Elevation of Serum Prestin in Patients With Tinnitus: Pathophysiological Implications and Biomarker Potential

Prestin enables outer hair cell (OHC) function in cochlear amplification and has been implicated in tinnitus. An experimental study of salicylate toxicity, known to cause tinnitus in humans, demonstrated increased expression of prestin. As prestin is quantifiable in the blood, we hypothesized that if prestin expression is increased in tinnitus patients, then serum prestin levels in those with tinnitus compared with those without tinnitus are elevated.

A prospective, case-control study.

Single-institution tertiary care center.

Patients with or without tinnitus.

Diagnostic.

Serum prestin was quantified through automated Western blot electropherograms. Key covariates, including age, hearing threshold, and daily noise exposure, were accounted for in multivariate analyses.

Eighty-nine participants (49 with chronic tinnitus and 40 controls) underwent audiometry, noise dosimetry, and blood sampling. The metrics of the 97 kDa prestin isoform were significantly increased in the tinnitus group, with differences in age, hearing thresholds, and daily noise exposure between the 2 groups accounted for in multivariate analyses. Correlations between prestin isoform expression and noise exposure seen in controls were disrupted in the tinnitus group, shifting from the 97 kDa isoform to the 140 kDa isoform.

These findings suggest OHC dysfunction involving prestin in those with tinnitus. Furthermore, the 97 kDa isoform of serum prestin represents a promising candidate biomarker in those with tinnitus. Prestin as a biomarker may serve to stratify tinnitus patients according to origin (eg, cochlear vs. central), inform further investigations of the pathophysiology of tinnitus, and potentially develop targeted treatments.