The role of soluble adhesion molecules and cytokines in sudden sensorineural hearing loss.

Abstract

The underlying pathology of sudden sensorineural hearing loss (SSNHL) is still not completely understood. Inflammatory and vascular factors are part of the present discussion. The aim of this study was to learn more about the possible role of adhesion molecules and cytokines in patients with SSNHL. These molecules are thought to contribute to endothelial dysfunction. Case-control study with planned data collection. Tertiary referral center. Blood samples of 35 patients presenting with SSNHL of more than 30 dB in at least 3 contiguous frequencies were compared to a gender- and age-matched control group of normal-hearing subjects. Levels of the soluble adhesion molecules intercellular adhesion molecule (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), endothelial selectin (E-selectin), and concentration of interleukin 6 (IL-6), interleukin 8 (IL-8), and monocyte chemoattractant protein 1 (MCP-1) were measured using established enzyme-linked immunosorbent assays. These parameters as well as fibrinogen and lipid values were statistically analyzed. Levels of soluble ICAM-1, VCAM-1, E-selectin, IL-6, IL-8, and MCP-1 were not significantly elevated in patients with SSNHL. The clinical chemistry and hematologic determinations showed no significant differences between patients and control subjects. This study revealed no association concerning SSNHL and typical vascular risk factors such as lipids and fibrinogen. Soluble adhesion molecules were not elevated in the SSNHL group. The role of endothelial dysfunction represented by increased levels of soluble adhesion molecules in the pathogenesis of SSNHL remains unclear. Further studies are necessary to elucidate the vascular etiology of SSNHL.