Trinh Hoang Kim Tu, Pham Le Duy, Le Kieu Minh, Park Hae-Sim
Center for Molecular Biomedicine, University of Medicine and Pharmacy at Ho Chi Minh City, Ho Chi Minh City, Vietnam.
Faculty of Medicine, University of Medicine and Pharmacy at Ho Chi Minh City, Ho Chi Minh City, Vietnam.
Front Genet. 2021 Jun 25;12:647257. doi: 10.3389/fgene.2021.647257. eCollection 2021.
Non-steroidal anti-inflammatory drugs (NSAIDs) are extensively prescribed in daily clinical practice. NSAIDs are the main cause of drug hypersensitivity reactions all over the world. The inhibition of cyclooxygenase enzymes by NSAIDs can perpetuate arachidonic acid metabolism, shunting to the 5-lipoxygenase pathway and its downstream inflammatory process. Clinical phenotypes of NSAID hypersensitivity are diverse and can be classified into cross-reactive or selective responses. Efforts have been made to understand pathogenic mechanisms, in which, genetic and epigenetic backgrounds are implicated in various processes of NSAID-induced hypersensitivity reactions. Although there were some similarities among patients, several genetic polymorphisms are distinct in those exhibiting respiratory or cutaneous symptoms. Moreover, the expression levels, as well as the methylation status of genes related to immune responses were demonstrated to be involved in NSAID-induced hypersensitivity reactions. There is still a lack of data on delayed type reactions. Further studies with a larger sample size, which integrate different genetic pathways, can help overcome current limitations of gen etic/epigenetic studies, and provide valuable information on NSAID hypersensitivity reactions.
非甾体抗炎药（NSAIDs）在日常临床实践中被广泛使用。NSAIDs是全球药物超敏反应的主要原因。NSAIDs对环氧化酶的抑制作用可使花生四烯酸代谢持续存在，转而进入5-脂氧合酶途径及其下游炎症过程。NSAID超敏反应的临床表型多种多样，可分为交叉反应性或选择性反应。人们已努力了解其致病机制，其中，遗传和表观遗传背景参与了NSAID诱导的超敏反应的各个过程。尽管患者之间存在一些相似之处，但在出现呼吸道或皮肤症状的患者中，有几种基因多态性是不同的。此外，与免疫反应相关的基因的表达水平以及甲基化状态也被证明与NSAID诱导的超敏反应有关。关于迟发型反应的数据仍然缺乏。进一步开展更大样本量的研究，整合不同的遗传途径，有助于克服目前遗传/表观遗传研究的局限性，并为NSAID超敏反应提供有价值的信息。
