Thrombocytopenia

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Thrombocytopenia may be a presenting laboratory finding in an otherwise asymptomatic HIV-infected person. HIV infection should be considered in the differential diagnosis of thrombocytopenia, and the history should include questions regarding risk factors for infection. Clinically asymptomatic but thrombocytopenic HIV-infected patients have a similar rate of progression to AIDS as asymptomatic HIV-seropositive persons without thrombocytopenia. Thrombocytopenia is not a criterion for more advanced HIV disease according to the staging system developed by the Centers for Disease Control and Prevention (CDC). Multiple causes need to be considered in evaluating thrombocytopenia in HIV infection. Immune-mediated destruction and ineffective hematopoiesis are generally both operative. In addition, cases of AIDS with apparent hemolytic-uremic syndrome or thrombotic thrombocytopenic purpura have been described, but are rare. Isolated thrombocytopenia is most often clinically similar to classic autoimmune thrombocytopenic purpura (ITP). Bone marrow examination reveals an increased number of megakaryocytes, and there are elevated levels of bound immunoglobulin on the platelet surface.

However, distinct from ITP, the immunoglobulin is generally immune complexes often involving anti-HIV antibodies, and splenomegaly is common. Detection of antibody on platelet surfaces does not correlate with thrombocytopenia, possibly because reliculoendothelial cell dysfunction often occurs in AIDS and may reduce platelet clearance. In addition to peripheral destruction of platelets, reduced production appears to be common in HIV disease. Even in patients with an ITP-like presentation, production is reduced. This mechanism predominates in patients with thrombocytopenia in the setting of AIDS.

The thrombocytopenia in HIV-infected patients has similar sequelae to classic immune thrombocytopenia, yet special attention to the issue of thrombocytopenia should be given in HIV-infected hemophiliacs. Complications from thrombocytopenia may be more severe in hemophiliacs, so therapy should be considered at a higher platelet count than in HIV-infected patients without other coagulation defects. An important observation has been the improvement in platelet count due to treatment with zidovudine (AZT) in HIV-infected patients with significant thrombocytopenia, regardless of risk group. Nearly two thirds of such patients may respond to AZT therapy and increase their platelet counts (mean, threefold increase) within 12 weeks of initiating treatment. There are a number of anecdotal reports of responses to other antiretroviral agents as well, should AZT be an unacceptable option. If there is no response to AZT, then several treatment modalities may be considered, including corticosteroids, interferon-alpha, splenectomy, danazol; for rapid temporary reversal of severe thrombocytopenia, intravenous gamma globulin and anti-RhD preparations have been shown to be quite active.

Theoretical risk of steroid use exists in an HIV-infected individual, including exacerbation of fungal infection, Kaposi’s sarcoma (KS), and the replicative activity of HIV itself. Nonetheless, most patients have tolerated corticosteroids for short intervals. Their long-term use in HIV-associated thrombocytopenia cannot be recommended.

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