Evaluation of angiotensin converting enzyme insertion/deletion, alpha adducin (ADD1) G460W, and IL-10 gene polymorphisms, and determination of prognostic effects in idiopathic sudden sensorineural hearing loss

The aim of this study was to examine angiotensin converting enzyme (ACE) insertion/deletion, alpha adducin, and interleukin-10 (IL-10) gene polymorphisms (GPs) in terms of both idiopathic sudden sensorineural hearing loss (ISSNHL) risk and their potential prognostic effects. The study group consisted of 70 patients and the control group consisted of 50 patients. Venous blood samples were analyzed for relevant GPs via kompetitive allele-specific polymerase chain reaction. Age, sex, affected side, tinnitus, and vertiginous symptom status, number of days between symptom onset and hospital admission, pure tone audiometry results at admission and after treatment were included in the study. Data were compared statistically. The D allele of ACE insertion/deletion GP was significantly more frequent in patients with ISSNHL than in the control group (p = 0.032). II genotype was associated with a reduced risk of ISSNHL (p = 0.036). The amount of hearing loss was significantly higher in patients with the TT genotype (p = 0.027) and T allele of the IL-10 GP (p = 0.035) than in the patients without this allele. Severe hearing loss was a poor prognostic factor (p = 0.008). The D allele of ACE insertion/deletion GP may be involved in the ISSNHL etiology. Due to the association of this allele with occlusive vascular pathologies, ischemia is believed to be a common pathway in the etiopathogenesis of ISSNHL. •The etiopathogenesis, treatment strategies, and prognosis of ISSNHL remain controversial.•In recent years, gene polymorphism studies in ISSNHL patients have progressively garnered attention.•GPs also help to determine individualized treatment strategies and predict treatment response.•The D allele of ACE I/D GP may be involved in the ISSNHL etiology.•Ischemia is believed to be a common pathway in the etiopathogenesis of ISSNHL.