The prevalence of pain in 211 HIV-infected patients with and without intravenous drug use was assessed and the prognostic information inherent in pain reporting was evaluated, using a questionnaire on pain and HIV-related symptoms combined with data on disease classification, route of HIV transmission, CD4+ lymphocyte counts in blood (CD4) and mortality rates at 15 months after completing the questionnaire. The pain prevalence was significantly higher among intravenous drug users (IDUs) compared with non-IDUs [76/89 (85%) vs 87/122 (71%);p<0.05], especially among the patients classified as asymptomatic [43/53 (81%) vs 35/59 (59%);p = 0.01]. No significant difference was found among AIDS patients. In non-IDUs, a strong correlation was found between HIV disease stages according to the Centers for Disease Control classification (CDC) and pain prevalence (CDC A: 59%vs B: 74%vs C: 96%, p<0.001), and between the number of concurrent pain sites and both the CD4 levels (no pains: CD4 0.26 x 10(9)/l vs 1-2 pain sites: CD4 0.22 vs>2 pain sites: CD4 0.09;r = 0.35, p<0.001), and the mortality rate [no pains: 2/35 (6%) vs 1-2 pain sites: 8/45 (18%) vs> 2 pain sites: 12/42 (29%), p<0.01]. In IDUs, no such correlations were found. Our data demonstrates differences in the development, prevalence and prognostic value of pain among HIV-infected patients, with and without intravenous drug use, clearly indicating the need to differentiate risk groups in pain related studies. Copyright 1999 European Federation of Chapters of the International Association for the Study of Pain.
This study evaluated the relation between cerebrospinal fluid (CSF) mononuclear cells (MNC) and CSF HIV-1 RNA levels. HIV-1 RNA levels in plasma and CSF were analyzed by reverse transcription-polymerase chain reaction (RT-PCR) in 58 consecutive patients with neurologic symptoms and late HIV-1 infection. The majority of the patients had no central nervous system (CNS) complication (n = 36), 11 had AIDS dementia complex (ADC) and 11 had CNS opportunistic infection (CNS OI). CSF cell counts were analyzed using a method that also evaluated hypocellular CSF (i.e., from 0.1 x 10(6) cells/L). A strong correlation was found between CSF MNC and CD4+ lymphocyte counts in blood (r = 0.58; p < .0001). HIV-1 RNA was detected in all plasma samples and in 38 of 58 (66%) of the cell-free CSF samples. CSF HIV-1 RNA was less frequently detected in patients with hypocellular CSF than in patients with normocellular or pleocytic CSF (13 of 28 patients [46%] versus 10 of 14 patients [71%] versus 15 of 16 patients [94%], respectively). The levels of CSF HIV-1 RNA correlated with the CSF MNC count (r = 0.61; p < .0001). The correlation also remained strong within the clinical subgroups of CNS asymptomatic patients (r = 0.55; p < .001) and ADC patients (r = 0.79; p < .001), but not among CNS OI patients (r = 0.19). Patients with CNS OI were found to have higher CSF HIV-1 RNA levels than the patients without evidence of CNS complication. Thus, a close relation was found between CSF HIV-1 RNA levels and CSF MNC counts. These data support the hypothesis that a substantial part of the virus in the CSF of HIV-1-infected patients is locally produced by CSF MNC.
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