indinavir-sulfate and Thrombophilia

Human immunodeficiency virus infection is an illness with protean manifestations including hematological abnormalities. Thromboembolic complications in HIV-infected patients have been described. Recent literature describes an incidence ranging from 0.26% to 7.6%; higher incidence is seen in patients with active opportunistic infections or malignancy, and in patients with the acquired immunodeficiency syndrome. A variety of potential mechanisms have been proposed to account for the observed hypercoagulability in HIV-infected patients. These include the presence of antiphospholipid-anticardiolipin antibodies, decreased activities of natural anticoagulants (especially protein S), and increased platelet activation. Recent epidemiological studies emphasize the increased incidence of thromboembolic events including myocardial infarction in the HIV-infected population after the introduction of highly active antiretroviral therapy. The use of protease inhibitors in particular is implicated. A hypercoagulable state and especially thromboses are emerging as clinical issues in HIV-infected patients. Further studies are in order to more clearly delineate the pathophysiologic mechanism(s) of thromboses in HIV-infected patients.

Topics: Adult; Antibodies, Antiphospholipid; Anticoagulants; Antiretroviral Therapy, Highly Active; Aspirin; Cohort Studies; HIV Infections; HIV Protease Inhibitors; Humans; Incidence; Indinavir; Middle Aged; Myocardial Infarction; Platelet Activation; Protein S Deficiency; Retrospective Studies; Risk Factors; Thromboembolism; Thrombophilia; Thrombosis