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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...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International AIDS Society
2014
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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 |
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author | Díaz-Pollán, Beatriz Estrada, Vicente Fuentes-Ferrer, Manuel Gómez-Garré, Dulcenombre San Román-Montero, Jesús |
author_facet | Díaz-Pollán, Beatriz Estrada, Vicente Fuentes-Ferrer, Manuel Gómez-Garré, Dulcenombre San Román-Montero, Jesús |
author_sort | Díaz-Pollán, Beatriz |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-4225389 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | International AIDS Society |
record_format | MEDLINE/PubMed |
spelling | pubmed-42253892014-11-13 Lp-PLA2 levels in HIV-infected patients Díaz-Pollán, Beatriz Estrada, Vicente Fuentes-Ferrer, Manuel Gómez-Garré, Dulcenombre San Román-Montero, Jesús J Int AIDS Soc Poster Sessions – Abstract P189 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. International AIDS Society 2014-11-02 /pmc/articles/PMC4225389/ /pubmed/25397467 http://dx.doi.org/10.7448/IAS.17.4.19721 Text en © 2014 Díaz-Pollán B et al; licensee International AIDS Society http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Poster Sessions – Abstract P189 Díaz-Pollán, Beatriz Estrada, Vicente Fuentes-Ferrer, Manuel Gómez-Garré, Dulcenombre San Román-Montero, Jesús Lp-PLA2 levels in HIV-infected patients |
title | Lp-PLA2 levels in HIV-infected patients |
title_full | Lp-PLA2 levels in HIV-infected patients |
title_fullStr | Lp-PLA2 levels in HIV-infected patients |
title_full_unstemmed | Lp-PLA2 levels in HIV-infected patients |
title_short | Lp-PLA2 levels in HIV-infected patients |
title_sort | lp-pla2 levels in hiv-infected patients |
topic | Poster Sessions – Abstract P189 |
url | 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 |
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