论文部分内容阅读
Background: Before the introduction of combination antiretroviral therapy (CAR T), neurological disease correlated with cerebrospinal fluid (CSF) levels of hum an immunodeficiency virus (HIV) RNA. Objective: To investigate the relationships among HIV RNA levels, immune activation markers, and neurological status in pat ients receiving CART. Design: Multicenter cohort study. Setting: Academic neurol ogy departments. Patients: A total of 371 patients unselected for neurological c omplaints and with CD4 cell counts less than 200/μL or with cognitive symptoms and CD4 cell counts less than 300/μL were enrolled into the Northeastern AIDS D ementia cohort in 1998-2002. Diagnoses of HIV associated dementia (HIV D) and minor cognitive motor disorder (MCMD) were obtained with a computerized algori thm. Plasma and CSF levels of HIV RNA, monocyte chemotactic protein 1, macrophag e colony stimulat ing factor, and tumor necrosis factor αwere quantified. Res ults: The mean±SD age was 41.5±7.2 years, and the mean±SD educational level w as 12.3±2.2 years. Seventy percent of the cohort was black, and 30%were women. The mean±SD CD4 cell count was 136.8±87.9/μL, and CART was used in 71%. Twe nty nine percent of the patients were unimpaired (n=106) , 36%had MCMD (n= 13 3), and 35%had HIV D (n=128). Mean log10 CSF HIV RNA copies per milliliter was 2.6±0.8, with no differences among the neurological groups, even after adjustm ents for baseline CD4 cell counts and antiretroviral therapy. Cerebrospinal flui d HIV RNA was undetectable in 47%of unimpaired, 46%of MCMD, and 43%of HIV D patients (P=.91). Plasma levels of monocyte chemotactic protein type 1 and tumor necrosis factor αcorrelated weakly with HIV RNA levels but did not distinguish those with neurological deficits. Conclusions: In contrast to observations in i ndividuals not treated with CART, we found no relationship between CSF markers a nd neurological status in this CART using cohort with advanced HIV/AIDS. This w as not explicable by demographic differences or plasma virological control. CART may substantially attenuate the degree of central nervous system HIV infection a nd immune activation, and in CART users, CSF HIV RNA and immune activation marke rs may fail to discriminate milder degrees of HIV D and MCMD.
Background: Before the introduction of combination antiretroviral therapy (CAR T), neurological disease correlated with cerebrospinal fluid (CSF) levels of hum an immunodeficiency virus (HIV) RNA. Objective: To investigate the associations among HIV RNA levels, immune activation markers, and Settings: Academic neurology departments. Patients: A total of 371 patients unselected for neurological c omplaints and with CD4 cell counts less than 200 / μL or with Cognitive symptoms and CD4 cells counts less than 300 / μL were enrolled into the Northeastern AIDS D ementia cohort in 1998-2002. Diagnoses of HIV associated dementia (HIV D) and minor cognitive motor disorder (MCMD) were obtained with a computerized algori thm. Plasma and CSF levels of HIV RNA, monocyte chemotactic protein 1, macrophag e colony stimulating factor, and tumor necrosis factor αwere quantified. Res ults: The mean ± SD age was 41.5 ± 7.2 ye ars, and the mean ± SD educational level w as 12.3 ± 2.2 years. Seventy percent of the cohorts was black, and 30% were women. The mean ± SD CD4 cell count was 136.8 ± 87.9 / μL, and the CART was used in 71 %. Twe nty nine percent of the patients were unimpaired (n = 106), 36% had MCMD (n = 13 3), and 35% had HIV D ± 0.8, with no differences among the neurological groups, even after adjusting for ents for baseline CD4 cell counts and antiretroviral therapy. Cerebrospinal flui d HIV RNA was undetectable in 47% of unimpaired, 46% of MCMD, and 43% of HIVD patients ( P = .91). Plasma levels of monocyte chemotactic protein type 1 and tumor necrosis factor αcorrelated weakly with HIV RNA levels but did not distinguish those with neurological deficits. Conclusions: In contrast to observations in i ndividuals not treated with CART, we found no relationship between CSF markers a nd neurological status in this CART using cohort with advanced HIV / AIDS. This w as not explicable by demographic differences or plasma virological control. CART may substantially attenuate the degree of central nervous system HIV infection a nd immune activation, and in CART users, CSF HIV RNA and immune activation marke rs may fail to discriminate milder degrees of HIV D and MCMD .