Iván Arias-de la Rosa, María Lourdes Ladehesa Pineda, Jesus Castellano-Curado, Leonardo Rodríguez-Pérez, Carlos M Collantes-Sánchez, Carlos Pérez-Sánchez, Miriam Ruiz-Ponce, Antonio Manuel Barranco, Jesús Eduardo Martín-Salazar, Pedro Ortiz-Buitrago, María Del Carmen Ábalos-Aguilera, Desiree Ruiz-Vilchez, María Ángeles Puche-Larrubia, Chary Lopez-Pedrera, Alejandro Escudero-Contreras, Eduardo Collantes-Estévez, Nuria Barbarroja, Clementina López-Medina
Hearing impairment is highly prevalent in axSpA and is associated with cumulative inflammation, structural damage, and an exploratory circulating neurobiological protein profile that requires validation in larger longitudinal studies.
OBJECTIVE: To characterize hearing impairment in patients with axial spondyloarthritis (axSpA) and identify associated clinical and molecular factors.
METHODS: A cross-sectional study was conducted including 53 patients with axSpA from the REGISPON-3 registry and 17 age- and sex-matched healthy controls (HCs). All participants underwent pure-tone audiometry. Clinical variables included disease duration, structural damage assessed by modified Stoke Ankylosing Spondylitis Spinal Score (mSASSS), inflammatory markers, and persistent inflammation status based on serial C-reactive protein (CRP) measurements during the previous 5 years. Serum proteomic profiling focused on neurobiological pathways was performed. Multivariable regression analyses were adjusted for potential confounding factors.
RESULTS: Hearing loss was significantly more frequent in patients with axSpA compared with HCs (86.8%), predominantly bilateral sensorineural hearing loss. Patients with axSpA showed higher hearing thresholds across multiple frequencies, particularly at high frequencies. Axial SpA patients with hearing impairment were older, had longer disease duration, worse ASAS-HI scores, higher structural damage, and greater persistent inflammatory burden in comparison with those without hearing impairment. Mean CRP levels during the previous 5 years were significantly higher in patients with hearing impairment, and the prevalence of hearing loss progressively increased across inflammation persistence groups. Multivariable analyses identified higher circulating levels of HAGH, GDF8, and SPOCK1 as independently associated with hearing impairment after adjustment for structural damage, inflammation, age, sex, disease duration, and NSAID use.
CONCLUSIONS: Hearing impairment is highly prevalent in axSpA and is associated with cumulative inflammation, structural damage, and an exploratory circulating neurobiological protein profile that requires validation in larger longitudinal studies.