Pathogenesis of Thrombocytopenia

Kim, Hugh C

Abstract

Thrombocytopenia may be due to 1) a decrease in production, as seen in patients with marrow aplasia or when the marrow is infiltrated by tumor, 2) disorders in which platelet destruction exceeds production, or 3) splenomegaly, in which the distribution of platelets is abnormal. In evaluating the patient with thrombocytopenia, one should look for splenomegaly on physical examination, which would suggest a syndrome characterized by platelet sequestration. Second, one should examine a bone marrow sample to detect aplasia, fibrosis, or infiltration. In patients with a normal spleen and normal bone marrow function, the underlying disorder must by excess destruction. This can be due to nonimmune disorders, such as disseminated intravascular coagulation, or prosthetic cardiac valves, or thrombotic thrombocytopenic purpura, or to the presence of either immune complexes or specific antiplatelet antibodies. Immune thrombocytopenia can be induced by a wide range of common drugs, including quinidine, penicillin, gold, and sulfonamides. Heparin is perhaps the most common drugs in inducing thrombocytopenia in 1~10% of patients who receive this anticoagulant. Acute immune thrombocytopenia seen primarily in children often occurs following a viral infection. About 90% of these patients recover within 4 to 6 weeks without therapy. In contrast a chronic form of immune thrombocytopenia is much more common in adults. Antibodies against specific target antigens, usually against GP IIb/IIIa or GP Ib/IX/V. Cognizant of pathogenesis of these various forms of thrombocytopenia will allow the diagnosis much easier and practical.

Pathogenesis of Thrombocytopenia

Abstract

MeSH Terms

Cited

Save citations to file

Email citations