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Clinical and Translational Allergy

Open Access

Use of in vitro tests to assess the causative drugs for NSAIDs-induced type I hypersensitivity

  • Wan-Chun Chang1,
  • Bi-Kai Hsu1,
  • Wen-Hung Chung2 and
  • Shuen-Iu Hung1
Clinical and Translational Allergy20144(Suppl 3):P31

https://doi.org/10.1186/2045-7022-4-S3-P31

Published: 18 July 2014

Non-steroidal anti-inflammatory drugs (NSAIDs) are associated with type I hypersensitivity, including cutaneous manifestations (e.g., urticaria and angioedema), respiratory manifestations (rhinitis, nasal polyposis, asthma), and anaphylaxis. To assess the sensitivity/specificity of in vitro tests for verifying the causative/tolerant drugs and cross-reactivity of different NSAIDs, we used three assays, including two ELISA tests for histamine/leukotriene C4 (LTC4) release, and a flow cytometric basophil activation test (BAT). We recruited 82 patients with NSAIDs-induced type I hypersensitivity (angioedema of the most cases), and isolated the peripheral leukocytes to perform histamine/LTC4 release tests in 38 patients, and BAT in 44 patients. The cell response to NSAIDs was examined in the incubation containing suspected or tolerant drugs with concentrations equal to 1-fold (physical level) or 10-fold Cmax. Comparing with the data of solve controls of the same subject, positive response was considered if the histamine/LTC4 release showed 1.2-fold increase, and BAT detected more than 5% increase of CD63+/CCR3+ cells. We found that histamine release test had a sensitivity of 41.9% (26/62), and specificity of 100% (10/10).LTC4 release test had a sensitivity of 32.3% (20/62), and specificity of 90% (9/10). BAT had a sensitivity of 46.4% (39/84) and specificity of 90% (18/20) for NSAIDs-induced type I hypersensitivity. Regarding drug classification, the four most common clinically suspected agents were aspirin, ibuprofen, diclofenac, and acetaminophen. The three assays have consistently >50% sensitivity for verifying aspirin, but various sensitivity and diverse individual response for the other NSAIDs. Heterogeneous mechanisms including both immunology and pharmacology may be involved in NSAIDs-induced type I hypersensitivity.

Authors’ Affiliations

(1)
National Yang-Ming University, Institution of Pharmacology, Taiwan
(2)
Department of Dermatology, Chang Gung Memorial Hospital, Taiwan

Copyright

© Chang et al; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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