AI Insight
This prospective study of 40 patients with sudden sensorineural hearing loss (SSNHL) and 40 healthy controls found that baseline homocysteine levels were significantly elevated in SSNHL patients and independently associated with the condition. However, homocysteine levels did not decrease after treatment despite hearing improvement, and were not associated with hearing recovery outcomes. The findings suggest homocysteine may function as a predisposing vascular risk factor for SSNHL rather than a prognostic marker.
Why it matters
This research identifies elevated homocysteine as a potential risk marker for sudden hearing loss, which could help identify at-risk individuals. However, since homocysteine levels were not linked to recovery, the current findings do not support homocysteine-lowering treatments as a therapeutic strategy, though larger studies are needed to confirm this.
Understand the Science
by Murat Akın, Orhan Kemal Kahveci
Objective
To compare baseline and post-treatment homocysteine levels in patients with sudden sensorineural hearing loss (SSNHL) and to evaluate the potential role of homocysteine in the pathogenesis of the disease as well as its association with hearing recovery.
Methods
A total of 40 patients diagnosed with SSNHL and 40 age- and sex-matched healthy controls were included in this prospective observational study. Serum homocysteine levels were measured at baseline and at the 4–6-week follow-up visit after treatment in the SSNHL group, and once at enrollment in the control group. Hearing thresholds were assessed using pure tone audiometry. Treatment response was classified according to Siegel criteria. Statistical analyses included group comparisons, correlation analyses, and multivariate logistic regression.
Results
Baseline homocysteine levels were significantly higher in the SSNHL group compared with controls. No significant change in homocysteine levels was observed after treatment, although hearing thresholds improved significantly. Homocysteine levels were not significantly associated with hearing recovery. In multivariate logistic regression analysis, baseline homocysteine was independently associated with SSNHL (OR = 1.742, 95% CI: 1.351–2.245, p < 0.001). ROC curve analysis demonstrated good discriminative ability for baseline homocysteine in distinguishing SSNHL patients from controls (AUC = 0.809, 95% CI: 0.712–0.905, p < 0.001).
Conclusion
Homocysteine may play a role in the pathophysiology of SSNHL as a potential vascular risk marker. However, the lack of significant post-treatment reduction and its absence of association with hearing recovery suggest that it may function more as a predisposing factor rather than a prognostic biomarker. Further large-scale prospective studies are needed to evaluate the potential therapeutic implications of homocysteine-lowering strategies in SSNHL.