Cugno Massimo, Borghi Alessandro, Marzano Angelo V
Medicina Interna, Dipartimento di Fisiopatologia Medico-Chirurgica e dei Trapianti, Università degli Studi di Milano, Ospedale Maggiore Policlinico, Fondazione IRCCS Ca' Granda, Via Pace, 9, 20122, Milan, Italy.
Dipartimento di Scienze Mediche, Sezione di Dermatologia e Malattie Infettive, Università degli Studi di Ferrara, Ferrara, Italy.
Am J Clin Dermatol. 2017 Aug;18(4):555-562. doi: 10.1007/s40257-017-0265-1.
Pyoderma gangrenosum (PG) is a neutrophilic dermatosis usually manifesting as skin ulcers with undermined erythematous-violaceous borders. It may be isolated, associated with systemic conditions or occurring in the context of autoinflammatory syndromes such as PAPA (pyogenic arthritis, PG and acne), PASH (PG, acne and suppurative hidradenitis) or PAPASH (pyogenic arthritis, acne, PG and suppurative hidradenitis). From a physiopathological point of view, all these conditions share common mechanisms consisting of over-activation of the innate immune system leading to increased production of the interleukin (IL)-1 family and 'sterile' neutrophil-rich cutaneous inflammation. From a genetic point of view, a number of mutations affecting the proteins of the inflammasome complex (the molecular platform responsible for triggering autoinflammation) or the proteins that regulate inflammasome function have been described in these disorders. As these debilitating entities are all associated with the over-expression of IL-1 and tumour necrosis factor (TNF)-α, biological drugs specifically targeting these cytokines are currently the most effective treatments but, given the emerging role of IL-17 in the pathogenesis of these syndromes, IL-17 antagonists may represent the future management of these conditions.
坏疽性脓皮病(PG)是一种嗜中性皮病,通常表现为具有潜行性红斑-紫罗兰色边缘的皮肤溃疡。它可以是孤立性的,与全身性疾病相关,或发生在自身炎症综合征的背景下,如PAPA(化脓性关节炎、PG和痤疮)、PASH(PG、痤疮和化脓性汗腺炎)或PAPASH(化脓性关节炎、痤疮、PG和化脓性汗腺炎)。从生理病理学角度来看,所有这些病症都有共同的机制,包括先天免疫系统的过度激活,导致白细胞介素(IL)-1家族的产生增加以及富含中性粒细胞的“无菌性”皮肤炎症。从遗传学角度来看,在这些病症中已经描述了一些影响炎性小体复合物蛋白(负责引发自身炎症的分子平台)或调节炎性小体功能的蛋白的突变。由于这些使人衰弱的病症都与IL-1和肿瘤坏死因子(TNF)-α的过度表达相关,目前专门针对这些细胞因子的生物药物是最有效的治疗方法,但是,鉴于IL-17在这些综合征发病机制中的新作用,IL-17拮抗剂可能代表了这些病症的未来治疗方法。