Risk Factors for Venous Thromboembolism in Patients with Human Immunodeficiency Virus Infection

Katie L. Kiser, Pharm.D.; Melissa E. Badowski, Pharm.D.

Disclosures

Pharmacotherapy. 2010;30(12):1292-1302. 

In This Article

Abstract and Introduction

Abstract

Prevention and treatment of venous thromboembolism are gaining attention in the lay and medical communities because of an increase in frequency, cost, and risk factors. Evidence shows that patients with human immunodeficiency virus (HIV) have multiple risk factors and a 2–10-fold increased risk for venous thromboembolism compared with the general population. A higher rate of venous thromboembolism also occurs in patients with HIV who are younger than 50 years (3.31% vs 0.53% in age-matched healthy controls, p<0.0001), have a CD4+ cell count less than 200 cells/mm3, or have a diagnosis of acquired immunodeficiency syndrome. Both protein S and C deficiencies—disorders that may predispose individuals to thrombotic disease—are considered risk factors; in addition, the use of protease inhibitors and the presence of active opportunistic infections or antiphospholipid antibodies may be associated with venous thromboembolism. It is imperative that all risk factors for venous thromboembolism be identified and incorporated into medical decision making for high-risk patients, including those with HIV. The classification and mechanism of these risk factors are not well understood. Long-term, prospective studies assessing the factors associated with venous thromboembolism in patients with HIV are needed. Risk stratification systems or screening tools, as well as effective preventive measures, must be developed.

Introduction

The number of venous thromboembolism (VTE) cases that occur each year is approximately 2 million at a cost of over $1.5 billion/year in the United States.[1] This has prompted national recognition to improve the awareness, prevention, and treatment of VTE.[2–5] Many cases of VTE are thought to be preventable with appropriate awareness and prophylaxis, especially in high-risk patients. Although there are many high-risk populations, those with the human immunodeficiency virus (HIV) or acquired immunodeficiency syndrome (AIDS) have not been addressed in national guidelines despite evidence to support an increased risk for VTE in this population.[6–8]

The frequency of VTE in patients with HIV ranges from 0.19–7.63%/year, with most reports citing 1–2%.[6,9–20] This frequency has been correlated to an approximate 10-fold increase in the risk for VTE in the HIV population compared with the general population.[8] The diagnosis of VTE in these studies was generally through International Classification of Disease, Ninth Revision codes, venous duplex ultrasonography, abdominal computed tomography (CT), ventilation-perfusion lung scans, or CT pulmonary angiography. This overall increased risk for VTE in patients with HIV is comparable to the risk for a patient without HIV who has commonly recognized thrombophilias such as heterozygous factor V Leiden, protein C deficiency, or protein S deficiency.[18]

There are many theories and proposed mechanisms as to why an increased risk for thrombosis has been found in HIV-infected individuals. Thrombosis can occur due to conventional risk factors such as venous stasis, impaired response of the anticoagulation cascade, damage to the vessel wall, and drug-induced effects. In patients with HIV, these risk factors may already be present and further complicated and/or exacerbated by the infection. Infection with HIV can interfere with the synthesis and/or metabolism of clotting factors and proteins, cause the release of procoagulant factors from AIDS-related cancers, cause intravascular coagulation due to severe immuno-suppression, alter the endothelium, and increase circulation of proinflammatory cytokines. When all of these factors are combined, abnormalities in hemostasis lead to a procoagulant state and potentially cause a VTE.[15,21]

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