|Year : 2015 | Volume
| Issue : 2 | Page : 138-143
Is sensorineural hearing loss related with thyroid metabolism disorders
Canan Filiz Karakus1, Emine Elif Altuntaş2, Fatih Kılıçlı3, Kasım Durmuş2, Zekiye Hasbek4
1 Department of Otorhinolaryngology, Ministry of Health, Hatay Antakya Public Hospital, Hatay, Turkey
2 Department of Otorhinolaryngology, Cumhuriyet University School of Medicine, Campus, 58140 Sivas, Turkey
3 Department of Endocrinology and Metabolic Diseases, Cumhuriyet University School of Medicine, Campus, 58140 Sivas, Turkey
4 Department of Nuclear Medicine, Cumhuriyet University School of Medicine, Campus, 58140 Sivas, Turkey
|Date of Web Publication||20-Apr-2015|
Dr. Emine Elif Altuntaş
Department of Otorhinolaryngology, Cumhuriyet University School of Medicine, Campus, 58140 Sivas
Source of Support: None, Conflict of Interest: None
Objectives: In this study, we measured hearing thresholds in patients diagnosed with hyperthyroidism or hypothyroidism with high-frequency audiometry and otoacoustic emission before and after treatment to determine whether hearing losses were cochlear or retrocochlear and whether they would improve with medical therapy. Materials and Methods: This study was conducted on patients diagnosed with hyperthyroidism and hypothyroidism at Cumhuriyet University, Faculty of Medicine, Department of Endocrinology and Metabolism and accepting to participate in the study. We measured the hearing thresholds of the study population during the pretreatment period and in posttreatment euthyroid period. Result: The audiometric findings of patients with hyperthyroidism were better than those of the control group especially at high frequencies. Sensorineural hearing loss was detected in the euthyroid period. We compared the audiometric findings of the patients with hypothyroidism and the controls. We found sensorineural hearing loss in patients with hypothyroidism, especially at low frequencies. Conclusions: The results of this study showed that both hyperthyroidism and hypothyroidism may have an effect on hearing pathway disorders. Medical therapy may lead to hearing loss in patients with hyperthyroidism, and the underlying factors should be investigated in detailed future studies. It was shown in our study that the hearing loss induced by hypothyroidism may improve with medical therapy. Therefore, in all patients with thyroid dysfunction, hearing levels should be monitored closely with audiometric tests.
Keywords: Audiometry, Hearing loss, Hyperthyroidism, Transient evoked otoacoustic emission
|How to cite this article:|
Karakus CF, Altuntaş EE, Kılıçlı F, Durmuş K, Hasbek Z. Is sensorineural hearing loss related with thyroid metabolism disorders. Indian J Otol 2015;21:138-43
|How to cite this URL:|
Karakus CF, Altuntaş EE, Kılıçlı F, Durmuş K, Hasbek Z. Is sensorineural hearing loss related with thyroid metabolism disorders. Indian J Otol [serial online] 2015 [cited 2019 May 26];21:138-43. Available from: http://www.indianjotol.org/text.asp?2015/21/2/138/155310
| Introduction|| |
Thyroid hormone deficiency may lead to severe cognitive dysfunction and deafness. Hypothyroidism is a cause of genetic and environmentally induced deafness. ,, Although many authors have reported on hearing loss in hypothyroidism, there is still no clear understanding on its pathology. The real incidence of hearing loss in patients with hypothyroidism is not known clearly yet; however, it has been reported that 25% of the patients with acquired hypothyroidism and 35-50% of those with congenital hypothyroidism may have hearing loss. , Hearing loss has been reported to be associated with thyroid disorders and treatment with propylthiouracil. Our literature review did not yield many studies on hearing changes in hypothyroid patients. , For this reason, in our study, we evaluated the hearing levels both in hypothyroid and hyperthyroid patients based on the results obtained by high frequency audiometry and temporarily stimulated otoacoustic emission (transient evoked otoacoustic emission [TEOAE]). Our aim was to determine whether hearing loss was of cochlear or retro-cochlear origin and to establish whether the hearing loss would improve with medical treatment in euthyroid cases.
| Materials and Methods|| |
A total of 62 patients composed of 31 patients (Group 1) having a diagnosis of hyperthyroidism and 31 patients (Group 2) having a diagnosis of hypothyroidism and undergoing medical treatment at the Department of Endocrinology and Metabolism between June 2011 and 2012 were included in the study. Control groups were formed by re-evaluating the patients in Group 1 and 2 with audiology tests during the euthyroid period.
This study was performed in accordance with the principles of the Declaration of Helsinki and approved by the Research Ethics Committee of Cumhuriyet University (Decision Number: 2011-05/31 Date: 31/05/2011-154). Oral and written consents were obtained from all those participating in the study.
Exclusion criteria were refusing to visit the ear-nose-throat polyclinic for the hearing tests, not giving consent to participate in the study, having an autologic disease/surgery, mechanic trauma, syphilis, malignancy, vascular disease, acute or chronic otitis media, congenital cochlear malformation or neurological disease (known as a cause of hearing loss), using autotoxin drugs within the 1-month prior to the study, having hypertension or etiological factors such as liver or renal failure causing hearing loss and receiving radiotherapy or chemotherapy treatment within 1-month prior to the study for any reason.
Besides, those with serum thyroid-stimulating hormone (TSH) levels below the normal value (<0.35 μIU/ml) but having normal free triiodothyronine (fT3) and free thyroxine (fT4) levels were regarded as subclinical hyperthyroid and thus excluded from the study, too.
On the other hand, patients having fT3 and fT4 levels above the normal value were regarded as clinic hyperthyroid and included in the study. Those with serum TSH levels above the normal value (>4.94 μIU/ml) but having normal fT3 and fT4 levels were regarded as subclinic hypothyroid and excluded from the study. Meanwhile, patients with fT3 and fT4 levels below the normal value were regarded as clinic hypothyroid and included in the study. In addition, patients having ear infection symptoms, not attending the hearing and hormone level follow-ups or wishing to withdraw from the study were also excluded from the study.
Comprehensive ear-nose-throat and head-neck examinations of the cases participating in the study were evaluated by the same researcher (CFK). All the patients underwent high-frequency audiometry and hearing tests with TEOAE (in pretreatment and posttreatment euthyroid periods) performed by a single audiometrist (VO).
Air-and bone-conduction thresholds of the patients were measured by a clinical audiometer device (INTERACOUSTICS AC 40 Clinical Audiometer) calibrated according to ISO standards. All the audiology tests were performed by masking the nontest ear. Pure tone hearing thresholds were measured at frequencies of 0.25, 0.5, 1, 2, 4, 6, 8, and 12 kHz. Pure tone thresholds were classified as follows: Normal hearing = between 0.20 dBs, mild = between 21 and 40 dBs, moderate = between 41 and 60 dBs, severe = between 61 and 80 dBs, profound = between 80 and 100 dBs and total hearing loss = over 100 dBs.  Then, all the patients were subjected to TEOAE performed with a TEOAE device (Maico ERO-Scan TEOAE). TEOAE tests and analysis were conducted by a commercial device (Maico, ERO Scan Analyzer, GmbH Salzufer, 13/14, 10587, Berlin GE) calibrated beforehand. During the test, disposable probe tip was used to close the ear canal. A response (better hearing than 30 decibels) to TEOAE was shown as "PASS" on the screen while no response (hearing loss range was 30 decibels or more) was shown as "REFER."
Screening test was repeated for the ears yielding "REFER." The stimulant in the form of a click sound occurred in the frequency range 0.7-4 kHz and 83 dB/SPL (±3 dB) degree of density. In each session, the results for both the right and the left ears were recorded. The results were recorded one by one in the frequency bandwidth of 1.5-4 kHz and at 1.5, 2, 2.5, 3, 3.5, and 4 kHz frequencies for TEOAE. In the bandwidth of 1.5-4 kHz, having an average amplitude below 6 dB meant that there was no response to otoacoustic emission.
A detailed anamnesis, fT3, fT4, and TSH results, otoscopic examination findings, high-frequency audiogram, and findings of TEOAE were recorded in the follow-up forms of the patients.
SPSS 14.0 (SPSS Inc., Chicago, IL, USA) statistical package software was used to record the results. Paired Student's t-test, "McNemar Test" and "Correlation Analysis" were used to evaluate the results obtained. P < 0.05 was accepted as significant.
| Results|| |
There were twenty-six (83.9%) females and 5 males (16.1%) in the hyperthyroid group (n = 31, Group 1), and their ages were between 21 and 74 years (approximately 43.03 ± 13 years). The ages of those in the hypothyroid group (n = 31, Group 2) composed of only female patients ranged between 19 and 66 years (approximately 46.03 ± 12 years).
High frequency audiometry test performed during the pretreatment period on 62 ears in Group 1 (n = 31) revealed no hearing loss in 55 (88.7%) ears, mild sensorineural hearing loss in 7 (11.3%) ears. During the posttreatment period, there was no hearing loss in 54 of the said 62 ears (87.1%) and mild sensorineural hearing loss was found in 8 (12.9%) ears. When the patients classified based on their hearing levels were compared before and after the treatment, there was a statically significant difference (P = 0.317; P > 0.05).
In the high frequency audiometry test made on 62 ears of 31 patients in Group 2; while there was not any hearing loss in 54 (87.1%) ears, mild sensorineural hearing loss was detected in 8 (12.9%) in pretreatment period. During the posttreatment period, there was no hearing loss in 60 of the said 62 ears (96.8%) and mild sensorineural hearing loss was found in 2 (3.2%) ears. The difference was statistically insignificant when we compared the patients classified according to their hearing levels before and the after the treatment (P = 0.034; P > 0.05).
The pure tone average of those in Group 1 was 12.24 ± 6.65 dB in the pretreatment period and 12.88 ± 6.79 dB in the posttreatment period. The increase observed in pure tone average during the euthyroid period was statistically insignificant (P = 0.052; P > 0.05). In Group 2, the pure tone average was 13.77 ± 5.53 dB in the pretreatment period and 11.51 ± 4.24 dB in the posttreatment period. This alteration detected in pure tone average in Group 2 during the euthyroid period was found to be statistically significant (P = 0.001; P < 0.05).
In Group 1, there were negative correlation coefficients between the pretreatment right ear pure tone averages and T3 (r = −0.15), T4 (r = −0.06) and TSH (r = −0.08) values. Posttreatment pure tone averages and T3 (r = −0.11), T4 (r = −0.32) and TSH (r = −0.23) had negative correlation coefficients too. These coefficients were statistically small and insignificant. Similarly, there were negative correlation coefficients between the pretreatment left ear pure tone averages and T3 (r = −0.07), T4 (r = −0.12) and TSH (r = −0.02) values. Posttreatment pure tone averages and T3 (r = −0.06), T4 (r = −0.14) and TSH (r = −0.01) had negative correlations too. These coefficients were statistically small and insignificant.
In Group 2, there were positive correlation coefficients between the posttreatment right ear pure tone averages and T3 (r = −0.05), T4 (r = −0.04) and TSH (r = −0.03) values. Posttreatment pure tone averages and T3 (r = −0.14) value had a positive correlation coefficient while there was a negative correlation coefficient between T4 (r = −0.07) and TSH (r = −0.14) values had negative correlation coefficients. These coefficients were statistically small and insignificant. Similarly, there were negative correlation coefficients between the pretreatment left ear pure tone averages and T3 (r = −0.02), T4 (r = −0.16) values. Posttreatment left ear pure tone averages and TSH (r = 0.03) value had a positive correlation coefficient. Posttreatment left ear pure tone averages had a positive correlation with T3 (r = 0.14) value and negative correlation with T4 (r = −0.06) and TSH (r = −0.15). These coefficients were statistically small and insignificant.
Comparison of the pretreatment and posttreatment airway hearing thresholds of Group 1 and Group 2 at different frequencies is given in [Table 1].
|Table 1: Comparison of the pretreatment and posttreatment airway hearing thresholds of Group 1 and Group 2 at different frequencies|
Click here to view
When we compared the pretreatment and posttreatment airway hearing thresholds measured in different thresholds in Group 1, euthyroid period airway thresholds were higher at 4000 Hz, 8000 Hz, and 12,000 Hz (P < 0.05).
When we compared the pretreatment and posttreatment airway hearing thresholds measured in different thresholds in Group 2, euthyroid period airway thresholds were higher at 250 Hz, 500 Hz, 1000 Hz, and 2000 Hz (P < 0.05).
In audiometry conducted by otoacoustic emission in Group 1, 58 (93.5%) of the 62 ears were recorded as "PASS" and 4 ears (6.5%) were recorded as "REFER" in the pretreatment period. The audiometry conducted by otoacoustic emission after the treatment did not yield any differences.
In audiometry conducted by otoacoustic emission in Group 2, 60 (96.8%) of the 62 ears were recorded as "PASS" and 2 ears (3.2%) were recorded as "REFER" in the pretreatment period. The audiometry conducted by otoacoustic emission after the treatment yielded "PASS" "for all the ears.
| Discussion|| |
Thyroid hormones influence the biological events in the body by direct or indirect ways and help all the cells, and thus the systems develop normally and work. ,
Although there are various studies evaluating hypothyroid patients' hearing, the studies conducted on hyperthyroid patients are limited. ,, In this study, conducted on 31 clinic hyperthyroid and 31 clinic hypothyroid patients, we evaluated the effects of the changes in thyroid functions on hearing levels with high-frequency audiometry and TEOAE measurements.
In a study on 14 hyperthyroid patients, Thornton and Jarvis  reported that there was not a significant difference between the results of audiometry and auditory brainstem response (ABR) when the hyperthyroid group was compared with the normal group. In our study, among the hyperthyroid patients, a mild sensorineural hearing loss was detected in 7 (11.3%) of the 62 ears in the pretreatment period while there were 8 (12.9%) ears with mild sensorineural hearing loss in the posttreatment period.
However, when we compared the patients classified based on their hearing levels in pretreatment and posttreatment periods, the difference was found to be statically insignificant. Moreover, pure tone average values of these patients were 12.24 ± 6.65 dB in the pretreatment period and 12.88 ± 6.79 dB in the posttreatment period. When these values were compared, there was an increase in the pure tone average values during the euthyroid period; however, this increase was statically insignificant. Taking these results into account, the results we obtained are similar to those of Thornton et al. 
In a study conducted by Karalı and Güçlü  in 2009 on 25 hyperthyroid patients, the airway threshold values the hyperthyroid group and the control group were compared audiometrically, and the airway thresholds of the hyperthyroid patients were found to be significantly higher at all frequencies (especially at 2000 Hz-8000 Hz), Similar to the results obtained by Karalı and Güçlü,  we found that the pretreatment and posttreatment airway hearing thresholds of the hyperthyroid cases were higher at 4000-12,000 Hz in the euthyroid period and the difference was statically significant.
In a case report presented by Fong et al.  in 1991, sensorineural hearing loss and additional side-effects such as high temperature, polyarthritis, anemia, and hepatotoxicity were observed in the hyperthyroid patient who became euthyroid after propiltiourasil (PTU) therapy. When the therapy was stopped due to drug-induced hypersensitivity, they observed a rapid improvement in the hearing loss and other symptoms.
Similarly, in 2004, Sano et al.  reported a 36 years old male hyperthyroidism patient with bilateral sensorineural hearing loss, high temperature, and polyarthritis occurring a result of vasculitis attack induced by PTU therapy. Distortion product otoacoustic emissions test results suggested the dysfunction of outer hair cells of the organ of Corti. PTU withdrawal and administering a high dose methylprednisolone improved hearing and other symptoms of the patient.
Although we observed a statistically significant increase at high frequencies in hearing thresholds of the hyperthyroid patients in our study which indicates the possibility of a drug-induced hypersensitivity, our aim was not to investigate the drug side effects and thus expressing an absolute judgment on this subject would not be appropriate. We believe that drug side-effects should be taken into consideration in future studies.
Insufficient synthesis of thyroid hormones for various reasons causes hypothyroidism. ,,,, The most common symptom of hypothyroidism regarding ear nose and throat is hearing insufficiency accompanied with cochleovestibular symptoms such as tinnitus and dizziness.  Hearing pathology occurring in thyroid function disorders has been studied by many researches. The relation between hypothyroidism and hearing insufficiency was first identified by Bircher in 1883. The second case was a 53-year-old, the female patient with hypothyroidism published in 1907 by Kemp. , Case studies by Moehlig, Howarth and Lloyd and Friedman are among the other publications on this issue. ,, The relation between hypothyroidism and hearing insufficiency gained acceptance for the 1 st time when the London Clinic Institution, Committee of Myxoedematous detected that 36 out of 69 hypothyroid patients had hearing loss.  Once it was accepted that there is a relationship between hypothyroidism and hearing loss, the location of the affected part in ear has been subject to many new studies which showed one or multiple parts such as endocochlear, retrocochlear or central hearing ways might be affected. ,
In 1989, Anand et al.  reported prolongation in the I-III and I-V interpeak latencies in hypothyroid patients, and a casual relation between hearing loss and the pathologies effecting retrocochlear or central hearing ways in hypothyroid patients.
Khedr et al.  found prolongation in all frequency latencies and interpeak latencies, and argued that there was a pathology in all cochlear, retrocochlear, and central hearing ways in hypothyroid patients.
In a study conducted on 30 hypothyroid patients, Santos et al.  detected moderate sensorineural hearing loss in 22 of the 60 ears and reported that these were bilateral hearing losses.
In a clinical study conducted in 1967, Ritter et al. reported that the hearing loss occurring in hypothyroidism was a bilateral, mild and moderate sensorineural type hearing loss. In 2008, Thornton and Jarvis  conducted a study on 21 hypothyroid patients, and the audiometric findings showed that 36% of this group had a pure tone average threshold >25 dB. In the same patients group, ABR measurements supported the retrocochlear pathology.
In our study, among the hypothyroid patients, a mild sensorineural hearing loss was detected in 8 (12.9%) of the 62 ears in the pretreatment period while there were 2 (3.2%) ears with mild sensorineural hearing loss in the posttreatment period. When we compared the patients who were classified according to their hearing levels, the difference was found statistically significant. In this aspect, our study similar to the studies conducted by Santos et al.  at different times. Our study revealed that the average pure tone of the patients with hypothyroidism was 13.77 ± 5.53 dB in the pretreatment period and 11.51 ± 4.24 dB in the posttreatment period, which is a result similar to that of Thornton and Jarvis. 
Dokianakis et al.  detected moderate sensorineural hearing loss in 8 and mixed type hearing loss in 4 of 23 hypothyroid patients. The hearing loss of the patients improved significantly after a 4-month therapy. The studies conducted by Ben-Tovim et al.  on rats and by Rubinstein et al.  on pigs, it was found that the hearing loss in hypothyroidism was remediable and reversible after treatment.
On the other hand, Anand et al.  claimed that the audiometric changes in hypothyroidism might improve with treatment but the brainstem electric response audiometry brainstem auditory evoked potential (BAEP) would be permanent despite the treatment. In a clinical study performed by Di Lorenzo et al.,  proved by BAEP measurements that the hearing loss in hypothyroid period improved in 6-12 months after hormone replacement therapy. Similarly, in our study, the hearing loss in hypothyroid patients improved after medical therapy.
In studies conducted by Ben-Tovim et al.  on rats and Himelfarb et al.  on people, a significant relation was found between the decrease of T4 level and the changes in audiometric measurements and BAEP results. Santos et al.  reported that there was no relationship between hearing thresholds and serum levels of hormones. Similarly, we could not find any statistically significant relation between the audiometric measurement results and an increase/decrease in T3 level T4 level or TSH level.
Karalı and Güçlü  studied 25 hypothyroid patients and reported that comparison of the airway threshold values obtained by audiometry revealed that the airway thresholds in the hypothyroid group were found higher at all frequencies when compared to the controls. However, while there was no significant difference at 500 Hz-4000 Hz, they found a statistically significant difference at 8000 Hz in the hypothyroid group. Likewise, when we compared the airway hearing thresholds of the hypothyroid patients measured at various frequencies during the pretreatment and posttreatment periods; the airway thresholds were statistically significantly lower at 250-2000 Hz in euthyroid period. On the other hand, the difference between measurements at 4000-12,000 Hz was found to be insignificant. The airway hearing thresholds, especially at low frequencies, in hypothyroidism period were significantly higher than the posttreatment euthyroid period, which differs our study from the one conducted by Karalı and Güçlü. 
In the study conducted on 50 hypothyroid patients, Khechinaschvili et al.  could not find any evoked otoacoustic emissions (EOAEs) response in patients having normal audiometric thresholds. In the same study, ABR changes were recorded in 30% of the patients. Inconsistency among EOAEs measurements, threshold values measured by audiometric tests and ABR results suggests that the involvement leading to changes in hearing levels in thyroid function disorders might be multifocal. In our study, there was no TEOAE response in 6.5% of the hyperthyroid patients and 3.2% of the hypothyroid patients during the pretreatment evaluation. As for the evaluation made after they became euthyroid with treatment, TEOAE results were obtained in all of the patients with hypothyroidism while no change was observed in hyperthyroid patients after treatment.
| Conclusion|| |
Based on the results we obtained, those in the hyperthyroid group had hearing losses at higher frequencies and their hearing loss increased during the euthyroid period. When the audiometric findings of the hyperthyroid cases were compared with the ones observed during the euthyroid period, sensorineural hearing loss was detected especially at low frequencies. When TEOAE results of the hypothyroid group and the controls were compared, there was no significant difference. In conclusion, the hearing loss in hyperthyroid cases was permanent while the hearing loss in hypothyroid cases was a temporary one caused by the treatment. We believe that one should take into consider that the hearing loss in hyperthyroid patients may result from a drug-induced hypersensitivity. For this reason, more comprehensive studies are required to evaluate the reasons of increased hearing loss during euthyroid period in hyperthyroid cases. Besides, similar to the literature, we showed that the hearing loss in hypothyroid patients may improve with medical therapy, and we believe that the hearing level should be clinically followed-up in these patients.
| References|| |
Debruyne F, Vanderschueren-Lodeweyckx M, Bastijns P. Hearing in congenital hypothyroidism. Audiology 1983;22:404-9.
Rovet J, Walker W, Bliss B, Buchanan L, Ehrlich R. Long-term sequelae of hearing impairment in congenital hypothyroidism. J Pediatr 1996;128:776-83.
Fang Q, Giordimaina AM, Dolan DF, Camper SA, Mustapha M. Genetic background of Prop1(df) mutants provides remarkable protection against hypothyroidism-induced hearing impairment. J Assoc Res Otolaryngol 2012;13:173-84.
Ben-Tovim R, Zohar Y, Zohiar S, Laurian N, Laurian L. Auditory brain stem response in experimentally induced hypothyroidism in albino rats. Laryngoscope 1985;95:982-6.
Vanasse M, Fischer C, Berthezène F, Roux Y, Volman G, Mornex R. Normal brainstem auditory evoked potentials in adult hypothyroidism. Laryngoscope 1989;99:302-6.
Thornton AR, Jarvis SJ. Auditory brainstem response findings in hypothyroid and hyperthyroid disease. Clin Neurophysiol 2008;119:786-90.
Berker D, Karabulut H, Isik S, Tutuncu Y, Ozuguz U, Erden G, et al.
Evaluation of hearing loss in patients with Graves' disease. Endocrine 2012;41:116-21.
Guidelines for screening for hearing impairment and middle-ear disorders. Working Group on Acoustic Immittance Measurements and the Committee on Audiologic Evaluation. American Speech-Language-Hearing Association. ASHA Suppl 1990;(2):17-24. PubMed PMID: 1970249.
Ritter FN. The effects of hypothyroidism upon the ear, nose and throat. A clinical and experimental study. Laryngoscope 1967;77:1427-79.
Santos KT, Dias NH, Mazeto GM, Carvalho LR, Lapate RL, Martins RH. Audiologic evaluation in patients with acquired hypothyroidism. Braz J Otorhinolaryngol 2010;76:478-84.
Karalı E. Güçlü E. Evaluation of auditory brainstem responses in hypothyroid and hyperthyroid disease. Duzce University School of Medicine Department of Otolaryngology, Master Thesis. Düzce, 13-26, 2009.
Fong PC, Pun KK, Tai YT, Wang C, Yeung RT. Propylthiouracil hypersensitivity with circumstantial evidence for drug-induced reversible sensorineural deafness: A case report. Horm Res 1991;35:132-6.
Sano M, Kitahara N, Kunikata R. Progressive bilateral sensorineural hearing loss induced by an antithyroid drug. ORL J Otorhinolaryngol Relat Spec 2004;66:281-5.
Wartofsky L. Diseases of the thyroid. In: Fauci AS, Braunwald E, editors. Harrison's Principles of Internal Medicine. 14 th
ed., Vol. 331. Philadelphia: McGraw-Hill Co.; 1998. p. 2012-35.
Loeb JN. Metabolic changes in hypothyroidism. In: Braverman LE, Utiger RD, editors. Werner and Ingbar's the Thyroid. 7 th
ed., Vol. 73. New York: Lippincott-Raven; 1996. p. 858-65.
Ladenson PW. Diagnosis of hypothyroidism. In: Braverman LE, Utiger RD, editors. Werner and Ingbar's the Thyroid. 7 th
ed., Vol. 76. New York: Lippincott-Raven; 1996. p. 878-82.
Lindsay RS, Toft AD. Hypothyroidism. Lancet 1997;349:413-7.
Woeber KA. Subclinical thyroid dysfunction. Arch Intern Med 1997;157:1065-8.
Günel C, Basak HS, Güney E. The relationship between hypothyroidism and rhinitis. Kulak Burun Bogaz Ihtis Derg 2010;20:163-8.
Stephens SD. Temporary threshold drift in myxoedema. J Laryngol Otol 1970;84:317-21.
Kemp WR. Deafness in myxoedema. Br Med J 1907;1:375.
Moehlig RC. Vertigo and deafness associated with hypothyroidism. Endocrinology 1927;11:229.
Howarth AE, Lloyd HE. Perceptive deafness in hypothyroidism. Br Med J 1956;1:431-3.
Friedman IH. Deafness in myxedema. N Y State J Med 1964;64:2792-3.
Meyerhoff WL. Hypothyroidism and the ear: Electrophysiological, morphological, and chemical considerations. Laryngoscope 1979;89:1-25.
Khechinaschvili S, Metreveli D, Svanidze N, Knothe J, Kevanishvili Z. The hearing system under thyroid hypofunction. Georgian Med News 2007;(144):30-3.
Anand VT, Mann SB, Dash RJ, Mehra YN. Auditory investigations in hypothyroidism. Acta Otolaryngol 1989;108:83-7.
Khedr EM, El Toony LF, Tarkhan MN, Abdella G. Peripheral and central nervous system alterations in hypothyroidism: Electrophysiological findings. Neuropsychobiology 2000;41:88-94.
Dokianakis G, Ferekidis E, Pantazopoulos P. Hearing loss and hyperthyroidism (author's transl). Arch Otorhinolaryngol 1978;219:351-3.
Rubinstein M, Perlstein TP, Hildesheimer M. Cochlear action potentials in experimentally induced hypothyroidism in guinea pigs. Acta Otolaryngol 1975;79 Suppl 331:1-10.
Di Lorenzo L, Foggia L, Panza N, Calabrese MR, Motta G, Tranchino G, et al
. Auditory brainstem response in thyroid diseases before and after therapy. Horm Res 1995;43:200-5.
Himelfarb MZ, Lakretz T, Gold S, Shanon E. Auditory brain stem responses in thyroid dysfunction. J Laryngol Otol 1981;95:679-86
|This article has been cited by|
||Untreated primary hypothyroidism with simultaneous rhabdomyolysis, pericardial effusion, and sudden sensorineural hearing loss: a case report
| ||Chung Gyo Seo,Kyoung Jin Kim,Euyhyun Park,Nam Hoon Kim,Joo Hyung Kim,Hee Young Kim,Sin Gon Kim,Kyeong Jin Kim |
| ||BMC Endocrine Disorders. 2019; 19(1) |
|[Pubmed] | [DOI]|
||l -Thyroxine does not prevent immunemediated sensorineural hearing loss in autoimmune thyroid diseases
| ||Antonio Rodríguez-Valiente,Óscar Álvarez-Montero,Carmen Górriz-Gil,José Ramón García-Berrocal |
| ||Acta Otorrinolaringológica Española. 2018; |
|[Pubmed] | [DOI]|
||Does the use of recombinant TSH in preparation for I-131 scintigraphy scan affect hearing function?
| ||Mehtap Dogan,Kasim Durmus,Zekiye Hasbek,Emine Elif Altuntas |
| ||Journal of Otology. 2017; |
|[Pubmed] | [DOI]|