Obstructive sleep apnea, characterised by intermittent hypoxia and sleep fragmentation, may influence thyroid hormone regulation. However, evidence regarding thyroid function in obstructive sleep apnea remains inconsistent, particularly for free triiodothyronine. We conducted a cross-sectional study including 168 adults with polysomnography-confirmed obstructive sleep apnea, rigorously selected to exclude overt thyroid disease, thyroid autoimmunity, and the use of thyroid-active medications. Demographic characteristics, body mass index, polysomnographic indices, and serum levels of free triiodothyronine, free thyroxine, and thyroid-stimulating hormone were collected. Disease severity was assessed using the apnea-hypopnea index, oxygen desaturation index, mean nocturnal oxygen saturation, and the percentage of sleep time spent with oxygen saturation below 90%, and patients were stratified according to median values. Individuals with apnea-hypopnea index values above the cohort median exhibited significantly higher free triiodothyronine concentrations (p = 0.014), whereas no differences were observed for free thyroxine or thyroid-stimulating hormone. In multivariable linear regression analyses, free triiodothyronine independently predicted both the apnea-hypopnea index (p = 0.004) and the oxygen desaturation index (p = 0.001), alongside age, sex, and body mass index. No significant associations were observed between free triiodothyronine levels and mean nocturnal oxygen saturation or the percentage of sleep time spent with oxygen saturation below 90%. No independent associations with any respiratory index were identified for free thyroxine or thyroid-stimulating hormone. These findings indicate that higher free triiodothyronine concentrations reflect respiratory event burden rather than hypoxemia severity, supporting its role as a sensitive marker of the response to intermittent hypoxia in obstructive sleep apnea.
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