Role of metabolic syndrome components in HIV-associated sensory neuropathy
- PMID: 19823068
- PMCID: PMC2896813
- DOI: 10.1097/QAD.0b013e328332204e
Role of metabolic syndrome components in HIV-associated sensory neuropathy
Abstract
Objectives: Sensory neuropathy is a common peripheral nerve complication of HIV infection and highly active antiretroviral therapy. Metabolic syndrome (MetS), a cluster of risk factors for atherosclerosis and microvascular disease, is associated with sensory neuropathy in HIV-uninfected (HIV-negative) persons. We examined whether MetS or its components predispose individuals to HIV-associated sensory neuropathy (HIV-SN).
Design: From a prospective multicenter cohort of 1556 HIV-positive patients, a subgroup (n = 130) with fasting laboratory tests and sensory neuropathy assessment was selected.
Methods: Sensory neuropathy was defined by symmetrically decreased reflexes or sensation loss in the legs. MetS was defined by presence of at least three risk factors: mean arterial pressure of at least 100 mmHg; triglycerides (TRGs) of at least 150 mg/dl and high-density lipoprotein cholesterol of less than 40 mg/dl for male patients, less than 50 mg/dl for female patients; body mass index of more than 25 kg/m; plasma glucose (GLU) of at least 100 mg/dl and self-reported diabetes mellitus type 2. Multivariate logistic regression examined the association between HIV-SN and MetS.
Results: After controlling for HIV-SN risk factors such as age, CD4 current, length of HIV infection, use of dideoxynucleoside reverse transcriptase inhibitors and protease inhibitors, MetS was not associated with HIV-SN (P = 0.72). However, when each MetS component was assessed, elevated TRG was a significant risk factor for HIV-SN. From the larger cohort, both diabetes mellitus type 2 (odds ratio = 1.4, P < 0.01) and elevated TRG (odds ratio = 1.4, P = 0.01) were risk factors for HIV-SN.
Conclusion: The risk of HIV-SN was increased for diabetes mellitus type 2 and elevated TRG but not for other MetS components. Both increase the risk of sensory neuropathy in HIV-populations, but the mechanism(s) remains unclear.
References
-
- Carr A, Samaras K, Thorisdottir A, Kaufmann GR, Chisholm DJ, Cooper DA. Diagnosis, prediction, and natural course of HIV-1 protease-inhibitor-associated lipodystrophy, hyperlipidaemia, and diabetes mellitus: a cohort study. Lancet. 1999;353:2093–2099. - PubMed
-
- Fantoni M, Del Borgo C, Autore C, Barbaro G. Metabolic disorders and cardiovascular risk in HIV-infected patients treated with antiretroviral agents. Ital Heart J. 2002;3:294–299. - PubMed
-
- Bacellar H, Munoz A, Miller EN, Cohen BA, Besley D, Selnes OA, et al. Temporal trends in the incidence of HIV-1-related neurologic diseases: Multicenter AIDS Cohort Study, 1985–1992. Neurology. 1994;44:1892–1900. - PubMed
-
- Tagliati M, Grinnell J, Godbold J, Simpson DM. Peripheral nerve function in HIV infection: clinical, electrophysiologic, and laboratory findings. Arch Neurol. 1999;56:84–89. - PubMed
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