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Aspirin Exacerbated Respiratory Disease

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Aspirin Exacerbated Respiratory Disease Journal of Allergy Aspirin Exacerbated Respiratory Disease Guest Editors: Luis M. Teran, Stephen T. Holgate, Hae-Sim Park, and Anthony P. Sampson Aspirin Exacerbated Respiratory Disease Journal of Allergy Aspirin Exacerbated Respiratory Disease Guest Editors: Luis M. Teran, Stephen T. Holgate, Hae-Sim Park, and Anthony P. Sampson Copyright © 2012 Hindawi Publishing Corporation. All rights reserved. This is a special issue published in “Journal of Allergy.” All articles are open access articles distributed under the Creative Commons At- tribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Editorial Board William E. Berger, USA Marek L. Kowalski, Poland H. Renz, Germany K. Blaser, Switzerland Ting Fan Leung, Hong Kong Nima Rezaei, Iran Eugene R. Bleecker, USA Clare M. Lloyd, UK Robert P. Schleimer, USA J. de Monchy, The Netherlands Redwan Moqbel, Canada Massimo Triggiani, Italy F. Hoebers, The Netherlands Desiderio Passali, Italy Hugo Van Bever, Singapore Stephen T. Holgate, UK Stephen P. Peters, USA A. van Oosterhout, The Netherlands S. L. Johnston, UK David G. Proud, Canada Garry M. Walsh, UK Young J. Juhn, USA F. Rance,´ France Alan P. Knutsen, USA Anuradha Ray, USA Contents Aspirin Exacerbated Respiratory Disease,LuisM.Teran,StephenT.Holgate,Hae-SimPark, and Anthony P. Sampson Volume 2012, Article ID 817910, 2 pages Aspirin Sensitivity and Chronic Rhinosinusitis with Polyps: A Fatal Combination, Hendrik Graefe, Christina Roebke, Dirk Schafer,¨ and Jens Eduard Meyer Volume 2012, Article ID 817910, 10 pages Rhinosinusitis and Aspirin-Exacerbated Respiratory Disease, Maria L. Garcia Cruz, M. Alejandro Jimenez-Chobillon, and Luis M. Teran Volume 2012, Article ID 273752, 8 pages Pathogenic Mechanisms and In Vitro Diagnosis of AERD,DirkSchafer¨ and Steffen Maune Volume 2012, Article ID 789232, 18 pages Exhaled Eicosanoids following Bronchial Aspirin Challenge in Asthma Patients with and without Aspirin Hypersensitivity: The Pilot Study, L. Mastalerz, M. Sanak, J. Kumik, A. Gawlewicz-Mroczka, N. Celejewska-Wojcik,´ A. Cmiel,´ and A. Szczeklik Volume 2012, Article ID 696792, 11 pages Interleukin-4 in the Generation of the AERD Phenotype: Implications for Molecular Mechanisms Driving Therapeutic Benefit of Aspirin Desensitization, John W. Steinke, Spencer C. Payne, and Larry Borish Volume 2012, Article ID 182090, 9 pages Comparison of CD63 Upregulation Induced by NSAIDs on Basophils and Monocytes in Patients with NSAID Hypersensitivity, N. Abuaf, H. Rostane, J. Barbara, C. Toly-Ndour, H. Gaouar, P. Mathelier-Fusade, F. Leynadier, C. Frances,` and R. Girot Volume 2012, Article ID 580873, 9 pages The IL1B-511 Polymorphism (rs16944 AA Genotype) Is Increased in Aspirin-Exacerbated Respiratory Disease in Mexican Population,Ramces´ Falfan-Valencia,´ Gandhi F. Pavon-Romero,´ Angel Camarena, Mar´ıa de la Luz Garc´ıa, Gustavo Galicia-Negrete, Mar´ıa Cristina Negrete-Garc´ıa, and Luis Manuel Teran Volume 2012, Article ID 741313, 5 pages Interleukin-13, but Not Indomethacin, Increases Cysteinyl-Leukotriene Synthesis in Human Lung Macrophages, Sarah E. Jackson, John W. Holloway, Jane A. Warner, and Anthony P. Sampson Volume 2012, Article ID 348741, 6 pages Genetic Mechanisms in Aspirin-Exacerbated Respiratory Disease, Nami Shrestha Palikhe, Seung-Hyun Kim, Hyun Jung Jin, Eui-Kyung Hwang, Young Hee Nam, and Hae-Sim Park Volume 2012, Article ID 794890, 6 pages Hindawi Publishing Corporation Journal of Allergy Volume 2012, Article ID 473863, 2 pages doi:10.1155/2012/473863 Editorial Aspirin Exacerbated Respiratory Disease Luis M. Teran,1 Stephen T. Holgate,2 Hae-Sim Park,3 and Anthony P. Sampson2 1 Department of Immunogenetics and Allergy, Instituto Nacional de Enfermedades Respiratorias, Mexico City, Mexico 2 Clinical & Experimental Sciences, University of Southampton Faculty of Medicine, Southampton, UK 3 Department of Allergy and Clinical Immunology, Ajou University School of Medicine, San-5, Woncheondong, Youngtonggu, Suwon 442-721, Republic of Korea Correspondence should be addressed to Luis M. Teran, [email protected] Received 14 June 2012; Accepted 14 June 2012 Copyright © 2012 Luis M. Teran et al. 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. As guest editors of this special issue of the Journal of Allergy, of the 5-lipoxygenase (5-LO) pathway that generates the we are pleased to be able to present a range of articles, both cysteinyl-leukotriene family of mediators. The most persis- reviews and original research papers, on the important topic tent anomaly described in AERD is that even in the absence of aspirin-exacerbated respiratory disease (AERD). AERD is of NSAID ingestion, the levels of cysteinyl-leukotrienes a synonym for the “aspirin triad” of asthma, nasal polyposis are constitutively elevated in the bronchoalveolar lavage and sensitivity to aspirin originally described by Widal fluid, sputum, exhaled breath condensate, nasal secretions, ninety years ago. AERD patients typically experience severe saliva, blood and urine of AERD patients compared to bronchoconstriction and/or rhinoconjunctival reactions to aspirin-tolerant individuals [4]. That the further triggering aspirin, and also to other non-steroidal anti-inflammatory of cysteinyl-leukotriene synthesis is important in acute drugs (NSAID), even those which they have not encountered AERD was established by studies with leukotriene synthesis previously [1]. The reactions reflect non-allergic hypersensi- inhibitors and leukotriene receptor antagonists [5]. The tivity as many AERD patients are not atopic and the reactions central mystery in AERD remains why only these patients, to NSAIDs are not usually IgE-mediated. While the aspirin and not others with comparably severe asthma, show acute triad has been described as emerging typically in early middle adverse responses to NSAIDs. This special issue of J. Allergy age, aspirin-intolerance, as determined in bronchoprovoca- includes papers from many of the leading laboratories and tion studies, may be apparent in 21% of adult asthmatics opinion leaders working on this question around the world. and 5% of asthmatic children, suggesting that it is under- In the review article by Dr Maria Garcia-Cruz and her recognised as a factor in asthma episodes [2]. Even in the colleagues in Mexico, AERD and the cyclooxygenase theory absence of NSAID ingestion, AERD patients have relatively are discussed with special emphasis on rhinosinusitis, its severe chronic asthma with a high proportion requiring diagnosis and its treatment. Pathophysiological mechanisms long-term oral corticosteroid therapy, representing an unmet are reviewed including recent studies of cytokine and chemo- need of poorly-controlled asthma [1]. Nasal polyposis in kine anomalies in AERD, particularly in relation to Staphylo- AERD can be severe and require recurrent surgery. coccus aureus enterotoxins which may drive abnormal allergic Many of the papers in this special issue hinge upon the responses. The theme of rhinosinusitis is extended by the key insight in the field of AERD made by the late Professor wide-ranging review paper from the group of Prof. Meyer in Andrzej Szczeklik of Krakow. His “cyclooxygenase theory” Hamburg, writing with Dr Schafer¨ from Erlangen, who stress recognised that the ability of NSAIDs to trigger adverse the life-threatening nature of AERD and survey its molecular reactions in AERD patients correlates with their potency mechanisms, treatment and future directions for research. as cyclooxygenase inhibitors [3]. He extended the theory Genetic studies into AERD, including candidate gene with the realisation that arachidonic acid, the substrate of approaches and genome-wide association studies, may throw the cyclooxygenase (COX) pathway, is also the substrate light on the underlying pathological mechanisms or provide 2 Journal of Allergy genetic biomarkers for improved diagnosis and treatment. Andrzej Szczeklik was born in 1938 and graduated with a The area is expertly reviewed by Dr Palikhe and colleagues Diploma in Medicine from Krakow in 1961. His postgrad- based in Korea, while its importance is underlined by the uate training included work in Sweden at the Karolinska original research presented by Dr Falfan-Valencia and colle- Institute and at Uppsala University, and in the USA at the agues in Mexico, describing a novel association between University of North Carolina, Chapel Hill. After several years AERD and a polymorphism in the gene encoding the inflam- in Wroclaw, Poland, he returned to Krakow in 1972 and rose matory cytokine interleukin-1β. to become the Chairman of the Department of Medicine at Over-production of cysteinyl-leukotrienes by LTC4 syn- the Jagiellonian University in 1989. From 1990 to 1993, he thase and over-expression of the cysteinyl-leukotriene was president of the Copernican Academy and in 1993–1996 CysLT1 receptor have been postulated as central components the Vice-Rector of Jagiellonian University Medical College. of AERD pathology in the upper and lower airways [5]. The Szczeklik was well known by his scientific reputation to paper by Dr Steinke and his colleagues in Virginia, USA, pro- all the contributors to this special issue for his lifelong vides a powerful argument that the Th2 cytokine interleukin- research into aspirin-intolerance. He led the international
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