Kastanioudakis I, Skevas A, Danielidis V, Tsiakou E, Drosos A A, Moustopoulos M H
Department of Otolaryngology, Medical School, University of Ioannina, Athens, Greece.
J Laryngol Otol. 1995 Aug;109(8):713-8. doi: 10.1017/s0022215100131135.
Sensorineural hearing loss in rheumatoid arthritis (RA) has been reported to be the result of the extra-articular manifestation of the disease (rheumatoid nodular vasculitis) or due to drug ototoxicity. In an attempt to investigate the presence of sensorineural hearing loss and the possible causes for it we investigated prospectively 45 RA patients (42 female; three male) with a mean age of 52.5 +/- 10.7 years and a mean disease duration of 8.5 +/- 7.3 years. All patients underwent a complete physical examination and audiological evaluation which included pure tone audiometry and impedance audiometry (tympanogram, static compliance, acoustic reflex, reflex decay, acoustic reflex latency test. We found a sensorineural hearing loss > 20 dB HL in 44.4 per cent (40/90) ears. In all cases the site of hearing loss was the cochlea and in most of them it was bilateral and symmetric (16 patients out of 45 had bilateral sensorineural hearing loss i.e. 35.5 per cent. There was no correlation between sensorineural hearing loss and age, sex, disease duration, articular and extra-articular manifestations and the presence of autoantibodies in our patients. In addition, no correlation was found between sensorineural hearing loss and drug therapy for one at least of the following drugs: NSAIDs, D-penicillamine, plaquenil and methotrexate. We noticed a prologation of acoustic reflex latency in five patients (10 per cent) which was found to be correlated with the temporomandibular joint involvement and the presence of rheumatoid factor (RF). We conclude that inner ear involvement in RA is expressed by: (1) mild symmetric, bilateral sensorineural hearing loss of cochlear type in 35.5 per cent of patients; (2) normal acoustic reflex thresholds; (3) nondecay; and (4) prologation of acoustic reflex latency which appeared in a small number of patients (10 per cent).
据报道，类风湿关节炎（RA）中的感音神经性听力损失是该疾病关节外表现（类风湿结节性血管炎）的结果，或由药物耳毒性引起。为了调查感音神经性听力损失的存在及其可能原因，我们对45例RA患者（42例女性，3例男性）进行了前瞻性研究，这些患者的平均年龄为52.5±10.7岁，平均病程为8.5±7.3年。所有患者均接受了全面的体格检查和听力学评估，包括纯音听力测定和阻抗听力测定（鼓室图、静态声顺、声反射、反射衰减、声反射潜伏期测试）。我们发现44.4%（40/90）的耳朵有感音神经性听力损失>20 dB HL。在所有病例中，听力损失部位均为耳蜗，且大多数为双侧对称（45例患者中有16例有双侧感音神经性听力损失，即35.5%）。在我们的患者中，感音神经性听力损失与年龄、性别、病程、关节和关节外表现以及自身抗体的存在之间没有相关性。此外，对于以下至少一种药物的药物治疗，感音神经性听力损失与药物治疗之间也没有相关性：非甾体抗炎药、D-青霉胺、羟氯喹和甲氨蝶呤。我们注意到5例患者（10%）有声反射潜伏期延长，发现其与颞下颌关节受累和类风湿因子（RF）的存在相关。我们得出结论，RA中的内耳受累表现为：（1）35.5%的患者出现轻度对称、双侧耳蜗型感音神经性听力损失；（2）声反射阈值正常；（3）不衰减；（4）少数患者（10%）出现声反射潜伏期延长。
