Hypersensitivity reactions to nonsteroidal anti-inflammatory drugs (NSAID) have traditionally been classified as either allergic, pseudoallergic, or idiosyncratic adverse reactions. Although allergic NSAID reactions are attributable to an immunologic mechanism (presumably immunoglobulin E [IgE] mediated), pseudoallergic reactions are believed to result from inhibition of the cyclooxygenase-1 pathway, and idiosyncratic reactions involve other types of immune mechanisms. Pseudoallergic reactions are frequently cross-reactive (or cross-intolerant) to chemically unrelated classes of NSAIDs. These reactions be classified into four types: NSAID-induced asthma and rhinosinusitis (type 1); NSAID-induced urticaria and/or angioedema in patients with chronic urticaria (type 2); NSAID-induced urticaria and/or angioedema in individuals who are otherwise asymptomatic (type 3); Blended (mixed respiratory and/or cutaneous) reactions in individuals who are otherwise asymptomatic (type 4).
In 2018, the European Network of Drug Allergy (ENDA) and the Drug Hypersensitivity interest group in the European Academy of Allergy and Clinical Immunology (EAACI) proposed a new classification of NSAID hypersensitivity reactions designed specifically for children.2 This classification was based on age, NSAID cross-reactivity status, and type of reaction. In this issue of the Proceedings, Arikoglu et al.3 present data to suggest that the EAACI/ENDA classification system of pediatric NSAID hypersensitivity reactions has significant limitations and that children with underlying allergic disease should be a separate subgroup because > 10% of reactors could not be categorized based on the EAACI/ENDA classification system. The authors suggest for this subgroup that the underlying mechanism may involve more than cyclooxygenase-1 inhibition.
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