Dona Inmaculada, Salas Maria, Perkins James R, Barrionuevo Esther, Gaeta Francesco, Cornejo-Garcia Jose A, Campo Paloma, Torres Maria Jose
Allergy Unit, pabellon 6, 1º planta, Hospital Regional Universitario de Malaga (Pabellon C), Plaza del Hospital Civil, 29009 Malaga, Spain.
Curr Pharm Des. 2016;22(45):6784-6802. doi: 10.2174/1381612822666160928142814.
Non-steroidal anti-inflammatory drugs (NSAIDs) are one of the leading causes of hypersensitivity reactions to drugs, and they are classified in two groups: those induced by nonspecific immunological mechanisms (non-allergic or cross-intolerance (CI) reactions), or by specific immunological mechanisms (allergic or selective reactions (SR)). The pathogenesis of CI is associated with their pharmacological activity (COX-1 inhibition), with symptoms due to an imbalance in the arachidonic acid pathway, independently of their chemical structure. SRs are mediated by specific IgE- or by a T-cell response and can be induced by a single NSAID or a class of chemically related NSAIDs, with patients tolerating chemically unrelated compounds. NSAIDs hypersensitivity reactions have been classified in five main groups: i) NSAIDs-exacerbated respiratory disease (NERD); ii) NSAIDs-exacerbated cutaneous disease (NECD); iii) NSAIDs-induced urticaria/angioedema (NIUA); iv) Single NSAID-induced urticaria/angioedema or anaphylaxis (SNIUAA); v) Single NSAID-induced delayed reactions (SNIDRs). Although this classification described above is widely accepted by most authors some phenotypes such as blended reactions do not fit. Therefore more research is needed in this topic.
非甾体抗炎药(NSAIDs)是药物过敏反应的主要原因之一,它们分为两组:由非特异性免疫机制(非过敏性或交叉不耐受(CI)反应)引起的,或由特异性免疫机制(过敏性或选择性反应(SR))引起的。CI的发病机制与其药理活性(COX-1抑制)有关,症状是由于花生四烯酸途径失衡所致,与它们的化学结构无关。SR由特异性IgE或T细胞反应介导,可由单一NSAID或一类化学相关的NSAIDs诱导,患者对化学无关的化合物耐受。NSAIDs过敏反应主要分为五组:i)NSAIDs加重的呼吸道疾病(NERD);ii)NSAIDs加重的皮肤疾病(NECD);iii)NSAIDs诱导的荨麻疹/血管性水肿(NIUA);iv)单一NSAID诱导的荨麻疹/血管性水肿或过敏反应(SNIUAA);v)单一NSAID诱导的迟发反应(SNIDRs)。尽管上述分类被大多数作者广泛接受,但一些表型如混合反应并不适用。因此,该主题需要更多的研究。