The selective response to AX appears consistent, and a response to penicillin determinants only develops in a minority of cases. For the case of CLV, the selective response appears not to be modified by exposure to penicillin determinants, meaning that patients with CLV allergy can take penicillin derivatives safely.

Selective immediate reactions to NSAIDs must be considered when a patient develops urticaria or anaphylaxis after intake of one drug with good tolerance to drugs from other groups or even a drug from the same group with a slightly different chemical structure. Further research is required to identify the antigenic determinant structures recognized.

NSAIDs are the most important group of drugs involved in hypersensitivity drug reactions, and include heterogeneous compounds with very different chemical structures. These reactions can be IgE dependent (immediate reactions), T cell-mediated (non-immediate), or induced by a non-specific immunological mechanism related with the blocking of the COX-1 enzyme and the shunting to the lipooxygenase pathway (cross-intolerant reactions). Cutaneous symptoms are the most frequent, with ibuprofen, naproxen and diclofenac being common culprit drugs worldwide, although others can be involved because patterns of consumption and exposure rates vary between countries. A very important proportion of immunological reactions are immediate, with urticaria and anaphylaxis being the typical clinical manifestations. Non-immediate reactions comprise a number of heterogeneous entities ranging from mild exanthema to severe TEN or DRESS syndrome, as well as organ-specific reactions such as hepatitis or pneumonitis. Cross-intolerant reactions appear to non-chemically related drugs, and involve respiratory airways, skin or both. In vivo diagnostic tests are based on the capacity of the skin to respond to the culprit drug, but their sensitivity is in many instances rather low. The approach for in vitro testing consists of either detecting specific IgE antibodies or studying the proliferation of T lymphocytes toward the eliciting drug. No appropriate tests are yet available for the in vitro validation of cross-intolerance reactions, although techniques based on the stimulation of basophils have been proposed. Based on these findings, the diagnostic approach is often based on the controlled administration of the drug to assess tolerance. In this work we review current knowledge on hypersensitivity reactions to NSAIDs, including diagnostic approach and genetic studies.

Hypersensitivity reactions to NSAIDs are more complex than for other drugs like betalactams in terms of the number and types of reactions elicited, and mechanisms involved. As NSAIDs are the most frequent cause of drug hypersensitivity, it is feasible to gather a sufficient number of cases for undertaking pharmacogenetic studies.

Background: Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most frequent agents involved in hypersensitivity drug reactions, with NSAID-induced urticaria and/or angioedema (NIUA) being the most common entity. Mast cells are key players in NIUA and are activated by thymic stromal lymphopoietin (TSLP). This cytokine functions through recognition by its receptor, composed of IL7Rα (interleukin-7 receptor alpha) and TSLPR (TSLP receptor). These genes have been previously associated with other inflammatory diseases. Methods: We assessed the genetic association between single nucleotide polymorphisms (SNPs) in TSLP, IL7R and TSLPR and NIUA in Spanish individuals, using genotyped and imputed data. A total of 369 unrelated NIUA patients and 580 NSAID-tolerant control subjects were included, and 6 SNPs in TSLP, 6 in IL7R and 3 in TSLPR were genotyped. Further variants were imputed using Mach and the 1,000 Genomes Project (Phase 3) data. Association testing and statistical analyses were performed with Mach2dat and R. Results: A total of 139 SNPs were tested for association following quality control. Two SNPs in TSLP (rs1816678 and rs764917) showed a nominal association (p = 0.033 and 0.024, respectively) with NIUA, although these results were not statistically significant after correcting for multiple comparisons. Conclusions: Although TSLP, IL7R and TSLPR are important genes involved in the development of the inflammatory response, we found no significant genetic association with NIUA in our population for common SNPs in these genes.

Table of contentsOral AbstractsO1 Functionally distinct HMGB1 isoforms correlate with physiological processes in drug-induced SJS/TENDaniel F. Carr, Wen-Hung Chung, Rosalind E. Jenkiins, Mas Chaponda, Gospel Nwikue, Elena M. Cornejo Castro, Daniel J. Antoine, Munir PirmohamedO2 Hypersensitivity reactions to beta-lactams, does the t cell recognition pattern influence the clinical picture?Natascha Wuillemin, Dolores Dina, Klara K. Eriksson, Daniel YerlyO3 Specific binding characteristics of HLA alleles associated with nevirapine hypersensitivityRebecca Pavlos, Elizabeth Mckinnin, David Ostrov, Bjoern Peters, Soren Buus, David Koelle, Abha Chopra, Craig Rive, Alec Redwood, Susana Restrepo, Austin Bracey, Jing Yuan, Silvana Gaudieri, Mary Carrington, David Haas, Simon Mallal, Elizabeth PhillipsO4 Do we need to measure total ige for the interpretation of analytical results of ImmunoCAP dnd 3gAllergy specific IgE?Douwe De Boer, Paul Menheere, Chris Nieuwhof, Judith BonsO5 Neutrophil activation in systemic anaphylaxis: results from the multicentric NASA studyFriederike Jonsson, Luc De Chaisemartin, Vanessa Granger, Caitlin Gillis, Aurelie Gouel, Catherine Neukirch, Fadia Dib, Pascale Roland Nicaise, Dan Longrois, Florence Tubach, Sylvie Martin, Pierre Bruhns, NASA Study GroupO6 Purpuric drug eruptions due to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) for non-small-cell lung cancer (NSCLC): a clinic-pathological study of 32 casesKai-Lung Chen, Shu-Ling Liao, Yi-Shuan Sheen, Yung-Tsu Cho, Che-Wen Yang, Jau-Yu Liau, Chia-Yu ChuPoster presentations: Poster Walk 1—Anaphylaxis (P01–P09)P1 Anaphylactic reactions during anaesthesia and the perioperative periodRita Aguiar, Anabela Lopes, Natália Fernandes, Leonor Viegas, M. A. Pereira-BarbosaP2 Anaphylaxis to chlorhexidine: is there a cross-reactivity to alexidine?Antonia Bünter, Nisha Gupta, Tatjana Pecaric Petkovic, Nicole Wirth, Werner J. Pichler, Oliver HausmannP3 Cefotaxime-induced severe anaphylaxis in a neonateMehtap Yazicioglu, Pinar G. Ozdemir, Gokce Ciplak, Ozkan KayaP4 Clinical features and diagnosis of anaphylaxis resulting from exposure to chlorhexidinePeter John CookeP5 Drug-induced anaphylaxis: five-year single-center surveyInês Mota, Ângela Gaspar, Filipe Benito-Garcia, Marta Chambel, Mário Morais-AlmeidaP6 Intraoperative severe anaphylactic reaction due to patent blue v dyeLuis Marques, Eva Alcoceba, Silvia LaraP7 Kounis syndrome in the setting of anaphylaxis to diclofenacLeonor Carneiro-Leão, Carmen Botelho, Eunice Dias-Castro, Josefina CernadasP8 Perioperative anaphylaxis audit: Royal Melbourne HospitalKatherine Nicholls, William Lay, Olivia Smith, Christine Collins, Gary Unglik, Kymble Spriggs, Priscilla Auyeung, Jeremy McComish, Jo A. DouglassP9 Recurrent peri-operative anaphylaxis: a perfect stormJonny G. Peter, Paul PotterPoster Walk 2: DH regions and patient groups (P10–P19)P10 A rare presentation of amoxicillin allergy in a young childFabrícia Carolino, Eunice Dias De Castro, Josefina R. CernadasP11 Adverse drug reactions in ...

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