During the current anti-retroviral era, the morbidity and mortality related to Human Immunodeficiency Virus (HIV) infection has shifted away from Acquired Immunodeficiency Syndrome (AIDS)-defining conditions and towards other clinical events. HIV-infected patients are at greater risk of developing venous thromboembolism (VTE) than the general population, with reports of up to a tenfold increased risk. Our clinical observations support these findings and suggest that degree of immunodeficiency and viral replication are predictive factors. Our aim is to identify characteristics common to HIV-positive patients who develop VTE.
All patients with HIV in the VA Loma Linda Healthcare System’s Clinical Case Registry (CCR) from 2000-2015 were screened to identify those with a history of deep venous thrombosis (DVT) or pulmonary embolism (PE); these patients were included in a retrospective case series. Each patient’s chart was reviewed to record epidemiological and clinical characteristics, which were described using frequencies for categorical variables, and mean and standard deviation (SD) for quantitative variables.
35 patients with HIV and history of DVT or PE were included in the retrospective case series. The incidence of VTE in this patient population is 3.5% from 2000-2015. All 35 patients were male (21 Caucasian, 10 African-American, and 4 Latin-American). Mean (SD) age at time of diagnosis of VTE was 58 (12), and mean (SD) BMI was 25.65 (4.51). 2.9% of patients (n=1) had used injection drugs. 85.7% (n= 30) were on anti-retroviral therapy (ART) at the time of diagnosis. 48.6% (n=17) had a history of opportunistic infection or malignancy, and 57.1% (n=20) had a history of recent hospitalization or surgery. Mean (SD) CD4 count at the time of diagnosis of VTE was 377 (244), while 34.3% (n=12) had detectable viral load and mean (SD) viral load was 16,697 (44,937).
Patients with HIV and who developed VTE often had relatively low CD4 counts and relatively high viral loads. This suggests a potential association of VTE with degree of immunodeficiency and viral replication, as seen in previous studies. Further investigation is necessary to determine correlation and/or causation.
M. Ing, None