Although several reports exist concerning the occurrence of hearing loss in patients withdisorders of thyroid function, there are still several unsettled issues, such as theincidence and the severity of hearing impairment, the anatomic site of the auditorypathway involved, and the possible pathogenetic mechanisms. Both congenitalhypothyroidism and environmentally based iodine deficiency are established causes ofhearing loss in humans and rodents. Congenital thyroid deficiency in humans can resultin a profound, hearing deficit, which may be prevented by early hormonal replacementtreatment in infants with hypothyroidism. However, the effect of acute or chronichypothyroidism in adults has not been adequately studied, and most information hasbeen obtained from animal experiments, whereas research in humans has been basicallybased on behavioral audiometry. The use of otoacoustic emissions may provide moreinsight into the hearing function of these patients than pure-tone audiometry, since it isconsidered as a sensitive test of the cochlear status. The aim of this study was toevaluate the hearing in a group of patients with acute hypothyroidism, using bothconventional audiometry and transiently evoked otoacoustic emissions (TEOAEs). Material and methods:A group of 52 patients with thyroid carcinoma who underwent total thyroidectomy wasstudied prospectively, All patients were examined before surgery and 6-8 weekspostoperatively. During this period there was no replacement with levothyroxine and themagnitude of thyroxin depletion was monitored by serum thyroid-stimulating hormone levels. On preoperative encounter with each patient, a detailed questionnaire of historyof hearing loss, tinnitus, vertigo, previous ear infections, noise exposure, medications,and recent upper respiratory tract infection was completed. Patients were excluded ifthey were older than 50 years, in order to avoid the phenomenon of presbycusis, or ifthey had a history of cochleovestibular, vascular or neurologic disease, or any other riskfactor for hearing impairment. Pure-tone audiometry, tympanometry and transientlyevoked otoacoustic emissions were performed. A group of healthy volunteers of similarage and sex were used for comparison.Results:(1) Tympanograms were normal, either on initial testing (75%) or on repeat testing(25%).(2) Audiometry showed elevation of all postoperative hearing thresholds, whereas thethresholds varied significantly across frequency.(3) TEOAE testing showed response signal to noise ratios lower in the postoperativesession (hypothyroid state) than in the preoperative session on all measured frequencies.(4) Emission levels varied significantly across frequency, with maximum responseobserved at 2 kHz.(5) Comparison of significant pure-tone and otoacoustic emission shifts for individualears showed more ears affected in otoacoustic emission testing, indicating subclinicalcochlear involvement.(6) Comparison of hearing thresholds and otoacoustic emission levels between patientsand controls showed significant differences on postoperative testing. Conclusions:Acute hypothyroidism in adults causes elevation of hearing thresholds and reducedotoacoustic emissions. The effect on otoacoustic emissions is greater, indicatingsubclinical damage of the cochlear function.