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Hypersensitivity reactions to nonsteroidal anti-inflammatory drugs: From phenotyping to genotyping

机译:对非甾体类抗炎药的超敏反应:从表型到基因型

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Purpose of Review: 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. Recent Findings: 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. Summary: 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.
机译:审查目的:非甾体抗炎药(NSAIDs)是超敏反应中最常见的药物。免疫和非免疫机制均可参与。我们描述了不同的表型,并分析了非甾体抗炎药超敏反应的遗传基础。最新发现:在对NSAID的超敏反应分类中目前接受了五个主要的临床实体。非特异性免疫机制介导了三种:NSAIDs加剧的呼吸道疾病,NSAIDs加剧的皮肤病和NSAIDs引起的荨麻疹/血管性水肿。两种是通过特定的免疫机制介导的:单非甾体抗炎药诱发的荨麻疹/血管性水肿或过敏反应和单种非甾体抗炎药诱发的迟发型超敏反应。如果我们认为在很多情况下会发生皮肤和气道受累以及其他器官的参与,则分类变得更加复杂。摘要:就引发的反应的数量和类型以及所涉及的机制而言,对NSAID的超敏反应比对其他药物(如β-内酰胺类)更为复杂。由于非甾体抗炎药是引起药物超敏反应的最常见原因,因此收集足够数量的病例进行药物遗传学研究是可行的。

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