Lipoprotein particle subclasses, cardiovascular disease and HIV infection

Duprez, Daniel; Kuller, Lewis H.; Tracy, Russell P.; Otvos, James D.; Cooper, David A.; Hoy, Jennifer; Neuhaus, Jacqueline; Paton, Nicholas I.; Friis-Møller, Nina; Lampe, Fiona; Liappis, Angelike P.; Neaton, James D.

doi:10.1016/j.atherosclerosis.2009.05.001

Cited by 103 publications

(104 citation statements)

References 19 publications

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“…However, and in contrast with our present observations, it has been reported that the concentration of cholesterol in large HDL particles was unaltered in HIV-infected patients as compared with uninfected controls ( 32 ). Interruption of HAART was associated with a reduction in HDL particles of medium and small size ( 35 ), or only in HDL particles of medium size with no change in HDL particles of small size ( 36 ). We presently observed a specifi c reduction of the large HDL2b subfraction in HIV-infected patients when compared with controls.…”

Section: Discussioncontrasting

confidence: 56%

Plasma cholesterol efflux capacity from human THP-1 macrophages is reduced in HIV-infected patients: impact of HAART

Khoury

Ghislain

Villard

et al. 2015

Journal of Lipid Research

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Coronary heart disease rates are expected to be higher as the human immunodefi ciency virus (HIV) population ages. Controversy still exists as to whether HIV infection per se or its treatment increases the rate of coronary heart disease. Highly active antiretroviral therapy (HAART) has been associated with the occurrence of cardiovascular events in HIV-infected patients ( 1, 2 ). However, in the Strategies for Managment of Antiretroviral Therapy (SMART) trial, the episodic use of HAART was associated with an increased risk of CVD when compared with continuous HAART use ( 3 ). It is now well-established that atherosclerosis Abstract The capacity of HDL to remove cholesterol from macrophages is inversely associated with the severity of angiographic coronary artery disease . The effect of human immunodefi ciency virus (HIV) infection or its treatment on the ability of HDL particles to stimulate cholesterol effl ux from human macrophages has never been studied. We evaluated the capacity of whole plasma and isolated HDL particles from HIV-infected subjects (n = 231) and uninfected controls (n = 200), as well as in a subset of 41 HIV subjects receiving highly active antiretroviral therapy (HAART) to mediate cholesterol effl ux from human macrophages. Plasma cholesterol effl ux capacity was reduced ( ؊ 12%; P = 0.001) in HIV patients as compared with controls. HIV infection reduced by 27% ( P < 0.05) the capacity of HDL subfractions to promote cholesterol effl ux from macrophages. We observed a reduced ABCA1-dependent effl ux capacity of plasma ( ؊ 27%; P < 0.0001) from HIV-infected subjects as a result of a reduction in the effl ux capacity of HDL3 particles. HAART administration restored the capacity of plasma from HIV patients to stimulate cholesterol effl ux from human macrophages (9.4%; P = 0.04). During HIV infection, the capacity of whole plasma to remove cholesterol from macrophages is reduced, thus potentially contributing to the increased coronary heart disease in the HIV population. HAART administration restored the removal of cholesterol from macrophages by increasing HDL functionality. -El Khoury, P., M. Ghislain,

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Section: Discussioncontrasting

confidence: 56%

Plasma cholesterol efflux capacity from human THP-1 macrophages is reduced in HIV-infected patients: impact of HAART

Khoury

Ghislain

Villard

et al. 2015

Journal of Lipid Research

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“…We could not demonstrate a significant change in the percentage of patients with atherogenic plasma levels of lipoproteins commonly associated with hypertriglyceridemia, such as slightly triglyceride-enriched VLDL and sdLDL-apoB. However, the risk of cardiovascular events in our population remains a concern mainly due to the high percentage of patients with low HDL, 42 frequent smoking, 43 and inflammatory factors associated with HIV infection. 44 …”

Section: Discussionmentioning

confidence: 54%

Lipid and Lipoprotein Profile in HIV-Infected Patients Treated with Lopinavir/Ritonavir as a Component of the First Combination Antiretroviral Therapy

Magenta

Dell-Kuster

Richter³

et al. 2011

AIDS Research and Human Retroviruses

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We characterized lipid and lipoprotein changes associated with a lopinavir/ritonavir-containing regimen. We enrolled previously antiretroviral-naive patients participating in the Swiss HIV Cohort Study. Fasting blood samples (baseline) were retrieved retrospectively from stored frozen plasma and posttreatment (follow-up) samples were collected prospectively at two separate visits. Lipids and lipoproteins were analyzed at a single reference laboratory. Sixty-five patients had two posttreatment lipid profile measurements and nine had only one. Most of the measured lipids and lipoprotein plasma concentrations increased on lopinavir/ritonavir-based treatment. The percentage of patients with hypertriglyceridemia (TG >150 mg/dl) increased from 28/74 (38%) at baseline to 37/65 (57%) at the second follow-up. We did not find any correlation between lopinavir plasma levels and the concentration of triglycerides. There was weak evidence of an increase in small dense LDL-apoB during the first year of treatment but not beyond 1 year (odds ratio 4.5, 90% CI 0.7 to 29 and 0.9, 90% CI 0.5 to 1.5, respectively). However, 69% of our patients still had undetectable small dense LDL-apoB levels while on treatment. LDL-cholesterol increased by a mean of 17 mg/dl (90% CI -3 to 37) during the first year of treatment, but mean values remained below the cut-off for therapeutic intervention. Despite an increase in the majority of measured lipids and lipoproteins particularly in the first year after initiation, we could not detect an obvious increase of cardiovascular risk resulting from the observed lipid changes. We characterized lipid and lipoprotein changes associated with a lopinavir/ritonavir-containing regimen. We enrolled previously antiretroviral-naive patients participating in the Swiss HIV Cohort Study. Fasting blood samples (baseline) were retrieved retrospectively from stored frozen plasma and posttreatment (follow-up) samples were collected prospectively at two separate visits. Lipids and lipoproteins were analyzed at a single reference laboratory. Sixty-five patients had two posttreatment lipid profile measurements and nine had only one. Most of the measured lipids and lipoprotein plasma concentrations increased on lopinavir/ritonavir-based treatment. The percentage of patients with hypertriglyceridemia (TG >150 mg/dl) increased from 28/74 (38%) at baseline to 37/65 (57%) at the second follow-up. We did not find any correlation between lopinavir plasma levels and the concentration of triglycerides. There was weak evidence of an increase in small dense LDL-apoB during the first year of treatment but not beyond 1 year (odds ratio 4.5, 90% CI 0.7 to 29 and 0.9, 90% CI 0.5 to 1.5, respectively). However, 69% of our patients still had undetectable small dense LDL-apoB levels while on treatment. LDL-cholesterol increased by a mean of 17 mg/dl (90% CI À3 to 37) during the first year of treatment, but mean values remained below the cut-off for therapeutic intervention. Despite an increase in the majority of measured...

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“…43 This association contributes to the consideration of HIV-infected patients at risk of coronary heart disease (CHD). In contrast, Duprez et al 44 found that, neither VLDL-p nor LDL-p concentrations were associated with CVD. 44 In general it's clear that HIV infection and subsequent treatment interfere with lipid metabolism to increase the possibility of cardiovascular complications for the patients.…”

Section: Nmr-based Metabonomics Of Hiv-infected Biofluidmentioning

confidence: 90%

Metabonomic analysis of HIV-infected biofluids

2013

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Monitoring the progression of HIV infection to full-blown acquired immune deficiency syndrome (AIDS) and assessing responses to treatment will benefit greatly from the identification of novel biological markers especially since existing clinical indicators of disease are not infallible. Nuclear magnetic resonance spectroscopy (NMR) and mass spectrometry (MS) are powerful methodologies used in metabonomic analyses for an approximation of HIV-induced changes to the phenotype of an infected individual. Although early in its application to HIV/AIDS, (biofluid) metabonomics has already identified metabolic pathways influenced by both HIV and/or its treatment. To date, biofluid NMR and MS data show that the virus and highly active antiretroviral treatment (HAART) mainly influence carbohydrate and lipid metabolism, suggesting that infected individuals are susceptible to very specific metabolic complications. A number of well-defined biofluid metabonomic studies clearly distinguished HIV negative, positive and treatment experienced patient profiles from one another. While many of the virus or treatment affected metabolites have been identified, the metabonomics measurements were mostly qualitative. The identities of the molecules were not always validated neither were the statistical models used to distinguish between groups. Assigning particular metabolic changes to specific drug regimens using metabonomics also remains to be done. Studies exist where identified metabolites have been linked to various disease states suggesting great potential for the use of metabonomics in disease prognostics. This review therefore examines the field of metabonomics in the context of HIV/AIDS, comments on metabolites routinely detected as being affected by the pathogen or treatment, explains what existing data suggest and makes recommendations on future research.

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Lipoprotein particle subclasses, cardiovascular disease and HIV infection

Cited by 103 publications

References 19 publications

Plasma cholesterol efflux capacity from human THP-1 macrophages is reduced in HIV-infected patients: impact of HAART

Plasma cholesterol efflux capacity from human THP-1 macrophages is reduced in HIV-infected patients: impact of HAART

Lipid and Lipoprotein Profile in HIV-Infected Patients Treated with Lopinavir/Ritonavir as a Component of the First Combination Antiretroviral Therapy

Metabonomic analysis of HIV-infected biofluids

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