OBJECTIVE: This study evaluates the degree of hearing impairment in patients with rheumatoid arthritis (RA) and examines the correlation between hearing impairment and the clinical data or chemical mediators. BACKGROUND: Both sensorineural hearing loss (SNHL) and conductive hearing loss (CHL) have been reported in patients with RA, but the results of most studies are not in agreement, and the pathophysiology of hearing impairment in RA is not well known. METHODS: Hearing in patients with RA and controls was examined using pure-tone audiometry and tympanometry. Also, the amounts of pro-inflammatory cytokines and matrix metalloproteinases in addition to antibodies against type II collagen in plasma of the patients with RA were determined using enzyme-linked immunosorbent assay. RESULTS: The frequency of SNHL in the patients with RA was higher than in normal controls (36.1% versus 13.9%), and bone conduction at 2,000 Hz differed significantly between the patients with RA and the controls (p < 0.01). Moreover, the presence of SNHL was related to ESR (p < 0.05), plasma interleukin-6 (p < 0.05), and plasma matrix metalloproteinase-3 (p < 0.001). On the other hand, CHL was not observed, whereas As-type tympanograms increased in the patients with RA (p < 0.01). Abnormal tympanograms were not related to any clinical findings or any chemical mediators tested. CONCLUSION: We demonstrated that there is increased SNHL in patients with RA, which may result from systemic inflammation and tissue injury, and increased latent-type CHL caused by stiffness of the middle ear system whose mechanisms are not yet clear.
OBJECTIVE: This study evaluates the degree of hearing impairment in patients with rheumatoid arthritis (RA) and examines the correlation between hearing impairment and the clinical data or chemical mediators. BACKGROUND: Both sensorineural hearing loss (SNHL) and conductive hearing loss (CHL) have been reported in patients with RA, but the results of most studies are not in agreement, and the pathophysiology of hearing impairment in RA is not well known. METHODS: Hearing in patients with RA and controls was examined using pure-tone audiometry and tympanometry. Also, the amounts of pro-inflammatory cytokines and matrix metalloproteinases in addition to antibodies against type II collagen in plasma of the patients with RA were determined using enzyme-linked immunosorbent assay. RESULTS: The frequency of SNHL in the patients with RA was higher than in normal controls (36.1% versus 13.9%), and bone conduction at 2,000 Hz differed significantly between the patients with RA and the controls (p < 0.01). Moreover, the presence of SNHL was related to ESR (p < 0.05), plasma interleukin-6 (p < 0.05), and plasma matrix metalloproteinase-3 (p < 0.001). On the other hand, CHL was not observed, whereas As-type tympanograms increased in the patients with RA (p < 0.01). Abnormal tympanograms were not related to any clinical findings or any chemical mediators tested. CONCLUSION: We demonstrated that there is increased SNHL in patients with RA, which may result from systemic inflammation and tissue injury, and increased latent-type CHL caused by stiffness of the middle ear system whose mechanisms are not yet clear.