Thyroid Disorders Causing Hearing Loss: A Scoping Review

Santosh Kumar Swain

doi:10.25259/AONO_12_2025

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Review Article

2025

:6;

e021

doi:

10.25259/AONO_12_2025

Thyroid Disorders Causing Hearing Loss: A Scoping Review

Santosh Kumar Swain^¹

1Department of Otorhinolaryngology and Head and Neck Surgery, All India Institute of Medical Sciences, Bhubaneswar, Odisha, India.

*Corresponding author: Dr. Santosh Kumar Swain, Department of Otorhinolaryngology and Head and Neck Surgery, All India Institute of Medical Sciences, Bhubaneswar, Odisha, India. santoshvoltaire@yahoo.co.in

Received: 2025-06-26, Accepted: 2025-08-11, Published: 2025-10-13

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This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

How to cite this article: Swain SK. Thyroid Disorders Causing Hearing Loss: A Scoping Review. Ann Otol Neurotol. 2025;6:e021. doi: 10.25259/AONO_12_2025

Abstract

The growth and maturation of the body as a whole depend on thyroid hormones. One of the crucial endocrine components required for the growth of inner ear function is thyroid hormone. It can modify the expression of numerous genes and proteins involved in the auditory system. These hormones play an important role in the development of the cochlea. Hypothyroidism and hyperthyroidism may cause conductive hearing loss due to mucosal edema of the eustachian tube or the middle ear, or sensorineural hearing loss (SNHL) due to endo-cochlear, retro-cochlear, or central hearing impairment. When it comes to the ears, nose, and throat, hypothyroidism frequently manifests as hearing loss combined with cochleovestibular symptoms, including vertigo and tinnitus. This review aims to comprehend the connection between SNHL and thyroid disorders. The thyroid hormone dysfunction is also associated with sudden sensorineural hearing loss (SSNHL). Hearing impairment may present alone or in association with tinnitus and vertigo in patients with thyroid disorders. Although all types of deafness, including sensorineural, conductive, and mixed varieties, are linked to hypothyroidism, it is still unknown how common this hearing impairment is and how it develops. This review discusses the prevalence, pathophysiology, clinical profile, investigations, and treatment of deafness due to thyroid disorders.

Keywords

Hearing loss

Hyperthyroidism

Hypothyroidism

Sensorineural hearing loss

Thyroid disorder

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INTRODUCTION

There are multiple factors affecting hearing loss, such as genetic factors and environmental factors.¹ A variety of metabolic and endocrine disorders can result in varying degrees of hearing loss.¹ The anatomical structure of the auditory pathway and neurophysiology of hearing are affected by changes in the metabolic and hormonal systems.² Thyroid disorders are common clinical conditions found in the general population. The thyroid disorders can be hyperthyroid or hypothyroid, which can manifest in all the systems of the body. Thyroid disorders can also affect the middle ear and cochlea. Thyroid dysfunctions are often associated with audiological manifestations such as hearing loss and tinnitus.³ Reduced cell energy production from hypothyroidism impairs microcirculation, which in turn affects oxygenation and metabolism in the affected organs.⁴ In the central nervous system, thyroid hormone also regulates the creation of proteins, myelin, enzymes, and lipid levels.⁵ Therefore, it is thought that hearing loss under hypothyroidism may start in the retro-cochlear region, the cochlea, or the central auditory pathways.⁵ Thyroid hormone deficiency plays a significant part in the process of SLC26A4-induced deafness and can cause hearing loss as well as some inner ear diseases, including Meniere’s disease.⁶ This systematic review summarizes the prevalence, history, thyroid disorders, pathophysiology, clinical profile, investigations, and treatment of deafness due to thyroid disorders.

METHODS OF LITERATURE SEARCH

A search was conducted for research articles on thyroid disorders associated with hearing loss. This began with searching online databases such as Google Scholar, Scopus, PubMed, and Medline. A search strategy was developed following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Articles were initially screened by their titles to determine eligibility, followed by a thorough review of each abstract to ensure they met the inclusion criteria. The search approach found published article abstracts, and citations were used to manually find more research publications. The review evaluated the suitability of incorporating observational studies, comparative studies, case series, case reports, and randomized controlled trials. A total of 69 articles (24 case reports, 17 case series, and 28 original articles) were found across various databases, with 46 being included in this review [Figure 1]. This article discusses the history, prevalence, thyroid disorders, mechanism of hearing loss, Graves’ disease, Pendred syndrome, clinical presentations, investigations, and treatment.

PREVALENCE

One of the most common endocrine problems in the world is thyroid disease. Hyperthyroidism and hypothyroidism are examples of aberrant fluctuations in blood thyroid hormone levels that can cause both sensorineural and conductive hearing loss.⁷ There is disagreement worldwide over the precise prevalence of hearing loss in acquired hypothyroidism. After receiving thyroid hormone replacement therapy, hearing loss is somewhat reversible in about 25% of people with acquired hypothyroidism.⁸ Approximately 35%–50% of patients with congenital hypothyroidism present with hearing impairment.⁸ Around 30%–40% of sensorineural hearing loss (SNHL) has been reported in myxoedema.⁹

HISTORY

Bircher initially reported the relationship between hypothyroidism and hearing loss in 1883.¹⁰ In 1907, a case of a female patient with hypothyroidism was reported with hearing loss.¹⁰ According to Ritter, the most common otorhinolaryngological sign of congenital and acquired hypothyroidism is deafness, which can manifest alone or in combination with vertigo and tinnitus.¹¹

THYROID DISORDERS

Hypothyroidism, hyperthyroidism, and low T3 syndrome are the three types of thyroid dysfunction.⁵ Insufficient inner ear blood supply, decreased cochlear blood perfusion, degeneration of inner ear blood vessel endothelial cells, and even the formation of inner ear microthrombi are all features of hyperthyroidism, which also causes increased tissue metabolism, blood supply, and oxygen consumption.⁵ All these changes may be responsible for deafness in hyperthyroidism. A decrease in thyroid hormone levels in the blood that causes an increase in thyroid stimulating hormone (TSH) levels is known as hypothyroidism. A low blood TSH level and an increase in the concentration of thyroid hormones are characteristics of hyperthyroidism. Serum values of free triiodothyronine (FT3), free thyroxine (FT4), and TSH typically vary between 0.2 and 0.5 ng/dl, 0.7 and 2.5 ng/dl, and 0.4 and 4.2 mU/l, respectively.¹² For the auditory system to develop normally, thyroid hormone is necessary. It has long been known that thyroid hormone and hearing development are related in patients with endemic cretinism, congenital hypothyroidism, and thyroid hormone resistance.¹³ Hypothyroidism can affect blood lipids, which can result in coronary atherosclerosis, high coagulation, damage from fibrous protein breakdown, aberrant platelet and endothelial function, elevated peripheral vascular resistance and blood pressure, endothelial-dependent vasodilation, and changes in arterial smooth muscles, in addition to influencing the development of inner ear function.¹³ All these changes affect blood vessels and hemodynamic changes, leading to hearing loss.¹⁴ Similar to hypothyroidism, low T3 syndrome is characterized by a decrease in T3, normal TSH, and normal T4. The auditory system may also be affected by low T3 syndrome. Therefore, any thyroid condition can have an indirect impact on the onset and course of treatment for hearing loss.

PATHOPHYSIOLOGY OF HEARING LOSS

The exact mechanism of SNHL in thyroid disorders is poorly understood. The critical period of thyroid-sensitive cochlear development in humans occurs between the close of the first trimester of intrauterine life and the first month after birth.¹⁵ However, hearing loss with cochlear and/or auditory nerve dysfunction has also been linked to hypothyroidism, which is brought on by exposure to chemicals that alter the thyroid.⁷ Hypothyroidism has also been linked to a decrease in the number of outer hair cells in the cochlea’s apical turn and upper middle turn, which are responsible for detecting lower frequency sounds.¹⁶ Thyroid hormones regulate hearing by stimulating the myelinogenesis of the vestibulocochlear nerve (VIII cranial nerve) through thyroid hormone β receptors prior to the start of hearing.¹⁷ Thyroid hormone insufficiency has also been shown to decrease the expression of prestin (cochlear protein), which controls the activities of outer hair cells.¹⁷ Chromosomes 3 and 17 contain the thyroid hormone receptor (TR) genes α and β, respectively.¹⁸ TRα and TRβ1, β2, and β3 are the active proteins. These proteins have tissue-specific preferences for the expression of distinct TRs, indicating that they have distinct roles in various tissues. TRβ2 is expressed in the cochlea. In both humans and animals, irreversible deafness can be caused by a shortage of thyroid hormones in late pregnancy and early infancy.¹⁹ The late fetal period of human Corti organ maturation is highly responsive to thyroid hormone. The defects in auditory physiology, histology, and anatomy are associated with a deficiency of thyroid hormones.¹⁹ Potassium voltage-gated channel subfamily Q member 4 (KCNQ4) gene, a potassium channel gene in outer hair cells (OHCs) of the cochlea, when abnormally expressed as in thyroid disorders, results in chronic depolarization of OHCs and finally loss of OHCs.²⁰ When the strial membrane’s potassium channel subfamily J member 10 (KCNJ10) gene is overexpressed, it causes an ionic imbalance that probably contributes to OHC malfunction, sporadic death, and diminished endo-cochlear potential.²¹ Tectorial membrane anomalies such as a noticeable Hensen’s stripe, increased beta tectorin composition, and a disturbed striated sheet matrix are linked to thyroid hormone deficiency. Intermediate cells deteriorate as a result of strial membrane anomalies.²²

PENDRED SYNDROME

It is a hereditary condition that causes goiter, congenital bilateral SNHL, and sporadic hypothyroidism.²³ Other than supportive measures for hearing loss and thyroid hormone supplements in hypothyroidism, there is no proven cure for Pendred syndrome. Pendred syndrome is an uncommon autosomal recessive condition that causes a Mondini-type cochlear malformation, which usually results in significant hearing loss, as well as impaired iodine transport to the follicular lumen, which causes an organification deficit with mild hypothyroidism.²⁴ The Pendrin/SLC26A4 gene encodes pendrin, an anion exchanger seen in the cochlea, thyroid, and kidney.²⁵ One study showed that cochlear hypothyroidism contributes to failure for developing the failure of hearing in mice lacking SLC 26 A4 or pendrin expression.²⁶ The mutations of SLC26A4 can cause enlarged vestibular aqueduct, non-syndromic deafness, and deafness as a component of Pendred syndrome.²⁶ The cochlea’s development is affected by endochondral and intramembranous ossification, tunnel opening, and the onset of efferent innervation at outer hair cells. One study looked at the distribution of thyroid hormone receptors in the outer and inner cochlear hair cells and spiral ganglion of rats; immunohistochemistry showed that thyroid hormone influences cochlear development.²⁷ Another study that employed in situ hybridization found that Thra and Thrb encode thyroid hormone receptors α1 and β in the middle ear mesenchyme, immature ossicles, and tympanic membrane of mice.²⁸

RESISTANCE TO THYROID HORMONE

The TRβ gene is mutated in the majority of people with the syndrome of resistance to thyroid hormone.²⁹ Patients with this autosomal dominant syndrome have higher thyroid hormone levels and are less sensitive to its effects.³⁰ Growth delay, attention deficit hyperactivity disorder, tachycardia, goiter, frequent infections of the ears, nose, and throat, hearing loss, and decreased bone mass are some of the clinical manifestations of this syndrome.⁸

GRAVE’S DISEASE

Grave’s disease is an autoimmune disorder, and the basic pathology is the production of antibodies against TSH receptors. This not only causes hyperplasia of the gland due to the thyrotropic effects of TSH but also promotes the formation of monoiodotyrosine and diiodotyrosine and the release of T3 and T4. Certain major histocompatibility complex susceptibility genes have been associated with Graves’ disease.³¹ Antibodies such as TR-Ab levels are positive in patients of Graves’ disease, where autoimmunity may play a role in the pathogenesis of hearing impairment.

CONGENITAL HYPOTHYROIDISM

Congenital hypothyroidism is a potential risk factor for hearing loss. It can affect hearing from the peripheral auditory pathway to central areas of hearing, which may also result in inappropriate auditory development.³² These defects can affect the comprehension and acquisition of acoustic information. Inappropriate development of auditory pathways can lead to scholarly, cognitive, language, behavioral and/or social-emotional problems.³² So, it is critical to evaluate and monitor the hearing with otoacoustic emissions and brain stem evoked audiometry as part of the clinical routine of these patients.³²

CLINICAL PROFILE

Thyroid disorders are usually seen in women in comparison to men and in individuals of middle age group. The most common cause of acquired hypothyroidism is Hashimoto’s thyroiditis. Hearing loss is the most frequently reported ear, nose, and throat symptom of hypothyroidism, often accompanied by cochleovestibular issues such as tinnitus and dizziness.³³ Therefore, assessing hearing function in individuals with hypothyroidism holds clinical significance and has been the focus of several studies.³⁴ Hypothyroidism affects the ear at different sites, resulting in different types of hearing impairment such as conductive, sensorineural, and mixed types of hearing loss. The hearing impairment in hypothyroidism ranges from mild to moderate in severity. There is a significant correlation between the duration of hypothyroidism and mean TSH levels with the severity of hearing loss. Patients with hypothyroidism may complain of dizziness. This unsteadiness may be due to vestibular or non-vestibular causes. The non-vestibular cause may be due to excessive weakness.

SUDDEN SENSORINEURAL HEARING LOSS (SSNHL)

Sudden onset of hearing loss of greater than 30 dB in three consecutive frequencies within 72 hours is known as SSNHL.¹ The etiology of SSNHL is still debated. There are several etiologies associated with SSNHL, such as infection, otologic disease, and trauma. Anemia, chronic kidney disease, systemic lupus erythematosus, HIV, psoriasis, osteoporosis, and chronic otitis media are among the various underlying comorbidities that may be associated with SSNHL.³⁵ A cross-sectional study revealed that thyroid disorders occur more frequently in individuals with SSNHL compared to the general population.³⁶ Normal thyroid function is considered a favorable prognostic factor for hearing recovery in sudden SSHL. Indicators such as T3 or FT3 may influence the prognosis, as there is a clear association between thyroid dysfunction involving T3 or FT3 levels and both the onset timing and hearing outcomes in SSHL.³⁷ Assessing thyroid function, particularly T3 levels, can be useful in predicting treatment outcomes in patients with prolonged SSHL.⁹

INVESTIGATIONS

Pure tone audiometry, tympanometry, otoacoustic emissions, and brainstem evoked response audiometry are important audiological investigations needed to evaluate hearing in thyroid disorders.³⁸ These investigations can detect the hearing thresholds and hearing loss due to subclinical damage to cochlear function.³⁹ Audiometric evaluation is done with otoscopy, tympanography, and assessment of middle ear function by immittance and acoustic reflex. In hypothyroidism, conductive hearing loss may be the result of reduced compliance due to hypertrophy and edema of the eustachian tube, resulting in eustachian catarrh with a retracted and thickened tympanic membrane. In hypothyroidism, potential complications may include changes in the ossicles and the round or oval windows, such as hard consistency of bone, fusion or malformation of the incus and stapes, and partial or complete blockage of the oval or round window. Impedance audiometry may reveal decreased compliance or unusually negative middle ear pressure, which can be attributed to mucosal hypertrophy and edema in the nose and Eustachian tube leading to its obstruction, as well as thickening of the middle ear mucosa and the tympanic membrane. The short increment sensitivity index score is more than 70% in many cases, indicating the cochlea to be the site of lesion, whereas the tone decay is more than 30 decibels in cases of retro-cochlear lesion. The cochlea has been identified as the primary site of damage, with acid mucopolysaccharide deposits observed within its scala. One study noted that the tectorial membrane is the earliest structure to exhibit changes in hypothyroidism.⁴⁰ Venous blood samples are taken from patients with thyroid disorders for estimation of serum levels of TSH, FT3, and FT4 levels measured by using the chemiluminescence microparticle immunoassay method. TRAb titers are determined by radioreceptor assay. These autoantibodies on hearing loss are helpful to distinguish whether hearing loss noted in Graves’ disease occurs due to autoimmunity or excess thyroid hormone level.⁴¹

TREATMENT

The most prevalent otorhinolaryngological symptom of both congenital and acquired hypothyroidism is hearing loss, which is strongly correlated with low free T4. The sooner the treatment for hearing loss due to thyroid dysfunction, the better the prognosis.⁴² The goal of the treatment is restoration of the euthyroid state, which can be done by oral administration of synthetic thyroxine (T4, levothyroxine). It is yet unknown if thyroxine therapy can improve hearing in hypothyroidism patients, as interactions are complex between thyroid hormones and associated receptors in the middle and inner ear.⁴³ Supplementation of thyroxine is helpful for middle ear compliance and pressure in case of hypothyroidism. Appropriate treatment is helpful to reverse all the clinical manifestations like hearing loss of hypothyroidism.

CONCLUSION

Thyroid hormones are essential for the development of hearing. Both hypothyroidism and hyperthyroidism are linked to hearing impairment, with potential for sensorineural, conductive, and mixed types of deafness. Hearing loss in hypothyroidism may improve with supplementation of thyroxine. So, prompt screening, treatment, and follow-up of the hearing loss should be done in patients with thyroid disorders. When thyroid dysfunction is diagnosed, a baseline audiogram is suggested to confirm hearing impairment. Both patients and medical professionals should be educated about this condition and the need for prompt treatment.

Ethical approval:

Institutional Review Board approval is not required.

Declaration of patient consent:

Patient’s consent not required as there are no patients in this study.

Financial support and sponsorship:

Nil.

Conflicts of interest:

There are no conflicts of interest.

Use of artificial intelligence (AI)-assisted technology for manuscript preparation:

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

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