Objective To investigate whether serum thyroid-stimulating hormone (TSH) levels are associated with primary subjective tinnitus and whether TSH provides clinically relevant information for the assessment of tinnitus. Materials and methods This case–control study included 557 patients with primary subjective tinnitus and 431 tinnitus-free controls without known thyroid disorders. All participants underwent otorhinolaryngological examination and serum TSH measurement. Patients with tinnitus additionally underwent comprehensive audiological assessment, including pure-tone audiometry, psychoacoustic tinnitus matching, and assessment of tinnitus-related handicap using the Tinnitus Handicap Inventory (THI). Differences in TSH levels between the groups were analysed using the Mann–Whitney U test. Linear regression and Bayesian analyses were performed to evaluate associations between TSH and tinnitus-related parameters. Receiver operating characteristic (ROC) curve analysis was used to assess the ability of TSH to discriminate between participants with and without tinnitus. Results Median TSH levels were 1.80 mIU/l (IQR 1.23–2.56) in the tinnitus group and 1.73 mIU/l (IQR 1.21–2.50) in the control group, with no significant difference between the groups ( p = 0.63). Bayesian analysis provided moderate evidence in favour of the null hypothesis regarding the difference in TSH levels between the two groups (BF₀₁ = 4.459). TSH was not significantly associated with total THI score, hearing level, tinnitus intensity, age, or symptom onset in linear regression analyses. Bayesian regression analyses likewise provided evidence against a meaningful contribution of TSH to tinnitus-related parameters. ROC analysis demonstrated no clinically useful ability of TSH to discriminate between participants with and without tinnitus (AUC = 0.509, 95% CI 0.471–0.547, p = 0.640). Conclusion These findings suggest that routine TSH measurement alone is unlikely to provide clinically relevant information for the assessment or management of primary subjective tinnitus in patients without known thyroid disease. However, these findings should not be extrapolated to patients with confirmed thyroid dysfunction or interpreted as a recommendation against thyroid function testing when clinical signs, symptoms, or other findings suggest underlying thyroid disease. Further studies incorporating comprehensive thyroid function assessment, including FT4, FT3, and thyroid autoantibodies, are warranted to clarify whether specific aspects of thyroid dysfunction may be relevant to selected tinnitus populations.
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Mavrogenis et al. (2026) studied this question.
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