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81st Annual Meeting of the German Society of Oto-Rhino-Laryngology, Head and Neck Surgery

German Society of Oto-Rhino-Laryngology, Head and Neck Surgery

12.05. - 16.05.2010, Wiesbaden

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The role of Cyclooxygensases, Vascular Endothelial Growth Factor and Survivin in the pathogenesis of chronic rhinosinusitis and analgetics intolerance

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  • corresponding author presenting/speaker Kai Fruth - HNO Universitätsmedizin Mainz, Germany
  • Chengjing Zhu - HNO Universitätsmedizin Mainz, Germany
  • Eduard Schramek - HNO Universitätsmedizin Mainz, Germany
  • Juergen Brieger - HNO Universitätsmedizin Mainz, Germany
  • Wolf Juergen Mann - HNO Universitätsmedizin Mainz, Germany

German Society of Oto-Rhino-Laryngology, Head and Neck Surgery. 81st Annual Meeting of the German Society of Oto-Rhino-Laryngology, Head and Neck Surgery. Wiesbaden, 12.-16.05.2010. Düsseldorf: German Medical Science GMS Publishing House; 2010. Doc10hno093

doi: 10.3205/10hno093, urn:nbn:de:0183-10hno0935

Published: July 6, 2010

© 2010 Fruth et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

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Background: The Cyclooxygenases (Cox) play a key role in arachidonic acid metabolism. An imbalance of leucotriens and prostaglandins is considered to be a major component in the pathogenesis of nasal polyps occurring in combination with analgetics intolerance. Recent findings suggest the involvement of Vascular Endothelial Growth Factor (VEGF) and Survivin in nasal polyp formation. However, the relevance of a dysregulated expression of the Cyclooxygenases, VEGF and Survivin in patients with aspirin intolerance is largely unknown.

Methods: 87 tissue specimens were stained by immunohistochemistry for Cox-1, Cox-2, VEGF and Survivin. These specimens were taken from patients with nasal obstruction without inflammatory disease during turbinate surgery and from patients suffering from chronic rhinosinusitis with polyposis. Staining intensities were semiquantitatively evaluated and statistically analyzed in terms of aspirin intolerance.

Results: In nasal polyps the expression of Cox-1 was significantly higher than in specimens without inflammatory disease. An upregulated expression of Survivin and VEGF was observed in nasal polyps, furthermore VEGF and Survivin expression was strongly upregulated in nasal polyps from patients with aspirin intolerance.

Conclusion: These data support the concept of an imbalanced Cyclooxygenases-, VEGF- and Survivin-expression as part of the pathogenesis of nasal polyp formation and is assumed to be an attribute in patients with aspirin intolerance.