indinavir-sulfate and Thrombosis

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

A 40-year-old HIV-infected woman developed nausea, vomiting, and epigastric pain and died following her third dose (per study protocol) of interleukin (IL)-2. Her HIV infection was diagnosed in 1996. Her last CD4 cell count was 390/microL, and her viral load was negligible (as of November 28, 1998). She had no known general risk factors for thrombosis other than HIV infection, injection drug abuse, and antiretroviral therapy with indinavir. Abdominal films showed no sign of mechanical obstruction but a generalized gas distention of the bowel, which was suggestive of paralytic ileus. Autopsy revealed dilation of the small bowel with extensive necrosis and hemorrhage involving all the segments. The superior and inferior mesenteric arteries revealed severe atherosclerosis. The stenotic celiac artery was occluded by a recent thrombus at the aortic ostium. Clinicians need to be aware of the potential for thrombosis and accelerated atherosclerosis in HIV-infected patients. Both injection drug abuse and protease inhibitors, such as indinavir, have been shown to be risk factors for thrombosis. However, it is likely IL-2 contributed to the severe thrombosis in this patient, although definitive proof is lacking. An acute awareness of intestinal infarction in HIV-infected patients is warranted.

Topics: Adult; Anti-HIV Agents; Celiac Artery; Female; HIV Infections; Humans; Indinavir; Infarction; Interleukin-2; Intestines; Mesenteric Arteries; Mesenteric Vascular Occlusion; Radiography; Thrombosis