BACKGROUND: In the pre-highly active antiretroviral therapy (HAART) era, distal sensory polyneuropathy (DSP) was associated with markers of advanced HIV infection and the use of neurotoxic antiretrovirals (ARVs). As HAART became widespread, and the AIDS epidemic shifted into minority populations, the risk factors for DSP became less clear. We explore the roles of ethnicity and ARV in the development of DSP in an HAART era cohort. METHODS: Data from 336 HIV-positive adults were obtained from the Manhattan HIV Brain Bank. One hundred four participants had no DSP at entry visit; at least 1 follow-up visit; and a self-identified ethnicity of non-Hispanic white, Hispanic, or African American. RESULTS: Fifty percent of participants developed DSP; of those, 67% were symptomatic. Participants who developed DSP were older (P = 0.02) and had higher CD4 counts (P = 0.001). ARV-DSP was more common in Hispanics (P = 0.02) and intravenous drug users (P = 0.02). There was a trend for higher pain scores in Hispanics with symptomatic DSP (P = 0.08). CONCLUSIONS: This study suggests that there are ethnic disparities in the clinical manifestations of HIV-related neuropathies including pain and the susceptibility to ARV-DSP. Further studies of larger cohorts are indicated to explore the etiology of these differences.
BACKGROUND: In the pre-highly active antiretroviral therapy (HAART) era, distal sensory polyneuropathy (DSP) was associated with markers of advanced HIV infection and the use of neurotoxic antiretrovirals (ARVs). As HAART became widespread, and the AIDS epidemic shifted into minority populations, the risk factors for DSP became less clear. We explore the roles of ethnicity and ARV in the development of DSP in an HAART era cohort. METHODS: Data from 336 HIV-positive adults were obtained from the Manhattan HIV Brain Bank. One hundred four participants had no DSP at entry visit; at least 1 follow-up visit; and a self-identified ethnicity of non-Hispanic white, Hispanic, or African American. RESULTS: Fifty percent of participants developed DSP; of those, 67% were symptomatic. Participants who developed DSP were older (P = 0.02) and had higher CD4 counts (P = 0.001). ARV-DSP was more common in Hispanics (P = 0.02) and intravenous drug users (P = 0.02). There was a trend for higher pain scores in Hispanics with symptomatic DSP (P = 0.08). CONCLUSIONS: This study suggests that there are ethnic disparities in the clinical manifestations of HIV-related neuropathies including pain and the susceptibility to ARV-DSP. Further studies of larger cohorts are indicated to explore the etiology of these differences.
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