Review:Thromboses among HIV-Infected Patients during the Highly Active Antiretroviral Therapy Era

Abstract

Venous thrombotic events (VTEs) may occur at higher rates among HIV patients; some studies suggest that HAART may increase the risk for these potentially life-threatening events. We performed a retrospective study among HIV patients to evaluate the incidence and risk factors for VTEs during the HAART era. A literature review was performed examining VTEs in the pre-and post HAART eras. Seventeen (3.7%) of 465 HIV patients experienced a VTE. The overall incidence rate of deep VTEs among HIV positive persons was 377 cases/100,000 person-years, a four-fold higher rate compared to age-matched males in the general population. The median age at VTE was 36 years (range 27-68). Patients with a thrombosis compared to those without had significantly lower current CD4 (153 vs. 520 cells/mm 3 , p<0.001) and nadir (76 vs. 276 cells/mm 3 , p<0.001) CD4 counts, higher viral loads (3.6 vs. 1.7 log 10 copies/ml, p=0.003), and more likely to have a diagnosis of AIDS (76% vs. 32%, p<0.001); there were no differences in demographics, hyperlipidemia, current use of HAART, the duration of HAART or PI exposure. A review of the literature noted 129 VTE cases; mean age was 40 years, mean CD4 count was 181 cells/mm 3 , the majority of patients were not receiving HAART, and the most common risk factor was an ongoing infection. Thrombotic events are occurring among HIV patients despite their relatively young ages. Advanced HIV disease is a risk factor for development of thromboses, possibly due to an increased inflammatory state or the presence of concurrent comorbidities such as infections. HAART or PI therapy does not appear to play a significant role in the occurrence of VTEs.

Emerging roles for platelets as immune and inflammatory cells

“…The risk of thrombosis, including deep vein thrombosis and pulmonary embolism, is increased in HIV1 individuals. 156,157 The mechanisms are not clear but may involve increased platelet activation, and with it broad inflammatory consequences. Studies using a primate simian immunodeficiency virus infection model have shown that platelets are activated early in infection, contributing to a drop in platelet count immediately following infection.…”

Warfarin Therapy in the HIV Medical Home Model: Low Rates of Therapeutic Anticoagulation Despite Adherence and Differences in Dosing Based on Specific Antiretrovirals

“…[1][2][3] The exact mechanism for this hypercoagulability is unknown, but may involve abnormal levels of antiphospholipid antibodies and anticoagulant proteins, monocyte overexpression of thromboplastin, concurrent malignancies, immobilization, and the administration of prothrombotic medications. [4][5][6] Confusing matters is the fact that abnormal levels of free protein S and antiphospholipid antibodies are common in HIV-infected individuals and are not necessarily associated with the development of thromboses.…”

Interaction between inherited thrombophilia and HIV infection: fact or fancy?

“…8 As Bibas et al correctly point out, ongoing oppor tunistic infections can further increase the risk of VTE in patients infected with HIV. 9 We agree that infections and inher ited thrombophilia might have a synergic…”