Publication Abstract Display
Type: Published Abstract
Title: HIV, Hepatitis C, and methamphetamine dependence independently worsen neuropsychological performance.
Authors: Letendre S, Cherner M, Marquie-beck J, Ellis R, Heaton R, Marcotte T, Harrington K, Gragg B, McCutchan J, Grant I, and the HNRC Group
Year: 2004
Publication: 11th Annual Conference on Retroviruses and Opportunistic Infections
Volume: Session 71 Issue: Pages: 469
Abstract:Background: HIV, HCV, and Meth are each associated with central nervous system (CNS) complications. All 3 may injure the CNS by similar mechanisms, such as macrophage activation, oxidative stress, and direct neuronal injury. The objective of this study was to determine if HIV, HCV, and Meth are independently associated with NP performance. Methods: We enrolled 401 subjects in a prospective study of the CNS effects of HIV and Meth. Subjects were recruited into 4 groups: HIV-Meth- (n=82), HIV+Meth- (n=110), HIV-Meth+ (n=115), and HIV+Meth+ (n=94). Meth+ subjects met DSM-IV criteria for dependence within 18 months but were not actively using meth, heroin, or cocaine. All subjects had standardized assessments, including NP tests, phlebotomy, and lumbar puncture. NP results were summarized as a global deficit score (GDS), a composite measure that adjusts for age, education, and ethnicity. HCV IgG and immune activation markers were measured by ELISA. HIV and HCV RNA levels were measured by RT-PCR. Data were analyzed using standard statistical methods, including non-parametric measures of association and linear regression. For some analyses, subjects were categorized by the number of risk conditions present (0, 1, 2, or all 3). Results: HCV IgG was detected in 78 (19%) subjects, 67 (86%) of whom were Meth+. HCV+ subjects did not have advanced liver disease, based on albumin, transaminase, and platelet levels. They were 2.4 times more likely to be globally impaired, compared to those who were HCV- (p<.001). In the entire cohort, impairment worsened as the number of co-existing risk conditions increased: 0 (median GDS 0.21), 1 (.32), 2 (.47), or all 3 (.74) (p<.001). In a linear regression, HIV, HCV, and Meth were independently associated with worse GDS, even after adjusting for CD4 counts and antiretroviral use (R2=.10, p<.001). HCV RNA levels in plasma were higher in those with memory, but not global, impairment (median 6.7 vs 5.9 log c/mL, p=.05). In CSF, HCV RNA was below 100 copies/mL in all specimens. Elevated immune activation markers in plasma and CSF were more frequently associated with HIV and HCV than with Meth. Conclusions: HIV, HCV, and Meth independently cause neural injury, leading to global impairment. HIV and HCV may mediate neural injury, in part, by activating monocyte-derived macrophages, which can release neurotoxins and replicate HIV and possibly HCV. Meth may injure the brain by other mechanisms, such as oxidative stress.

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