HIV-related thrombocytopenia

Abstract

About 5-10% of HIV seropositive individuals, in all risk groups, develop a syndrome of immunological thrombocytopenic purpura (ITP). Despite the clear association between HIV infection and thrombocytopenia, the exact immune mechanism leading to the peripheral platelet destruction remains unclear. Whereas some data support the direct effect of autoantibodies to platelet constituents, other findings argue in favour of the deposition of immune complexes containing anti-HIV antibodies. Although viral components could not be detected in the immune complexes or on the platelet membrane, megakaryocytes were shown to contain viral RNA and there is some evidence for a direct or indirect role of HIV in the pathophysiology of this disorder. Steroids, intravenous high dose polyvalent immunoglobulin, anti-rhesus immunoglobulin, danazol and vincristine usually induce only a transient increase in platelet counts. Zidovudine was shown to provide a sustained response in 40-60% of the patients and appears to be the treatment of choice for HIV-related thrombocytopenia. Splenectomy has been effective in many cases with persistent, profound and symptomatic thrombocytopenia and, on a 4-year follow-up, does not influence the progression rate to AIDS or survival. Patients with thrombocytopenia are not at greater risk for the development of AIDS than seropositive non-thrombocytopenic patients. Thus, thrombocytopenia should not be viewed as a stage in the progression from asymptomatic infection to AIDS.