Blanca-López Natalia, Barrionuevo Ester, Andreu Inmaculada, Canto María G
aAllergy Service, Hospital Infanta Leonor, Madrid bAllergy Service, Carlos Haya Hospital, Malaga cUnidad mixta de investigación IIS La Fe - UPV, Hospital La Fe, Valencia, Spain.
Curr Opin Allergy Clin Immunol. 2014 Aug;14(4):271-7. doi: 10.1097/ACI.0000000000000077.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most frequent drugs involved in hypersensitivity drugs reactions. Both immunological and nonimmunological mechanisms can be involved. We describe the different phenotypes as well as analyze the genetic basis for NSAIDs hypersensitivity.
Five major clinical entities are currently accepted in the classification of hypersensitivity reactions to NSAIDs. Three are mediated by nonspecific immunological mechanisms: NSAIDs-exacerbated respiratory disease, NSAIDs-exacerbated cutaneous disease and NSAIDs-induced urticaria/angioedema. Two are mediated by specific immunological mechanisms: single-NSAID-induced urticaria/angioedema or anaphylaxis and single-NSAID-induced delayed hypersensitivity reactions. The classification becomes more complex if we consider that in an important number of cases skin and airway involvement can occur, as well as the participation of other organs.
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.
非甾体抗炎药（NSAIDs）是药物超敏反应中最常涉及的药物。免疫和非免疫机制均可能参与其中。我们描述了不同的表型，并分析了NSAIDs超敏反应的遗传基础。
目前，NSAIDs超敏反应的分类中有五个主要临床类型。三种由非特异性免疫机制介导：NSAIDs加重的呼吸道疾病、NSAIDs加重的皮肤疾病和NSAIDs诱发的荨麻疹/血管性水肿。两种由特异性免疫机制介导：单一NSAID诱发的荨麻疹/血管性水肿或过敏反应以及单一NSAID诱发的迟发型超敏反应。如果考虑到在相当数量的病例中会出现皮肤和气道受累以及其他器官的参与，分类会变得更加复杂。
NSAIDs超敏反应在引发的反应数量和类型以及涉及的机制方面比其他药物（如β-内酰胺类）更为复杂。由于NSAIDs是药物超敏反应最常见的原因，收集足够数量的病例进行药物遗传学研究是可行的。
