Abstract

Background and Aims : Several studies have demonstrated higher incidence, prevalence and progression of subclinical atherosclerosis in HIV infected individuals. Chronic disease of people living with human immunodeficiency virus (HIV) infection are now approaching those of the general population. Previous, in vitro studies shown that HIV causes arterial injuries resulting in inflammation and atherosclerosis but direct relationship between HIV infection clinical stages and lower extremity arterial disease (LEAD) remain controversial. No study assessed, with an accurate method, both the prevalence of LEAD and the influence of HIV severity on LEAD in HIV outpatients in Central Africa.Methods: A cross-sectional study was conducted among 1250 HIV-infected outpatients in Burundi. Inclusion criteria were as follows: age ≥ 20 years, positive HIV status, and currently receiving ART. Clinical data were extracted from Centre records. Personal information and details of PAD-related symptoms were obtained through face-to-face interviews. All patients underwent ankle-brachial index (ABI) measurement and LEAD was diagnosed by ABI≤0.9.Results: The prevalence of LEAD was 14.72 % (CI 95%: 13.2-22.1). The mean age was 42, 8±7, 4 years. On multivariable analysis, factors associated with LEAD were diabetes (OR= 1.7; 95% CI: 1.09–2.79), obesity (OR=2.5, 95% CI: 1.27–5.02) and stage IV HIV clinical infection (OR=4.7, 95% CI: 2.29–9.85).Conclusions: This is the first study performed on a large HIV population in Central Africa, reporting high LEAD prevalence. It underlines the influence of HIV infection on peripheral atherosclerosis at latest clinical stage and the need for LEAD screening in HIV-infected patients. Background and Aims : Several studies have demonstrated higher incidence, prevalence and progression of subclinical atherosclerosis in HIV infected individuals. Chronic disease of people living with human immunodeficiency virus (HIV) infection are now approaching those of the general population. Previous, in vitro studies shown that HIV causes arterial injuries resulting in inflammation and atherosclerosis but direct relationship between HIV infection clinical stages and lower extremity arterial disease (LEAD) remain controversial. No study assessed, with an accurate method, both the prevalence of LEAD and the influence of HIV severity on LEAD in HIV outpatients in Central Africa. Methods: A cross-sectional study was conducted among 1250 HIV-infected outpatients in Burundi. Inclusion criteria were as follows: age ≥ 20 years, positive HIV status, and currently receiving ART. Clinical data were extracted from Centre records. Personal information and details of PAD-related symptoms were obtained through face-to-face interviews. All patients underwent ankle-brachial index (ABI) measurement and LEAD was diagnosed by ABI≤0.9. Results: The prevalence of LEAD was 14.72 % (CI 95%: 13.2-22.1). The mean age was 42, 8±7, 4 years. On multivariable analysis, factors associated with LEAD were diabetes (OR= 1.7; 95% CI: 1.09–2.79), obesity (OR=2.5, 95% CI: 1.27–5.02) and stage IV HIV clinical infection (OR=4.7, 95% CI: 2.29–9.85). Conclusions: This is the first study performed on a large HIV population in Central Africa, reporting high LEAD prevalence. It underlines the influence of HIV infection on peripheral atherosclerosis at latest clinical stage and the need for LEAD screening in HIV-infected patients.

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