The stealthy onset of sudden sensorineural hearing loss in hypothyroidism – literature review

 Debutul subliminal al surdităţii neurosenzoriale brusc instalate în hipotiroidism – revizuire a literaturii

First published: 24 mai 2024

Editorial Group: MEDICHUB MEDIA

DOI: 10.26416/ORL.63.2.2024.9625


Sudden sensorineural hearing loss (SSNHL) is a frequent oc­cur­rence in audiology and otolaryngology. It refers to a sen­so­rineural hearing loss of 30 dB or more across three con­se­cu­tive audiometric frequencies, developing within 72 hours. While the causes of SSNHL vary widely, most cases lack a clear origin. Studies have suggested a po­ten­tial re­la­tion­ship between thyroid dysfunction and the onset of SSNHL, yet establishing a definitive causal link re­mains un­cer­tain. Our review aims to meticulously explore the impact of thyroid function on SSNHL. The treatment for SSNHL with iden­ti­fiable causes typically targets the un­der­lying agent, often resulting in poor hearing outcomes due to inner ear hair cell damage. In cases of idiopathic SSNHL, steroid the­r­apy is the current standard of care. The prognosis for hea­r­ing recovery in idiopathic SSNHL hinges on factors such as the severity of hearing loss, age, presence of vertigo, and le­­­vels of thyroid hormones.

sudden sensorineural hearing loss (SSNHL), hypothyroidism, thyroid disorders


Surditatea neurosenzorială brusc instalată (SSNHL) este o pro­ble­mă des întâlnită în practica audiologică şi oto­larin­go­lo­gică. Pentru a putea stabili diagnosticul, hipoacuzia trebuie să fie de tip neurosenzorial, cu o pierdere auditivă de peste 30 dB, să afec­teze trei frecvenţe consecutive şi să se instaleze în maximum trei zile. Deşi există numeroase cauze determinante ale SSNHL, pentru majoritatea pacienţilor, etiologia nu poate fi stabilită. Studiile observaţionale au sugerat o posibilă le­gă­tu­ră între dis­func­ţia tiroidiană şi debutul brusc al SSNHL. Cu toate acestea, sta­bi­lirea exactă a conexiunii cauzale rămâne incertă. Scopul re­vi­zuirii noastre este de a investiga impactul funcţiei tiroidiene asupra SSNHL. Întrucât pierderea auditivă este asociată în prin­ci­pal cu pierderea celulelor ciliate din urechea internă, tra­ta­men­tul SSNHL se concentrează pe această cauză, în timp ce te­ra­pia cu corticosteroizi reprezintă standardul de îngrijire pen­tru forma idiopatică. Prognosticul în SSNHL idiopatic depinde de severitatea hipoacuziei, de vârstă, prezenţa vertijului şi de va­lo­ri­le hormonilor tiroidieni.


Sudden sensorineural hearing loss (SSNHL) is usually defined as acute loss of more than 30 dB in three contiguous frequencies in less than 72 hours. This represents an infrequent condition affecting the inner ear, although, in recent times, the prevalence of SSNHL worldwide has been on a gradual rise due to evolving lifestyles and habits, with 5 to 20 cases per 100,000 persons per year in the United States of America(1-3). The incidence in Japan has increased from 3.9/100,000 to 27.5/100,000 in 1972. The incidence in China is also increasing yearly, but it lacks a large sample epidemiological investigation(4). The declared incidence rates in Taiwan were 7.79 and 8.85 per 100,000 women and men, respectively(5).

According to one study reported before in Brazil, the incidence of thyroid dysfunction in SSNHL was 21.6% during the year 2008, significantly higher than the incidence of abnormal thyroid function which was about 10% in the general population. An increasing trend of this association has been observed, with a prevalence of 24.41% in recent years(6).

The cause of SSNHL is still unknown, although its clinical course might result in hearing disability. The pathophysiological mechanism is not fully elucidated, so numerous factors may cause SSNHL. Currently, potential etiologies underlying the disease and its potential mechanisms encompass inner ear vasospasm, vascular dysfunction, vascular embolization or thrombosis, as well as membranous labyrinth and hair cell injury(7,8). Simultaneously, the incidence and result of SSNHL hearing were influenced differently by various systemic disorders such as iron deficiency anemia, chronic kidney disease, systemic lupus erythematosus, diabetes mellitus (DM), human immunodeficiency virus (HIV), psoriasis, osteoporosis, and chronic otitis media (COM)(9-15).

The most prevalent endocrine diseases globally are thyroid disorders, which can manifest with a range of symptoms. The thyroid gland plays a crucial role in the endocrine system, impacting various systems within the human body. Additionally, thyroid hormone is a critical factor in the development of fetal ear and auditory function(4). In this context, several studies have indicated that aberrant alterations in serum thyroid hormone levels, such as hyperthyroidism and hypothyroidism, are associated with the development of both sensorineural and conductive hearing impairments(16,17). Furthermore, a cross-sectional investigation found that thyroid disorders are more prevalent in SSNHL patients than in the general population. Still, the specific types of thyroid disorders are not well known(6). Relying on those research results, it seems acceptable to speculate that thyroid disorders and SSNHL may be associated.

Materials and method

This review was performed through an extensive examination of scientific literature pertinent to the topic, entailing a meticulous and comparative evaluation of these publications. We used the following strategy to search the U.S. National Library of Medicine’s PubMed database and Google Scholar for relevant articles published over the past 10 years, using the terms: “sudden sensorineural hearing loss”, “hearing loss” and “sudden deafness”, as well as keywords such as “etiology”, “hypothyroidism and SSNHL”, “risk factors”, “thyroid disease and SSNHL”, “management”, “therapy”, and “prognosis”.

We chose to review articles that had a rigorous picture of the incidence of thyroid disease in patients with SSNHL, epidemiology, suspected risk factors, particularly hypothyroidism, and also the involvement of thyroid hormones in prognosis after treatment. As exclusion elements of the studies, we chose not to include those that did not contain several suspected risk factors for SSNHL. The limitations of our work were that there was no distinction between types of thyroid disease when analyzing the associated risk of SSNHL and most of the previous studies were based on a small number of cases and focused on only one type of thyroid disease, such as Graves’ disease or Hashimoto’s thyroiditis.


SSNHL is defined as sensorineural hearing loss grea­ter than 30 dB over at least three contiguous pure‐tone frequencies occurring within three days(18). One of the prevalent conditions among ENT outpatients is SSNHL. Because of the accelerated social rhythm and increased life pressure, the incidence of SSNHL is increasing yearly and is trending toward younger age groups than in previous years. Even while SSNHL can affect persons of all ages, there are variations in the peak onset age of the illness across the study subjects and different groups.

Prevalence data

Based on international research findings, the onset of SSNHL typically reaches its highest occurrence between the ages of 50 and 60 years old. Tsai’s research further corroborates this, indicating that when grouped by age, the correlation between SSNHL and hypothyroidism was noteworthy solely among individuals aged 50 years and older, and this relationship was absent in those aged 50 years or younger(5). Supporting this idea, physicians should be aware that patients with thyroid dysfunction who have already been identified are at a higher risk of developing SSNHL, particularly women and patients who are older than 50.

An extensive study conducted by Kim et al. on a large, representative population cohort revealed that, among individuals with SSNHL, those with hypothyroidism were predominantly men under the age of 60 and women aged 60 or older(19). Furthermore, SSNHL patients were also more likely to have goiter in the subgroups of men above 60 years old and in women below 60 years old(1) in the final model.

Regarding gender distribution, in Tsai’s study, the subgroup analysis revealed a significantly increased odds ratio of SSNHL for female patients with hyperthyroidism, but no significant relationships between thyroid diseases and increased SSNHL risk among men(5). Because the study did not focus on distinguishing between types of thyroid diseases, in our review we cannot specifically discuss the gender distribution of patients with hypothyroidism presenting with SSNHL as a complication. However, in attempting to elucidate the high occurrence of SSNHL in females with thyroid disorders, it has been proposed that the gender disparities in this correlation could be partially attributed to the relatively low frequency of thyroid diseases observed in men in the current study. Thyroid conditions exhibit a higher prevalence among women, with the exact etiology remaining unclear. The presence of extrathyroidal iodine storage in breast and cervical tissues, coupled with the impact of estradiol on thyroid function are likely contributing factors.

The involvement of thyroid hormones in the mechanism of SSNHL development

Thyroid hormones are integral endocrine factors crucial for the intricate development and function of the auditory system. Their influence spans from the initial embryological stages, guiding the differentiation and maturation of auditory structures, to the ongoing maintenance of cellular processes essential for sound perception and processing(7,20). Research findings suggest that optimal levels of thyroid hormones are essential for the proper development of the auditory system in both humans and animals. Consequently, insufficient levels of thyroid hormones may lead to notable alterations within the middle and inner ear(20).

Various systemic consequences – such as vascular insufficiency, electrolyte imbalance, and autoimmune disease – are brought on by thyroid-related disorders and may be linked to SSNHL. Given that the production of the endocochlear potential via ion transport in the stria vascularis entails significant energy consumption, and considering the labyrinthine artery’s status as an end artery, it becomes particularly vulnerable to alterations in vascular functionality. As a result, any impairment in vascular function may lead to hearing loss(19,21).

It is widely acknowledged that thyroid hormone receptors are instrumental in regulating the functional development of the cochlea by modulating fast-acting potassium channels. Given the vital role of maintaining the electrolyte composition in the endolymph and perilymph for sound conduction within the inner ear, any imbalance in these electrolytes could result in inner ear dysfunction(19). Additionally, individuals with SSNHL may be more susceptible to electrolyte imbalances brought on by their thyroid conditions, which might exacerbate their hearing loss. While hyperthyroidism has been linked to electrolyte abnormalities such as hypokalemia, hyperkalemia and hypercalcemia, there is evidence suggesting that hypothyroidism can also contribute to disturbances in these electrolyte levels.

Thyroid hormone receptors control the myelination of the cochleovestibular nerve, in addition to inner or outer hair cells. Consequently, it has been documented that sensorineural hearing loss could occur from hypothyroidism during the stages of development(22). Additionally, in rat models, hypothyroidism was found to postpone the connection of efferent neurons to outer hair cells in the cochlea and hinder the elimination of both type I and type II spiral ganglion neurons. This was associated with reduced expression of fibroblast growth factor receptors and phosphorylated cofilin, leading to decreased microtubules in cochlear supporting pillar cells and to alterations in the morphology of outer hair cells. Thyroid dysfunction and SSNHL may be connected to abnormalities of these several signaling pathways between the thyroid hormones and the inner ear(19).

To get a more comprehensive picture of the pathophysiological mechanism that is responsible for the development of SSNHL as a complication of hypothyroidism, Cordas et al., using in situ hybridization, discovered that the mouse tympanic membrane, immature ossicles, and middle ear mesenchyme all contain the thyroid hormone receptors a1 and b, which are encoded by Thra and Thrb genes. These results also suggest that the middle and inner ear could be potential targets that are sensitive to fluctuations in thyroid hormone levels(23).

In addition to compromising the development of inner ear function, hypothyroidism may further increase blood pressure and peripheral vascular resistance, damage endothelial-dependent vasodilation, alter the smooth muscle structure of blood vessels, induce high coagulation status, damage fibrous protein decomposition, and alter platelet function and endothelial function. These hemodynamic and blood vessel alterations could subsequently lead to hearing loss(24).

Additionally, it is pertinent to acknowledge the absence of collateral circulation within the cochlea, where a singular labyrinthine artery serves as the sole blood supply to this intricate auditory structure. Patients with hypothyroidism could present hypercoagulability, which raises the risk of venous thrombosis thus causing SSNHL(7,25).

It can also be added that SSNHL is linked to deficiencies in antithrombin, elevated homocysteine and factor VIII, and cardiovascular risk factors (diabetes, hyperlipidemia, arterial hypertension, and smoking), hypothyroidism in particular being recognized as a potential etiological factor contributing to the pathogenesis of these cardiovascular conditions. Consequently, the presence of hypothyroidism may exert an influence on the development of these cardiovascular risk factors, thereby potentially impacting the occurrence of SSNHL(26).

Thyroid hormone levels as risk and prognostic factors for SSNHL

Several studies have further searched the risk factors associated with SSNHL. In case-control research including 109 patients, Nakashima et al. investigated the risk factors for SSNHL, and found that individuals with a history of thyroid disease had a greater odds ratio for SSNHL than those without such a history(5,27). Potential risk factors for the development of SSNHL included histories of goiter, hypothyroidism, thyroiditis, hyperthyroidism, and levothyroxine therapy. In the Korean National Health Insurance Service-Health Screening Cohort, SSNHL patients were more likely than controls to have a history of goiter or hypothyroidism, according to Kim et al.(19)

The onset time and hearing outcome of SSNHL were correlated with the T3 and FT3 item of thyroid dysfunction, as shown by the research conducted by Zhu et al., suggesting that T3 or FT3 indicator may be one of the variables responsible for the SSNHL. They also discovered that the low T3 group’s time duration following the onset of SSHL was significantly shorter compared with the T3 normal group and the high T3 group. Other significant information from this study is that patients in the low T3 group may have received therapy for a shorter period after their condition began, which suggests that the patient’s chances of not recovering from SSNHL remained reduced. This time, we may also take into consideration low T3 syndrome, which is a situation with reduced T3, normal TSH and T4, and the potential to have effects similar to hypothyroidism, including alterations to the auditory system(4).

Hence, it becomes apparent that any dysfunction or irregularity in thyroid function can potentially impact the development, prevalence and outcomes of treatments for hearing loss, whether through direct physiological pathways or indirect influences(28).

Focusing on risk factors over SSNHL, in the prospective study of Zheng et al., low FT3 and TSH levels were independent predictors of the occurrence of the early stages of moderately severe-to-profound SSNHL; conversely, a rise in TSH can function as an independent predictor of a favorable prognosis(29). Moreover, research has shown positive correlations regarding the elevation of TSH levels after treatment which predicted a favorable outcome of hearing recovery, this notion being substantiated by the findings presented in Narozny’s publication.

Is there a link between hypothyroidism and the prognosis of SSNHL after treatment?

As the exact etiology of sudden sensorineural hearing loss (SSNHL) remains elusive, there exists no definitive treatment protocol leading to complete cure. Consequently, numerous therapeutic modalities have been explored for this condition. These include the administration of glucocorticoids, vasodilators, vitamins, anticoagulants, and hyperbaric oxygen therapy, either individually or in combination. However, determining their therapeutic efficacy poses a challenge due to the complex nature of SSNHL and its multifactorial etiology.

In our review, we focus on the treatment of SSNHL with glucocorticoids and the influences of hypothyroidism upon it. The most recent classification of hearing loss by the World Health Organization (WHO) classifies those who have hearing loss of more than 50 dB in the moderate-to-severe deafness category, meaning they would have difficulties comprehending conversational speech. The exhaustive therapy included intravenous injections of prednisone (1 mg/kg/day) for 3-5 days, with subsequent adjustments to a lower dosage contingent upon improvements in hearing. Additionally, intravenous batroxobin was administered initially at a dose of 10 U, subsequently reduced to 5 U, given once every other day, with a total of 1-3 doses, depending on the individual’s fibrinogen levels(29).

Even with appropriate therapy, hearing loss with a frequency drop of more than 50-60 dB results in a recovery of no more than 20-30 dB, as stated by Enache et al.(30) Alternatively, Sheehy et al. found that primary hearing loss with a reduction in intensity of 45 dB or less displayed a favorable prognosis for recovery(31). A higher severity of hearing loss is often associated with a poorer prognosis. While steroid therapy proves efficacious in the majority of instances, its effectiveness in restoring hearing is observed to be limited in cases where the initial hearing loss exceeds 90 dB.

The association found between hypothyroidism and glucocorticoid treatment indicates that the majority of patients showed an increase in thyroid-related hormone levels following glucocorticoid therapy. This observation might elucidate the occurrence of thyroid hormone elevation following glucocorticoid therapy in certain patients, thereby correlating with an improved prognosis. It is noteworthy to highlight that the elevation of thyroid stimulating hormone (TSH) levels post-treatment has been consistently associated with a positive prediction of hearing recovery outcomes.

Globally, the incidence rate of SSNHL is progressively increasing. By 2050, the World Health Assembly predic­ted that over 2.5 billion individuals globally would suffer from hearing loss of various degrees(32). In this context, clinicians should be aware that hypothyroidism may be associated as a rare complication with SSNHL. Within Table 1, we have compiled a concise overview of the pertinent findings extracted from the studies encompassed within our review.

Table 1. The main findings of the studies examined in the review
Table 1. The main findings of the studies examined in the review

While a comprehensive meta-analysis examining the relationship between hypothyroidism and sudden sensorineural hearing loss remains to be undertaken, the primary focus of this review underscores the critical importance of evaluating the thyroid profile. This meticulous assessment serves as a cornerstone not only in the identification of potential causes of SSNHL, but also in the early detection and efficacious management of hearing impairment. The intricate interplay between thyroid dysfunction and SSNHL necessitates a thorough understanding of thyroid hormone levels in patients presenting with sudden hearing loss, thereby guiding clinicians toward appropriate diagnostic and therapeutic interventions tailored to individual cases(33,34). Consequently, integrating thyroid profile assessment into the diagnostic workup of SSNHL patients may offer valuable insights into the underlying pathophysiological mechanisms and optimize the prospects for successful treatment outcomes(35).


Hearing loss poses a significant impact on the overall well-being of individuals, leading to a marked reduction in the quality of life, diminished productivity, and heightened societal burden. Its effects extend beyond audiological impairments, often manifesting in a spectrum of neurological and psychological sequelae. As such, prompt and decisive actions by otologists are imperative in formulating comprehensive preventive and therapeutic interventions.

Moreover, a noteworthy association has been established between hypothyroidism and an increased susceptibility to sudden sensorineural hearing loss (SSNHL). In light of this, it is recommended that healthcare providers counsel patients with thyroid disorders to promptly seek medical evaluation upon onset of any auditory deficits. Such patients may be at heightened risk for the development of SSNHL, necessitating early intervention and management.

The systemic repercussions stemming from thyroid dysfunction, including autoimmune manifestations, vascular insufficiencies and electrolyte imbalances, are intricately linked with the pathogenesis of SSNHL. By elucidating the mechanistic relationship between thyroid function and SSNHL, clinicians can develop tailored strategies for prevention and treatment. This targeted approach holds promise in mitigating the incidence of SSNHL among individuals with hypothyroidism and other thyroid hormone dysregulations, thereby optimizing clinical outcomes and enhancing patient well-being.   n


Conflicts of interest and sources of funding. The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results. This research received no external funding.

Authors’ contribution. All authors have read and agreed to the published version of the manuscript.

Ethics approval and consent to participate. Not applicable.

Corresponding author: Dana-Mihaela Tilici, e-mail:


CONFLICT OF INTEREST: none declared.

FINANCIAL SUPPORT: none declared.

This work is permanently accessible online free of charge and published under the CC-BY.



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