Detectable HIV Viral Load Is Associated With Metabolic Syndrome
Detectable HIV Viral Load Is Associated With Metabolic Syndrome
Background: The aim of our study was to assess the association between HIV viral load (HIV-VL) and metabolic syndrome (MS) in a cohort of HIV-infected patients.
Methods: This is a cross-sectional study including 1324 consecutive HIV-infected patients on stable antiretroviral therapy regimens.
Results: Variables significantly associated with MS in univariate analysis were: age [mean ± SD: 47.04 ± 7.41 vs 44.07 ± 6.82, (P < 0.0001)]; male sex [224 (69.35%) vs 614 (61.34%) (P = 0.009)]; Apo B (mg/dL) [111.51 ± 29.64 vs 100.57 ± 31.22, (P < 0.0001)]; homeostasis model assessment equation [median (interquartile range), 5.14 (3.00–8.15) vs 2.95 (1.93–4.57), (P < 0.0001)]; body mass index [25.17 ± 4.40 vs 22.80 ± 3.38, (P < 0.0001)]; protease inhibitor current use (%) [199 (61.61) vs 529 (52.85), (P = 0.006)]; and log10 HIV-VL [2.17 ± 0.94 vs 2.02 ± 0.79, (P = 0.0048)]. MS associated variables in multivariable analysis were: log10 HIV-VL [odds ratio (OR): 1.25; P = 0.003], age (per 10-year increment) [OR: 1.60; P < 0.0001], homeostasis model assessment equation ≥3.8 [OR: 2.77; P < 0.0001].
Conclusions: Persistent viremia is a significant predictor for the development of MS. Viral control through effective antiretroviral therapy is paramount not only for the control of HIV disease progression but also for the prevention of MS and associated cardiovascular disease.
Metabolic syndrome (MS) has been identified as a constellation of abnormalities that lead to an increased risk of cardiovascular disease (CVD). MS is affecting the general population in epidemic proportion, for example, up to 26.5% in the National Health and Nutrition Examination Survey (NHANES) cohort. The prevalence of MS in HIV-infected individuals is comparable with that in the general population and varies from 15% to 25.5%. But the studies to-date have shown conflicting results with regard to the roles of both HIV and antiretroviral therapy (ART) on the diagnosis of MS. It has been established that HIV itself may produce lipid abnormalities both in ART-naive patients and experienced patients. It is well known that several of the diagnostic criteria of MS overlap with common features of metabolic and morphologic abnormalities frequently observed in ART-experienced HIV-infected individuals. In particular, increased abdominal waist circumference (WC), elevated triglycerides, low high-density lipoprotein (HDL) cholesterol, and glucose abnormalities are commonly observed in patients with HIV infection and have been associated with ART. A positive association of MS with lopinavir/ritonavir and stavudine was found by Jericò et al, lopinavir/ritonavir and didanosine by Jacobson et al, and stavudine alone by Sobieszczyk et al. Samaras et al confirmed the association of MS with the protease inhibitor (PI) class, whereas Sobieszczyk et al did not find a significant association with ritonavir-boosted PIs, but a protective role of the nonnucleoside reverse transcriptase inhibitor (NNRTI) nevirapine.
Three case–control studies have investigated the impact of HIV on MS diagnosis. In a cohort of 1243 patients compared with 1922 controls. Bonfanti et al observed an increased prevalence of MS in HIV-infected patients compared with HIV-negative controls. Sobieszczyk et al confimed these results. On the contrary, Mondy et al did not find an association of MS and HIV in a cohort of 471 HIV-infected patients compared with NHANES. However, HIV diagnosis was related to both elevated triglyceride levels and low HDL cholesterol.
It further remains unclear if HIV RNA levels may better discriminate the role of the virus in the development of MS. Mangili et al showed significantly higher HIV-VL in those defined as having MS in a cohort of 314 HIV-infected patients. Jacobson et al found a higher risk of MS in patients with clinically relevant increase in HIV-VL in the previous 6 months in a sample of 477 patients. Sobieszczyk et al showed that HIV-VL greater than 50,000 copies per milliliter conferred an increased risk of MS in a large sample of HIV-infected women. On the contrary, 5 other studies did not find a significant relationship between HIV-VL and MS diagnosis. In all these studies, patients who were both ART naive and ART experienced were included.
The objective of our study was to assess the association between detectable HIV-VL and MS prevalence in a cohort of HIV patients on stable ART regimen.
Abstract and Introduction
Abstract
Background: The aim of our study was to assess the association between HIV viral load (HIV-VL) and metabolic syndrome (MS) in a cohort of HIV-infected patients.
Methods: This is a cross-sectional study including 1324 consecutive HIV-infected patients on stable antiretroviral therapy regimens.
Results: Variables significantly associated with MS in univariate analysis were: age [mean ± SD: 47.04 ± 7.41 vs 44.07 ± 6.82, (P < 0.0001)]; male sex [224 (69.35%) vs 614 (61.34%) (P = 0.009)]; Apo B (mg/dL) [111.51 ± 29.64 vs 100.57 ± 31.22, (P < 0.0001)]; homeostasis model assessment equation [median (interquartile range), 5.14 (3.00–8.15) vs 2.95 (1.93–4.57), (P < 0.0001)]; body mass index [25.17 ± 4.40 vs 22.80 ± 3.38, (P < 0.0001)]; protease inhibitor current use (%) [199 (61.61) vs 529 (52.85), (P = 0.006)]; and log10 HIV-VL [2.17 ± 0.94 vs 2.02 ± 0.79, (P = 0.0048)]. MS associated variables in multivariable analysis were: log10 HIV-VL [odds ratio (OR): 1.25; P = 0.003], age (per 10-year increment) [OR: 1.60; P < 0.0001], homeostasis model assessment equation ≥3.8 [OR: 2.77; P < 0.0001].
Conclusions: Persistent viremia is a significant predictor for the development of MS. Viral control through effective antiretroviral therapy is paramount not only for the control of HIV disease progression but also for the prevention of MS and associated cardiovascular disease.
Introduction
Metabolic syndrome (MS) has been identified as a constellation of abnormalities that lead to an increased risk of cardiovascular disease (CVD). MS is affecting the general population in epidemic proportion, for example, up to 26.5% in the National Health and Nutrition Examination Survey (NHANES) cohort. The prevalence of MS in HIV-infected individuals is comparable with that in the general population and varies from 15% to 25.5%. But the studies to-date have shown conflicting results with regard to the roles of both HIV and antiretroviral therapy (ART) on the diagnosis of MS. It has been established that HIV itself may produce lipid abnormalities both in ART-naive patients and experienced patients. It is well known that several of the diagnostic criteria of MS overlap with common features of metabolic and morphologic abnormalities frequently observed in ART-experienced HIV-infected individuals. In particular, increased abdominal waist circumference (WC), elevated triglycerides, low high-density lipoprotein (HDL) cholesterol, and glucose abnormalities are commonly observed in patients with HIV infection and have been associated with ART. A positive association of MS with lopinavir/ritonavir and stavudine was found by Jericò et al, lopinavir/ritonavir and didanosine by Jacobson et al, and stavudine alone by Sobieszczyk et al. Samaras et al confirmed the association of MS with the protease inhibitor (PI) class, whereas Sobieszczyk et al did not find a significant association with ritonavir-boosted PIs, but a protective role of the nonnucleoside reverse transcriptase inhibitor (NNRTI) nevirapine.
Three case–control studies have investigated the impact of HIV on MS diagnosis. In a cohort of 1243 patients compared with 1922 controls. Bonfanti et al observed an increased prevalence of MS in HIV-infected patients compared with HIV-negative controls. Sobieszczyk et al confimed these results. On the contrary, Mondy et al did not find an association of MS and HIV in a cohort of 471 HIV-infected patients compared with NHANES. However, HIV diagnosis was related to both elevated triglyceride levels and low HDL cholesterol.
It further remains unclear if HIV RNA levels may better discriminate the role of the virus in the development of MS. Mangili et al showed significantly higher HIV-VL in those defined as having MS in a cohort of 314 HIV-infected patients. Jacobson et al found a higher risk of MS in patients with clinically relevant increase in HIV-VL in the previous 6 months in a sample of 477 patients. Sobieszczyk et al showed that HIV-VL greater than 50,000 copies per milliliter conferred an increased risk of MS in a large sample of HIV-infected women. On the contrary, 5 other studies did not find a significant relationship between HIV-VL and MS diagnosis. In all these studies, patients who were both ART naive and ART experienced were included.
The objective of our study was to assess the association between detectable HIV-VL and MS prevalence in a cohort of HIV patients on stable ART regimen.