{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,24]],"date-time":"2025-10-24T20:51:26Z","timestamp":1761339086605},"reference-count":31,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2009,10,7]],"date-time":"2009-10-07T00:00:00Z","timestamp":1254873600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Experimental Allergy"],"published-print":{"date-parts":[[2010,3]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p><jats:bold>Background\n\t\t\t\t\t<\/jats:bold> Hypersensitivity reactions towards non\u2010steroidal anti\u2010inflammatory drugs (NSAID) are common, although true allergies are detectable only in a subgroup of patients. The current study was prompted by a case observation, where a patient experienced generalized urticaria following his second course of diclofenac and proton pump inhibitor medication, and was found to have diclofenac\u2010specific IgE. During recent years, our group has been investigating the importance of gastric digestion in the development of food allergies, demonstrating anti\u2010acid medication as a risk factor for sensitization against food proteins.<\/jats:p><jats:p><jats:bold>Objective\n\t\t\t\t\t<\/jats:bold> Here, we aimed to investigate whether the mechanism of food allergy induction described can also be causative in NSAID allergy, using diclofenac as a paradigm.<\/jats:p><jats:p><jats:bold>Methods\n\t\t\t\t\t<\/jats:bold> We subjected BALB\/c mice to several oral immunization regimens modelled after the patient's medication intake. Diclofenac was applied with or without gastric acid suppression, in various doses, alone or covalently coupled to albumin, a protein abundant in gastric juices. Immune responses were assessed on the antibody level, and functionally examined by <jats:italic>in vitro<\/jats:italic> and <jats:italic>in vivo<\/jats:italic> crosslinking assays.<\/jats:p><jats:p><jats:bold>Results\n\t\t\t\t\t<\/jats:bold> Only mice receiving albumin\u2010coupled diclofenac under gastric acid suppression developed anti\u2010diclofenac IgG1 and IgE, whereas no immune responses were induced by the drug alone or without gastric acid suppression. Antibody induction was dose dependent with the group receiving the higher dose of the drug showing sustained anti\u2010diclofenac titres. The antibodies induced triggered basophil degranulation <jats:italic>in vitro<\/jats:italic> and positive skin tests <jats:italic>in vivo<\/jats:italic>.<\/jats:p><jats:p><jats:bold>Conclusion\n\t\t\t\t\t<\/jats:bold> Gastric acid suppression was found to be a causative mechanism in the induction of IgE\u2010mediated diclofenac allergy.<\/jats:p><jats:p> <jats:italic>Cite this as<\/jats:italic>: A. B. Riemer, S. Gruber, I. Pali\u2010Sch\u00f6ll, T. Kinaciyan, E. Untersmayr and E. Jensen\u2010Jarolim, <jats:italic>Clinical &amp; Experimental Allergy<\/jats:italic>, 2010 (40) 486\u2013493.<\/jats:p>","DOI":"10.1111\/j.1365-2222.2009.03363.x","type":"journal-article","created":{"date-parts":[[2009,10,8]],"date-time":"2009-10-08T03:38:27Z","timestamp":1254973107000},"page":"486-493","source":"Crossref","is-referenced-by-count":34,"title":["Suppression of gastric acid increases the risk of developing Immunoglobulin E\u2010mediated drug hypersensitivity: human diclofenac sensitization and a murine sensitization model"],"prefix":"10.1111","volume":"40","author":[{"given":"A. 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