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Age, Race, Gender--But Not HIV--Tied to Hearing Loss in HIV+ People
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6th IAS Conference on HIV Pathogenesis, Treatment and Prevention, July 17-20, 2011, Rome
Mark Mascolini
Older age, male gender, and nonblack race raised the risk of hearing loss in two US HIV cohorts--the male Multicenter AIDS Cohort Study (MACS) and the female Women's Interagency HIV Study (WIHS) [1]. But HIV infection itself did not make hearing loss more likely; neither did lower nadir CD4 count or higher viral load.
Hearing loss may affect people with HIV because of medication toxicities, neurologic infection, or HIV-related pathological changes in the ear. MACS and WIHS investigators collaborated on this assessment of hearing loss in men and women enrolled in these prospective cohort studies.
The cochlea is the hearing apparatus in the middle ear. This study assessed cochlear function noninvasively by gauging "distortion product otoacoustic emissions" (DPOAEs). The study involved 334 HIV-positive or negative gay men (152/182) in the Baltimore-Washington MACS group, and 178 HIV-positive or negative women (137/41) in the Washington WIHS group. The investigators excluded people who used hearing aids or had conditions or medication histories that could contribute to hearing loss.
Study participants reported any hearing loss, tinnitus (ringing), and noise exposure at work and during leisure activities. People had DPOAEs measured twice in both ears. The investigators determine nonresponse in each ear, defining nonresponse as an absolute DPOAE less than -15 dB or the difference between the absolute DPOAE and the background noise level less than 6 dB. A person could have 0 to 4 nonresponses.
Median age for the study group stood at 51.2 years, and the group was nearly evenly divided between blacks and nonblacks. Slightly fewer than one quarter (22.3%) reported occupational noise exposure, whereas 57.5% reported nonoccupational noise exposure. While one quarter of study participants (25.2%) had 0 nonresponses, 30.7% had 1 nonresponse, 14.1% had 2, 14.8% had 3, and 15.2% had 4.
Almost one third of the group (31.5%) had taken antiretroviral monotherapy, 52.6% had taken two antiretrovirals, and 88.2% had taken 3 or more antiretrovirals in a regimen. Nadir CD4 count averaged 279, while peak CD8 count averaged 1423.
A multivariate model that factored in age, gender, race, and history of noise exposure identified three independent predictors of nonresponse (hearing loss), at the following odds ratios (OR) (and 95% confidence intervals):
--Every 10 years of age: OR 2.78 (2.07 to 3.73), P < 0.001
--Male gender: OR 5.60 (2.98 to 10.49), P < 0.001
--Nonblack race: OR 2.75 (1.57 to 4.83), P < 0.001
Factors that did not affect risk of hearing loss in this analysis were HIV status, occupational noise exposure, and nonoccupational noise exposure.
A second multivariate analysis considered age, gender, race, history of noise exposure, nadir CD4 count, peak CD8 count, viral load, and ever using antiretroviral therapy (categorized as none, monotherapy, combination therapy, or highly active antiretroviral therapy). In this analysis, age, male gender, and nonblack race remained independent predictors of nonresponse. But none of the HIV-related variables predicted hearing loss:
--Every 10 years of age: OR 2.17 (1.41 to 3.34), P = 0.001
--Male gender: OR 6.51 (3.04 to 13.94), P < 0.001
--Nonblack race: OR2.56 (1.27 to 5.15), P = 0.01
A 7-person case series of HIV-positive people who had cochlear implantation for profound hearing loss found the procedure safe and overall results good [2].
References
1. Torre III P, Hoffman H, Springer G, et al. Cochlear function among Multicenter AIDS Cohort Study (MACS) and Women's Interagency HIV Study (WIHS) participants. 6th IAS Conference on HIV Pathogenesis, Treatment and Prevention. July 17-20, 2011. Rome. Abstract TUPE138. For the study poster: http://pag.ias2011.org/EPosterHandler.axd?aid=2957.
2. Roland JT Jr, Alexiades G, Jackman AH, Hillman D, Shapiro W. Cochlear implantation in human immunodeficiency virus-infected patients. Otol Neurotol. 2003;24:892-895.
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