromboplastin; Platelet membrane glycoproteins; Thrombin; Interleukin-6
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