Abstract
Problem
Although sudden hearing loss (SHL) remains to be a frequent indication for emergency treatment in ENT departments, the pathogenesis leading to this disease is yet unknown. There is increasing evidence that vascular risk factors like hypercholesterolemia and chronic inflammation contribute to a disease-provoking environment and, thus, enhance the risk for sudden hearing loss. We have shown in the past that patients with acute ischemic stroke display signifantly elevated plasma levels of oxLDL as well as significantly elevated gene expression of proinflammatory (CD40, TNF-alpha and COX-2), proapoptotic (Caspase-3 and PARP) and proadhesive (CD38) genes. The aim of our study was to elucidate the possible role of hypercholesterolemia, inflammation and oxidative stress in sudden hearing loss and to show possible parallels with ischemic events like stroke.
Methods
Mononuclear cells from patients with SHL and healthy controls were isolated from blood and plasma. Analysis was performed using ELISA and FACS-analysis.
Results
We measured the levels of blood lipids, oxLDL, TNF-alpha and CD40L in the plasma of patients with sudden hearing loss in comparison to healthy controls using ELISAs. Furthermore, we isolated mononuclear cells from the blood of patients and controls and measured the protein expression of proinflammatory (CD40, TNF-alpha and COX-2), proapoptotic (Caspase-3 and PARP), oxidative stress associated (Mn-SOD) and adhesion relevant (CD38) proteins by FACS-analysis and ELISA.
Conclusion
We found that both plasma levels of the above mentioned markers and protein expression in mononuclear cells showed distinct changes compared to healthy controls.
Significance
We therefore postulate that a proinflammatory environment and oxidative stress might trigger the onset of sudden hearing loss and influence the clinical outcome.
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