Background: Nonsteroidal anti-inflammatory drugs (NSAIDS) are among the most common causes of drug hypersensitivity (HS) reactions. The diagnosis is based on a careful clinical history, and provocation tests are considered the gold standard for diagnosis. Skin tests have some value to study reactions to pyrazolones. Laboratory investigations are mostly used for research purposes. Different phenotypes have been described. Objective and Methods: Our aim was to describe the most common clinical manifestations of NSAID HS in a large population of adult patients, the drugs involved, the association with previously described risk factors, and the outcome of diagnostic procedures. The classification of reactions proposed by the European Academy of Allergy and Clinical Immunology (EAACI) Drug Allergy Interest Group was adopted. Results: Acetylsalicylic acid was the drug most often involved in reactions (34%), isolated cutaneous symptoms were the most reported (60%), and immediate reactions (58%) were the most common. There was an overall female predominance (64%) and 35% of the patients were atopic. HS to NSAIDs was confirmed in 21% of the patients. The most common phenotypes encountered among HS patients were NSAID-induced urticaria/angioedema and single-NSAID-induced urticaria/angioedema or anaphylaxis. Logistic regression analysis showed that gender and atopy were not significant risk factors for HS confirmation, but diagnosis depended on the number of previous reactions, the type of reaction, and the time interval between drug intake and reaction. Conclusion: Only 21% of suspected HS reactions were confirmed after diagnostic workup. Patients describing >1 previous reaction and suffering immediate reactions had a higher probability of a positive investigation.

Fixed drug eruptions are common cutaneous drug reactions, often misdiagnosed. A detailed anamnesis and physical examination are the key to suspect this condition.

A 56-year-old white woman developed a distinctive skin eruption over her mammary, lumbosacral, and pubic areas 2 weeks after the start of esomeprazole therapy for dyspeptic symptoms. Skin biopsy disclosed a spongiotic dermatitis with predominantly lymphocytic dermal infiltrate. Treatment with a tapering dose of corticosteroid and withdrawal of the suspected drug led to a rapid resolution of the eruption without residual dyschromia. Patch testing with esomeprazole 2% in petrolatum was negative at 48 and 72 hours but became positive on day 6. Oral-controlled provocation test induced the reappearance of the lesions over the mammary areas, confirming the putative involvement of this drug. Therefore, the patient was diagnosed as having a nonpigmented fixed drug eruption associated with esomeprazole. This compound is a proton-pump inhibitor developed as the S-isomer of omeprazole to improve its pharmacokinetic properties. Reports of cutaneous reactions to proton-pump inhibitors are quite common, but reports of such reactions to esomeprazole are rare, which demonstrates the need for higher clinical awareness and knowledge of reactions to these drugs.

Of the 67 studied cases with history of beta-lactam hypersensitivity reactions, 18 (27%) were confirmed after testing. A combination of skin testing, specific IgE determination and drug challenge is necessary since none has sufficient sensitivity to be used alone.

The interest of this case lies in the rarity of allergic reactions from inhaled CS in patients with asthma and/or rhinitis. These reactions therefore represent a diagnostic and therapeutic challenge.

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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Methylphenidate is the treatment of choice in attention-deficit/hyperactivity disorder (ADHD). The authors report the case of a 7 year old boy with ADHD and psoriasis who developed generalised erythema, pruritus and fever 5 hours after the first oral administration of methylphenidate. After 2 days of treatment the drug was discontinued with complete resolution of symptoms. Later on, the drug was re-introduced with recurrence of the same clinical symptoms. Patch tests were performed with negative results. Desensitization was proposed and performed because there is no alternative treatment for ADHD. After the therapeutic dose was achieved, the mother interrupted drug intake because of a misunderstanding of instructions, and a mild rash subsided when another pill was administered. After this event the same desensitization procedure was carefully repeated. Interruption of drug intake during desensitization and consequent recurrence of clinical symptoms highlights the importance of continued exposure to the culprit drug in this kind of procedure. This modified protocol may enable patients with cutaneous reactions to this drug, to maintain therapy without recurrent reactions.