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. 2011;3(1):e2011030.
doi: 10.4084/MJHID.2011.030. Epub 2011 Jul 8.

HIV-Associated Venous Thromboembolism

Affiliations

HIV-Associated Venous Thromboembolism

Michele Bibas et al. Mediterr J Hematol Infect Dis. 2011.

Abstract

HIV infection has been recognized as a prothrombotic condition and this association has now been proven by a large number of studies with a reported VTE frequency among HIV-infected patients ranging from 0.19% to 7,63 %/year. HIV infection is associated with a two to tenfold increased risk of venous thrombosis in comparison with a general population of the same age. Some risk factors demonstrated a strongest association with VTE such as, low CD4(+) cell count especially in the presence of clinical AIDS, protein S deficiency, and protein C deficiency. Whereas other risk factors are still controversial like protease inhibitor therapy, presence of active opportunistic infections and presence of antiphospholipid antibodies, including anticardiolipin antibodies and lupus anticoagulant. Physicians caring for HIV positive patients should be able to recognize and treat not only the well-known opportunistic infections and malignancies associated with this chronic disease, but also be alert to the less well-known complications such as thromboses. Pulmonary embolism should be included in the differential diagnosis when patients with HIV/AIDS have unexplained dyspnea or hypoxemia. In younger individuals with VTE, especially men, without other identifiable risk factors for VTE, HIV should be considered. Because interactions between warfarin and antiretrovirals is possible, health care providers should also be alert to the potential of dangerously high or low INRs when they are giving anticoagulants to patients with HIV infection who are undergoing antiretroviral therapy.

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Figures

Figure 1:
Figure 1:
Multi-factorial etiology of HIV-related venous thromboembolism. AT, antithrombin; sTM, soluble thrombomodulin; TFPI, tissue factor pathway inhibitor; v-WF, von Willebrand Factor; PAI-I, plasminogen activator inhibitor-1; tPA, tissue plasminogen activator. Stronger risk factors for VTE are listed in bold.
Figure 2:
Figure 2:
Diagram summarizing the pathogenesis of HIV-related VTE. HIV, human immunodeficiency virus; LPS, lipopolysaccharide; TLR, toll-like receptor; AT, antithrombin; ACA, anticardiolipin antibodies; LA, lupus anticoagulant; TF, Tissue Factor; TNF-a, tumor necrosis factor alpha; IL-6, interleukin six; hsCRP, high-sensitivity C-reactive protein; MCP1, monocyte chemotactic protein-1; sTM, soluble thrombomodulin; TFPI, tissue factor pathway inhibitor; v-WF, von Willebrand Factor; PAI-I, plasminogen activator inhibitor-1; tPA, tissue plasminogen activator

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