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HAART-associated dyslipidemia varies by biogeographical ancestry in the multicenter AIDS cohort study.

ABSTRACT: Highly active antiretroviral therapy (HAART) has been successful in delaying the progression to AIDS in HIV-1-infected individuals. Exposure to HAART can result in metabolic side effects, such as dyslipidemia, in a subset of recipients. Longitudinal data and frozen peripheral blood mononuclear cell pellets were obtained from 1,945 men enrolled in the Multicenter AIDS Cohort. Individuals were genotyped for ancestry informative markers (AIMs) and stratified by biogeographical ancestry (BGA). Then serum levels of total cholesterol (TCHOL), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglyceride (TRIG) were examined controlling for a number of HIV and HAART-related covariates using multivariate mixed-effects linear regression. HIV-1 infection, in the absence of HAART, was associated with altered lipid levels for all phenotypes tested when compared to HIV-negative men. HIV-1-infected men receiving HAART also had significantly different lipid levels compared to HIV-negative men, except for LDL-C. There were statistically significant interactions between BGA and HIV/HAART status for all lipids tested. BGA remained significantly associated with lipid levels after controlling for other HIV and HAART-related covariates. There was low concordance between self-reported race (SRR) and BGA in admixed populations. BGA performed better than SRR in our statistical models. Lipid profiles in untreated HIV-1-positive men and HIV-1-positive men receiving HAART differ from HIV-negative men and this effect varies by BGA. BGA performed better in our statistical analysis as a racial classifier but SRR remains a good clinical surrogate for BGA.

SUBMITTER: Nicholaou MJ

PROVIDER: S-EPMC3653392 | biostudies-literature | 2013 Jun

REPOSITORIES: biostudies-literature

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HAART-associated dyslipidemia varies by biogeographical ancestry in the multicenter AIDS cohort study.

Nicholaou Matthew J MJ Martinson Jeremy J JJ Abraham Alison G AG Brown Todd T TT Hussain Shehnaz K SK Wolinsky Steven M SM Kingsley Lawrence A LA

AIDS research and human retroviruses 20130308 6

Highly active antiretroviral therapy (HAART) has been successful in delaying the progression to AIDS in HIV-1-infected individuals. Exposure to HAART can result in metabolic side effects, such as dyslipidemia, in a subset of recipients. Longitudinal data and frozen peripheral blood mononuclear cell pellets were obtained from 1,945 men enrolled in the Multicenter AIDS Cohort. Individuals were genotyped for ancestry informative markers (AIMs) and stratified by biogeographical ancestry (BGA). Then ...[more]

PMID: 23343448

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Project description:BackgroundThough the initiation of Highly Active Antiretroviral Therapy (HAART) has led to decreased HIV/AIDS related mortality, the regimen has been reported to be associated with lipid toxicities. Baseline data on such disturbances are required to induce countrywide interventional HIV/AIDS programs. The aim of this study was to determine the frequency and risks of dyslipidemia in HIV patients on HAART medication in Eritrea.MethodsA cross sectional study was conducted on HIV/AIDS patients in two national referral hospitals in Asmara, Eritrea. A structured questionnaire was used to collect demographic data and blood sample was taken for analyses of lipid profile tests. Data was analyzed using chi-square test, Post Hoc and logistic regression in SPSS software.ResultsThe study included 382 participants of whom 256(67%) were females. Their median age, CD4+ T cell count (cell/microliter) and duration of HAART (years) was 45(IQR: 38-51), 434(IQR: 294-583) & 5(IQR: 3-5) respectively. The prevalence of dyslipidemia was 331(86.6%). Increased Low Density Lipoprotein-C (LDL-C) 213(55.8%) was the predominant abnormality. Abacavir was significantly related with highest means of triglycerides (TG) (228.17 ± 193.81) and lowest means of High Density Lipoprotein (HDL-C) (46.94 ± 12.02). Females had substantially higher proportions of TG (aOR = 2.89, 95% CI: 1.65-5.05) and TC/HDL ratio (aOR = 2.33, 95% CI: 1.40-3.87) and low HDL-C (aOR = 2.16, 95% CI: 1.34-3.48). Increased age was related with increased pro-atherogenic lipid parameters. High LDL-C was more infrequent in non-smokers (aOR = 0.028, 95% CI: 0.12-0.69).ConclusionThe study showed a high prevalence of dyslipidemia in HIV-patients receiving HAART in Eritrea. Sex, age and smoking practice were among key factors associated with dyslipidemia. The necessity to assess lipid profiles and other cardiovascular risk factors before initiation of HAART treatment and continuous monitoring during therapy is mandatory.

Project description:BackgroundPeople living with human immunodeficiency virus (HIV+) have greater risk for sudden arrhythmic death than HIV-uninfected (HIV-) individuals. HIV-associated abnormal cardiac repolarization may contribute to this risk. We investigated whether HIV serostatus is associated with ventricular repolarization lability by using the QT variability index (QTVI), defined as a log measure of QT-interval variance indexed to heart rate variance.MethodsWe studied 1123 men (589 HIV+ and 534 HIV-) from MACS (Multicenter AIDS Cohort Study), using the ZioXT ambulatory electrocardiography patch. Beat-to-beat analysis of up to 4 full days of electrocardiographic data per participant was performed using an automated algorithm (median analyzed duration [quartile 1-quartile 3]: 78.3 [66.3-83.0] hours/person). QTVI was modeled using linear mixed-effects models adjusted for demographics, cardiac risk factors, and HIV-related and inflammatory biomarkers.ResultsMean (SD) age was 60.1 (11.9) years among HIV- and 54.2 (11.2) years among HIV+ participants (P<0.001), 83% of whom had undetectable (<20 copies/mL) HIV-1 viral load (VL). In comparison with HIV- men, HIV+ men had higher QTVI (adjusted difference of +0.077 [95% CI, +0.032 to +0.123]). The magnitude of this association depended on the degree of viremia, such that in HIV+ men with undetectable VL, adjusted QTVI was +0.064 (95% CI, +0.017 to +0.111) higher than in HIV- men, whereas, in HIV+ men with detectable VL, adjusted QTVI was higher by +0.150 (95% CI, 0.072-0.228) than in HIV- referents. Analysis of QTVI subcomponents showed that HIV+ men had: (1) lower heart rate variability irrespective of VL status, and (2) higher QT variability if they had detectable, but not with undetectable, VL, in comparison with HIV- men. Higher levels of C-reactive protein, interleukin-6, intercellular adhesion molecule-1, soluble tumor necrosis factor receptor 2, and soluble cluster of differentiation-163 (borderline), were associated with higher QTVI and partially attenuated the association with HIV serostatus.ConclusionsHIV+ men have greater beat-to-beat variability in QT interval (QTVI) than HIV- men, especially in the setting of HIV viremia and heightened inflammation. Among HIV+ men, higher QTVI suggests ventricular repolarization lability, which can increase susceptibility to arrhythmias, whereas lower heart rate variability signals a component of autonomic dysfunction.

Project description:ObjectivesHuman immunodeficiency virus (HIV) infection and antiretroviral therapy (ART) may increase the risk of fatty liver disease. We determined the prevalence of and risk factors for fatty liver by comparing HIV-infected men with HIV-uninfected men who have sex with men in the Multicenter AIDS Cohort Study (MACS).MethodsIn 719 MACS participants who consumed less than three alcoholic drinks daily, fatty liver was defined as a liver-to-spleen attenuation ratio <1 on noncontrast computed tomography (CT). We genotyped single nucleotide polymorphisms in the patatin-like phospholipase domain-containing 3 (PNPLA3) gene and in other genes previously associated with nonalcoholic fatty liver disease. Risk factors for fatty liver were determined using multivariable logistic regression.ResultsAmong 254 HIV-uninfected men and 465 HIV-infected men, 56% were White with median age 53 years and median body mass index 25.8 kg/m(2). The vast majority of HIV-infected men (92%) were on ART, and 87% of the HIV-infected men were treated with a nucleoside reverse transcriptase inhibitor for a median duration of 8.5 years. Overall, 15% of the cohort had fatty liver, which was more common in the HIV-uninfected compared with the HIV-infected men (19 vs. 13%, P=0.02). In multivariable analysis, HIV infection was associated with a lower prevalence of fatty liver (odds ratio (OR)=0.44, P=0.002), whereas a higher prevalence of fatty liver was seen in participants with PNPLA3 (rs738409) non-CC genotype (OR=2.06, P=0.005), more abdominal visceral adipose tissue (OR=1.08 per 10 cm(2), P<0.001), and homeostatic model assessment of insulin resistance (HOMA-IR) ≥4.9 (OR=2.50, P=0.001). Among HIV-infected men, PNPLA3 (rs738409) non-CC genotype was associated with a higher prevalence of fatty liver (OR=3.30, P=0.001) and cumulative dideoxynucleoside exposure (OR=1.44 per 5 years, P=0.02).ConclusionsCT-defined fatty liver is common among men at risk for HIV infection and is associated with greater visceral adiposity, HOMA-IR, and PNPLA3 (rs738409). Although treated HIV infection was associated with a lower prevalence of fatty liver, prolonged exposure to dideoxynucleoside analogs is associated with higher prevalence.

Dataset Information

HAART-associated dyslipidemia varies by biogeographical ancestry in the multicenter AIDS cohort study.

Publications

HAART-associated dyslipidemia varies by biogeographical ancestry in the multicenter AIDS cohort study.

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