SERUM 25-HYDROXYVITAMIN D LEVELS IN PATIENTS WITH PROGRESSIVE SENSORINEURAL HEARING LOSS
DOI:
https://doi.org/10.37219/03hwed87Keywords:
sensorineural hearing loss, progressive course, 25-hydroxyvitamin D, deficiency, inner ear, electrochemiluminescence immunoassayAbstract
Abstract
Background. Sensorineural hearing loss (SNHL) is a common auditory pathology with a polyetiological nature. Vitamin D deficiency is considered one of the potential modifiable factors in its development and progression due to its crucial role in maintaining ion homeostasis of the inner ear cells and providing neuroprotection.
Objective: to evaluate serum 25-hydroxyvitamin D [25(OH)D] levels in patients with progressive sensorineural hearing loss.
Materials and Methods. A total of 62 patients with SNHL were examined and divided into two groups: the primary group (n = 35) with a progressive course of the disease and the comparison group (n = 27) with a stable course. The control group consisted of 15 practically healthy individuals with normal hearing. The severity of hearing impairment was assessed using pure-tone threshold and speech audiometry. Serum 25(OH)D levels were determined by electrochemiluminescence immunoassay (ECLIA) on a Cobas e 411 automated analyzer (Roche Diagnostics, Germany). Statistical analysis was performed using the StatSoft Statistica 9.1 software package with Student's t-test and the Shapiro–Wilk test.
Results. Decreased vitamin D status (< 30.0 ng/mL), encompassing both deficiency and insufficiency, was recorded in 91.4% (32 out of 35) of patients in the primary group, significantly exceeding the rates in the comparison group — 77.8% (21 out of 27) and the control group — 53.3% (8 out of 15). The most severe vitamin D deficiency (< 20.0 ng/mL) was detected in the primary group of patients with progressive SNHL, reaching 68.6% (24 patients), whereas it was 40.7% (11 patients) in the comparison group, and only 20.0% (3 individuals) in the control group. A sufficient level of 25(OH)D was observed in only 5.7% of patients with a progressive course of SNHL.
Conclusions. A clear clinical and laboratory parallelism was identified between the severity of vitamin D deficiency and the nature of the hearing loss course, suggesting a pathogenic link between impaired cholecalciferol metabolism and the progression of cochlear degeneration. The population-wide hypovitaminosis in the control group (53.3%) reflects the modern stress factors of martial law in Ukraine; however, the critically higher frequency of deficiency in progressive SNHL confirms its nosological specificity. The findings substantiate the appropriateness of including 25(OH)D screening in the examination protocol for SNHL patients to timely identify high-risk groups and incorporate therapeutic doses of vitamin D into treatment regimens.
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