Dyslipidemia and Cardiovascular Risk in Human Immunodeficiency Virus Infection

Kelesidis, Theodoros; Currier, Judith S.

doi:10.1016/j.ecl.2014.06.003

Cited by 38 publications

(53 citation statements)

References 98 publications

(130 reference statements)

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“…Los pacientes que no han sido previamente tratados con TARGA también pueden presentar dislipidemia aterogénica, pero los niveles de CT y LDL, por lo general, no están elevados (11,12) .…”

Section: Discussionunclassified

“…La utilización de IP está asociada a dislipidemia, independientemente de la carga viral, recuento de linfocitos CD4 y sexo, e incluso de otros factores de riesgo cardiovascular como el tabaquismo (11) . Por tal motivo, el uso de IP ya se incluye como factor en algunas escalas de riesgo cardiovascular (14) .…”

Section: Discussionunclassified

“…En el Perú, el uso de fármacos IP se ha indicado, principalmente, en los casos de fracaso terapéutico o intolerancia a drogas de primera línea, y es utilizado por casi el 20% de los pacientes actualmente en tratamiento (15) . Si bien los IP tienen un mayor riesgo para el desarrollo de dislipidemia, los INTR y los INNTR también presentan asociación (11) . En el análisis por cada grupo farmacológico encontramos diferencias significativas entre los INNTR, con una menor frecuencia de dislipidemia entre quienes usaban esquemas que incluían nevirapina, en comparación con los que incorporan efavirenz.…”

Section: Discussionunclassified

“…A pesar de sus múltiples efectos adversos, el uso de TARGA es necesario para suprimir la carga viral y reconstituir el sistema inmune; además, disminuye el estado de inflamación crónica y otras vías de desarrollo de enfermedad cardiovascular (11) . Las guías de manejo de las PVVS en TARGA recomiendan controles lipídicos periódicos.…”

Section: Discussionunclassified

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Elevada frecuencia de dislipidemia en pacientes infectados por VIH en un hospital público peruano

Taype‐Rondan

Flores-Flores

Doria

et al. 2017

Rev Peru Med Exp Salud Publica

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RESUMENEl objetivo del estudio fue determinar la frecuencia y características de la dislipidemia en pacientes con VIH en terapia antirretroviral de gran actividad (TARGA) en un hospital público peruano. Se realizó un estudio transversal en pacientes que tuvieran un perfil lipídico completo luego de recibir al menos seis meses de TARGA. La dislipidemia se definió según los criterios NCEP-ATP III. Se revisaron 2975 historias clínicas, 538 (18.1%) fueron incluidas en el análisis. La frecuencia de dislipidemia fue 74.7%. Los esquemas de TARGA que incluían inhibidores de la proteasa (IP) (OR 1.22; IC95% 1,11-1,34) y la edad mayor de 40 años (OR 1.17; IC95% 1,06-1,29) mostraron asociación con dislipidemia, ajustado por carga viral, nivel de células CD4 y sexo. En conclusión, la dislipidemia fue muy frecuente en la muestra estudiada y estuvo asociada principalmente al uso de IP. Es necesario promover el control de la dislipidemia como parte de la atención integral del paciente con infección por VIH. Palabras clave: Dislipidemias; VIH; Terapia antirretroviral altamente activa (fuente: DeCS BIREME). HIGH FREQUENCY OF DYSLIPIDEMIA IN HIV-INFECTED PATIENTS IN A PERUVIAN PUBLIC HOSPITAL ABSTRACTThe objective of the study was to determine the frequency and characteristics of dyslipidemia in patients with HIV in highly active antiretroviral therapy (HAART) in a Peruvian public hospital. A cross-sectional study was carried out in patients with complete lipid profile after receiving at least six months of HAART. Dyslipidemia was defined according to the criteria of the NCEP-ATP III. We reviewed 2 975 clinical histories, and included 538 (18.1%) in the analysis. The frequency of dyslipidemia was 74.7%. HAART regimens which include protease inhibitors (PI) (odds ratio [OR]: 1.22; confidence interval at 95% [CI 95%]: 1.11-1.33) and to be older than 40 years (OR: 1.17; CI 95%: 1.05-1.28) were associated with dyslipidemia, adjusted by viral load, CD4 lymphocyte level and gender. In conclusion, dyslipidemia was very common in our sample and was mainly associated with the use of PI. It is necessary to promote the dyslipidemia control as part of the comprehensive care of the patient with HIV.

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Section: Discussionunclassified

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Elevada frecuencia de dislipidemia en pacientes infectados por VIH en un hospital público peruano

Taype‐Rondan

Flores-Flores

Doria

et al. 2017

Rev Peru Med Exp Salud Publica

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“…Despite potent antiretroviral therapy (ART) HIV-1-infected (HIV + ) individuals have an approximately twofold increased risk of atherosclerotic cardiovascular disease (CVD), but the mechanisms are unclear [1]. High-density lipoprotein (HDL) levels are a powerful independent negative predictor of CVD; however, HDL structure and function rather than absolute level may more accurately predict atherosclerosis [1].…”

Section: Introductionmentioning

confidence: 99%

Dysfunctional high-density lipoprotein from HIV+ individuals promotes monocyte-derived foam cell formation in vitro

Angelovich

Hearps

Oda

et al. 2017

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Objective The role of high-density lipoprotein (HDL) function in HIV-related atherosclerotic cardiovascular disease (CVD) is unclear. HDLs isolated from HIV+ [HIV(+)HDL] and HIV-uninfected individuals [HIV(−)HDL] were assessed for HDL function and ability to promote monocyte-derived foam cell formation (MDFCF; a key event in HIV-related CVD) ex vivo. Design/methods Using an established in-vitro model of atherogenesis and plasma samples from an established cross-sectional study of virologically suppressed HIV+ men on stable effective antiretroviral therapy and with low CVD risk (median age: 42 years; n = 10), we explored the impact of native HDL [HIV(+)HDL] on MDFCF. In this exploratory study, we selected HIV(+)HDL known to be dysfunctional based on two independent measures of impaired HDL function: antioxidant (high HDLox) ability of HDL to release apoA-I (low HDL-apoA-I exchange). Five healthy men matched by age and race to the HIV+ group were included. Given that oxidation of HDL leads to abnormal HDL function, we also compared proatherogenic effects of HIV(+)HDL vs. chemically derived HDLox. The ex-vivo atherogenesis assay was performed using lipoproteins (purchased or isolated from plasma using ultracentrifugation) and monocytes purified via negative selection from healthy donors. Results HIV(+)HDL known to have reduced antioxidant function and rate of HDL/ApoAI exchange promoted MDFCF to a greater extent than HDL (33.0 vs. 26.2% foam cells; P = 0.015). HDL oxidized in vitro also enhanced foam cell formation as compared with nonoxidized HDL (P < 0.01). Conclusion Dysfunctional HDL in virologically suppressed HIV+ individuals may potentiate atherosclerosis in HIV infection by promoting MDFCF.

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Intravascular hemolysis triggers NAFLD characterized by a deregulation of lipid metabolism and lipophagy blockade

Rayego‐Mateos

Morgado‐Pascual

García‐Caballero

et al. 2023

The Journal of Pathology

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Intravascular hemolysis is a common feature of different clinical entities, including sickle cell disease and malaria. Chronic hemolytic disorders are associated with hepatic damage; however, it is unknown whether heme disturbs lipid metabolism and promotes liver steatosis, thereby favoring the progression to nonalcoholic fatty liver disease (NAFLD). Using an experimental model of acute intravascular hemolysis, we report here the presence of liver injury in association with microvesicular lipid droplet deposition. Hemolysis promoted serum hyperlipidemia and altered intrahepatic triglyceride fatty acid composition, with increments in oleic, palmitoleic, and palmitic acids. These findings were related to augmented expression of transporters involved in fatty acid uptake (CD36 and MSR1) and deregulation of LDL transport, as demonstrated by decreased levels of LDL receptor and increased PCSK9 expression. Hemolysis also upregulated hepatic enzymes associated with cholesterol biosynthesis (SREBP2, HMGC1, LCAT, SOAT1) and transcription factors regulating lipid metabolism (SREBP1). Increased LC3II/LC3I ratio and p62/SQSTM1 protein levels were reported in mice with intravascular hemolysis and hepatocytes stimulated with heme, indicating a blockade of lipophagy. In cultured hepatocytes, cell pretreatment with the autophagy inductor rapamycin diminished heme‐mediated toxicity and accumulation of lipid droplets. In conclusion, intravascular hemolysis enhances liver damage by exacerbating lipid accumulation and blocking the lipophagy pathway, thereby promoting NAFLD. These new findings have a high translational potential as a novel NAFLD‐promoting mechanism in individuals suffering from severe hemolysis episodes. © 2023 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

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Dyslipidemia and Cardiovascular Risk in Human Immunodeficiency Virus Infection

Cited by 38 publications

References 98 publications

Elevada frecuencia de dislipidemia en pacientes infectados por VIH en un hospital público peruano

Elevada frecuencia de dislipidemia en pacientes infectados por VIH en un hospital público peruano

Dysfunctional high-density lipoprotein from HIV+ individuals promotes monocyte-derived foam cell formation in vitro

Intravascular hemolysis triggers NAFLD characterized by a deregulation of lipid metabolism and lipophagy blockade

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