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Lp-PLA2 levels in HIV-infected patients

INTRODUCTION: HIV-infected patients show an increased risk of cardiovascular disease (CVD). In the general population, lipoprotein-associated phospholipase A2 (Lp-PLA2) appears to be an independent predictor of CVD. We aimed to study associations between Lp-PLA2 plasma levels and other risk factors...

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Detalles Bibliográficos
Autores principales: Díaz-Pollán, Beatriz, Estrada, Vicente, Fuentes-Ferrer, Manuel, Gómez-Garré, Dulcenombre, San Román-Montero, Jesús
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International AIDS Society 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4225389/
https://www.ncbi.nlm.nih.gov/pubmed/25397467
http://dx.doi.org/10.7448/IAS.17.4.19721
Descripción
Sumario:INTRODUCTION: HIV-infected patients show an increased risk of cardiovascular disease (CVD). In the general population, lipoprotein-associated phospholipase A2 (Lp-PLA2) appears to be an independent predictor of CVD. We aimed to study associations between Lp-PLA2 plasma levels and other risk factors for CVD in HIV patients. MATERIALS AND METHODS: A cross-sectional, comparative study of two series of cases (HIV patients, n=116 and age-matched non-HIV healthy controls, n=113) was conducted. Eighty-seven percent HIV patients on antiretroviral therapy (ART), 72.4% with HIV-1 viral load <50 cop/mL. Inflammatory biomarkers (CRP, Lp-PLA2) and internal carotid intima-media thickness (IMT) were measured and CVD risk (Framingham and SCORE algorithms) was calculated. Univariate and multivariable associations between these variables were performed. RESULTS: HIV patients presented higher Lp-PLA2 levels [276.81 ng/mL (209.71–356.58)] than uninfected healthy controls [220.80 ng/mL (172.70–256.90)], p≤0.01. In univariate analysis of the global sample, only cigarette smoking was associated with higher Lp-PLA2 levels, p≤0.001. In HIV group, female and smoker patients showed higher Lp-PLA2 levels, p≤0.05. No significant association was found between Lp-PLA2 levels and another CVD risk factors, carotid IMT, Framingham and SCORE algorithms, ART, HIV-1 viral load neither and CD4+ T lymphocyte count. In multivariate analysis, cigarette smoking remained significantly associated with Lp-PLA2 levels [β=64.8 (95% CI 10.8–118.9) ng/mL, p=0.020]. CONCLUSIONS: HIV-infected patients present higher Lp-PLA2 levels than healthy controls, and in this population, tobacco smoking is significantly associated with increased Lp-PLA2 levels. Smoking cessation should be a priority in CVD prevention in HIV-infected patients.