HIV/AIDS and the Risk of Deep Vein Thrombosis: A Study of 45 Patients with Lower Extremity Involvement

Abstract

Many aspects of acquired immunodeficiency syndrome (AIDS) have been described in detail in the literature. However, there have been very few articles on the phenomenon of deep vein thrombosis (DVT) in the lower extremities of human immunodeficiency virus (HIV)/AIDS patients. The objective of this communication is to record the incidence of DVT in HIV/AIDS patients and the risks for development of embolic events and to emphasize the need for prevention and for the vigorous treatment of this complication. We conducted a retrospective review of HIV/AIDS-infected patients with DVT admitted to Mount Sinai School of Medicine/Cabrini Hospital in New York during the last 5 years. Analysis includes demographic data; risk factors for HIV/AIDS infection; associated medical problems; recent surgery; and laboratory findings including CD4 counts, platelet counts, prothrombin times, partial thromboplastin times, and plasma albumin levels; and image studies. From January 1995 to January 2000 4752 HIV/AIDS-infected patients were admitted. Of those admitted to the hospital 45 (0.95%) were found to have DVT. There were 36 males and nine females (mean age 43 years). Of the 45 patients 38 had infectious complications and 13 developed a malignancy. The distribution of the thromboses were the femoral vein in 23 patients, the popliteal vein in 20 patients, and the iliofemoral system in 2 patients. Twelve patients had recurrent DVT and three patients developed a pulmonary embolism. HIV/AIDS infection is a considerable risk for development of DVT in the lower extremity. Statistically DVT in HIV/AIDS is approximately 10 times greater than in the general population. Emphasis upon prevention and vigorous treatment of DVT is recommended.

Venous thromboembolism in viral diseases: A comprehensive literature review

“…Therefore, opportunistic infections and developed HIV being concomitantly present can be an additional risk for VTE. 36 , 43 , 58 VTE is mostly established with Mycobacterium avium intracellular, CMV, and pneumocystis jiroveci pneumonia (PCP).…”

“…Despite HAART efficacy, HIV‐positive patients can develop opportunist infections relying on their immunologic condition. Therefore, opportunistic infections and developed HIV being concomitantly present can be an additional risk for VTE 36,43,58 . VTE is mostly established with Mycobacterium avium intracellular, CMV, and pneumocystis jiroveci pneumonia (PCP).…”

“…The occurrence of thromboembolism in KS and HIV patients ranged from 9.3% to 20%. Other malignancies were rare including colon cancer, prostate cancer, B‐cell NHL, anal cancer, primary central nervous system (CNS) Lymphoma, and Hodgkin's disease 45,51,58 …”

Plasminogen Activator Inhibitor 1 (PAI-1) and Haematologic Parameters in HIV- Positive Patients on Protease Inhibitor-Based HAART Regimen: A Case-Control Study

“… 4 The risk of deep vein thrombosis in patients with HIV infection has been estimated to be 2–10 fold higher than in the general population. 5 Other thrombotic complications such as coronary artery events (myocardial infarction) have also been reported in HIV-infected persons. 6 …”

“…4 The risk of deep vein thrombosis in patients with HIV infection has been estimated to be 2-10 fold higher than in the general population. 5 Other thrombotic complications such as coronary artery events (myocardial infarction) have also been reported in HIV-infected persons. 6 The interplay of the components of Virchow triad has been reported to play a role in the pathogenesis of thrombotic events in HIV infection.…”