376 Epidemiology of Immediate Type Adverse Drug Reactions and Rashes Elicited by Nsaid

Abstract

BackgroundNSAID are frequently used and can often cause adverse drug reactions (ADR) ranging from generally mild to sometimes severe and life-threatening reactions. ADRs are in most cases interpreted as pseudo-allergic, presumably non immunologic, but their dynamics and appearance in a subgroup of patients is suggestive for an IgE-mediated mechanism.MethodsIn this study, we retrospectively analysed data of 501 patients from our outpatient clinic population of the past 7 years with ADR to NSAID. Data was evaluated regarding the culprit drug or drugs, type and severity of reactions, age, gender, atopy, number of co-medication, co-morbidity and infections etc. as risk factors. Further, skin test and provocation test results were reviewed for their clinical relevance and reliability.ResultsAcetylsalicylic acid (ASA), paracetamol, diclofenac, mefenamic acid and propyphenazone were found as top five of causative drugs for ADR. The most common symptoms were angioedema, urticaria, pruritus, exanthema and dyspnea. ASA caused dyspnea, angioedema and urticaria in the majority of the cases. Diclofenac was found to be the most common culprit for severe anaphylactic reactions, followed by paracetamol and propyphenazone. Sixty percent of the NSAID reactors suffered from an atopic disease or had an atopic predisposition. There was a significant association between proven hypersensitivity reactions and reaction initiation after drug intake regarding the time interval.ConclusionsOur data suggest that -atopic predisposition is a risk factor for intolerance reaction to NSAID, -ASS accounts for non-immunologic, intolerance reactions, whereas severe anaphylactic reactions to diclofenac and/or propyphenazone seem to be IgE-mediated, -a shorter time interval between drug intake and appearance of symptoms is supportive for clinical relevance and could be an indicator for IgE-mediated ADR. Acknowledgements: FWF project L467-B05.

Genetic variants of the arachidonic acid pathway in non‐steroidal anti‐inflammatory drug‐induced acute urticaria

“…Association of SNPs in genes from the AA pathway with the risk of NSAIDs-induced AU in the two populations studied and in meta-analysis. Note that rs320995 is located in the Xchromosome and therefore, genotypes are presented separately for females ( by selective responses and airway involvement [7][8][9], up to now most genetic association studies in HSR to NSAIDs have been carried out in patients with respiratory disease and, to a lesser extent with CU [17,18]. The approaches mostly consisted of candidate gene studies focused on leukotriene-related genes, with variable and often not replicable results, as has been recently reviewed [17,18].…”

“…Although recent studies show that AU is the most frequent clinical entity in patients with HSR to NSAIDs, followed by selective responses and airway involvement , up to now most genetic association studies in HSR to NSAIDs have been carried out in patients with respiratory disease and, to a lesser extent with CU . The approaches mostly consisted of candidate gene studies focused on leukotriene‐related genes, with variable and often not replicable results, as has been recently reviewed .…”

“…Patients experiencing specific reactions are usually classified as selective responders because the reaction is induced by a single drug and they have good tolerance to other chemically unrelated drugs . Those with non‐specific reactions, the most common, are usually described as having HSR with cross‐intolerance (CRI) because their response is triggered by chemically unrelated NSAIDs .…”

“…Clinical manifestations of CRI to NSAIDs can involve both the respiratory system (asthma and/or rhinitis and nasal polyposis) and the skin (urticaria). Although cutaneous reactions are considered the most common manifestations , respiratory airway involvement has long been the best‐studied model. The underlying mechanism of these reactions (Fig.…”