基于引起慢性瘙痒的原因,国际瘙痒研究论坛(international forum for the study of itch,IFSI)将瘙痒分为:①皮肤疾病源性瘙痒:由皮肤病特别是炎症性皮肤病引起;②系统疾病源性瘙痒:由系统疾病如肝肾疾病、感染或肿瘤等引起;③神经病理性瘙痒:由中枢或外周神经病变引起;④躯体障碍性瘙痒:由心理、精神或身心疾病引起;⑤混合性瘙痒:即存在上述2种或2种以上类型;⑥原因不明性瘙痒(chronic pruritus of unknown origin,CPUO):暂时找不到引起慢性瘙痒的原因[4]。见表1。慢性瘙痒常为一种症状,但也有以瘙痒症状为主命名的诊断,如:CPUO、结节性痒疹等。推荐尽可能基于引起瘙痒的原因进行分类诊治(推荐强度:强推荐;专家意见的一致性强度:一致)。
根据致痒介质的不同,瘙痒机制分为组胺依赖性与非组胺依赖性。组胺依赖性瘙痒途径是经典机制,即组胺由皮肤肥大细胞和/或嗜碱性粒细胞释放,激活初级感觉神经元上的组胺受体,从而引起痒觉[19]。组胺依赖性瘙痒是荨麻疹瘙痒的重要机制[20]。非组胺依赖性瘙痒中,多种炎症因子均能直接激活初级感觉神经元上的相应受体,引起痒觉。其中白细胞介素4(IL-4)、IL-13、IL-31可分别与感觉神经元上受体(IL-4Rα与IL-31RA)直接结合[21,22],这可能是2型炎症反应参与的皮肤病如AD、大疱性类天疱疮等引起剧烈瘙痒的共同机制。有研究显示,CPUO的发生也与2型炎症密切相关[23]。其他炎症介质,如蛋白酶、白三烯类、胸腺基质淋巴细胞生成素(TSLP)、IL-33等,也能够直接结合神经元上的受体引发或加重瘙痒[22,24,25,26]。非皮肤疾病源性瘙痒中,肝硬化黄疸引起的瘙痒可能与胆汁酸激活神经元上的Mas相关G蛋白偶联受体家族(Mas-related G protein coupled receptor,MRGPR)X4或Takeda G蛋白偶联受体5有关[27,28]。氯喹引起的瘙痒则是激活痒觉神经元的MRGPRX1所致[29]。
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