Evaluation of autoimmune and inflammatory markers in bilateral sudden hearing loss.

Abstract

Background: Bilateral sudden hearing loss (BSHL) is a rare otologic emergency, representing 1-2% of all sudden hearing loss cases. Autoimmune processes are considered one of the key contributors to BSHL, with immune responses targeting inner ear structures. The aim of our study is to identify the role of autoimmune and inflammatory markers in patients with BSHL and assess their prognostic significance.

Materials and methods: This retrospective study reviewed 30 BSHL patients out of 420 sudden hearing loss cases. Data including audiometric results, medical histories, autoimmune and inflammatory markers (ANA, RF, ESR, CRP, ACA, ANCA), and autoimmune diseases such as Ankylosing Spondylitis (AS), Hypothyroidism (HT), Rheumatoid Arthritis (RA), and Systemic Lupus Erythematosus (SLE) were analyzed. Audiometric recovery was assessed using Siegel's criteria, and the presence of autoimmune markers was evaluated for their impact on clinical outcomes and recovery.

Results: Autoimmune markers were detected in 60% of the patients with BSHL, with elevated levels of ANA, RF, ESR, and CRP observed most frequently. Patients who tested positive for autoimmune markers demonstrated significantly lower recovery rates compared to those without marker positivity. Specifically, 13% of patients with positive markers showed partial hearing recovery, while 100% of patients without markers exhibited partial recovery. The average hearing improvement across all frequencies was around 21.5 dB. These results suggest that autoimmune marker positivity is associated with poorer clinical outcomes and lower recovery rates following standard corticosteroid treatment.

Conclusion: Our study demonstrates that autoimmune and inflammatory markers play a significant role in the prognosis of BSHL. Patients with positive autoimmune markers exhibit poorer recovery rates, indicating the potential importance of these markers in predicting treatment outcomes for BSHL.