Table of Contents
Journal of Allergy
Volume 2012, Article ID 789232, 18 pages
Review Article

Pathogenic Mechanisms and In Vitro Diagnosis of AERD

1Allergie- und Intoleranzlabor, Medizinisch Klinik III, Friedrich-Alexander-Universität Erlangen-Nürnberg, Glückstraße 4a, 91054 Erlangen, Germany
2Klinik für HNO-Heilkunde, Kopf- und Halschirurgie, Krankenhaus Holweide, Neufelder Straße 32, 51067 Köln, Germany

Received 13 January 2012; Accepted 27 February 2012

Academic Editor: A. P. Sampson

Copyright © 2012 Dirk Schäfer and Steffen Maune. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Aspirin-exacerbated respiratory disease (AERD) refers to chronic rhinosinusitis, nasal polyposis, bronchoconstriction, and/or eosinophilic inflammation in asthmatics following the exposure to nonsteroidal anti-inflammatory drugs (NSAIDs). A key pathogenic mechanism associated with AERD is the imbalance of eicosanoid metabolism focusing on prostanoid and leukotriene pathways in airway mucosa as well as blood cells. Genetic and functional metabolic studies on vital and non-vital cells pointed to the variability and the crucial role of lipid mediators in disease susceptibility and their response to medication. Eicosanoids, exemplified by prostaglandin E2 (PGE2) and peptidoleukotrienes (pLT), are potential metabolic biomarkers contributing to the AERD phenotype. Also other mediators are implicated in the progress of AERD. Considering the various pathogenic mechanisms of AERD, a multitude of metabolic and genetic markers is suggested to be implicated and were introduced as potential biomarkers for in vitro diagnosis during the past decades. Deduced from an eicosanoid-related pathogenic mechanism, functional tests balancing PGE2 and pLT as well as other eicosanoids from preferentially vital leukocytes demonstrated their applicability for in vitro diagnosis of AERD.