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抗中性粒细胞胞浆抗体相关性血管炎的最新进展。

Updates in ANCA-associated vasculitis.

机构信息

Division of Rheumatology, Department of Medicine, Vasculitis Clinic, Mount Sinai Hospital, University of Toronto, Ontario, Canada.

Division of Internal Medicine, Vasculitis Clinic, Hopital Sacre´-Coeur de Montre´al, University of Montreal, Montreal, Quebec, Canada.

出版信息

Eur J Rheumatol. 2022 Jul;9(3):153-166. doi: 10.5152/eujrheum.2022.20248.

Abstract

Antineutrophil cytoplasm antibody (ANCA)-associated vasculitides (AAV) are small-vessel vasculitides that include granulomatosis with polyangiitis (formerly Wegener's granulomatosis), microscopic polyangiitis, and eosinophilic granulomatosis with polyangiitis (Churg - Strauss syndrome). Renal-limited AAV can be considered a fourth entity. Despite their rarity and still unknown cause(s), research into AAV has been very active over the past decades and has allowed for the development of new therapeutic regimens. The pathogenesis is a complex process of immune dysregulations with genetic and environmental influences. Recent genome-wide association studies have identified multiple genetic predisposing variants, especially at the major histocompatibility complex region. The pathogenic role of antimyeloperoxidase ANCA (MPO-ANCA) is well supported by several animal models, but that of antiproteinase 3 ANCA (PR3-ANCA) is not as strongly demonstrated. B cells likely play a major role in the pathogenesis because they produce ANCAs, as do neutrophil abnormalities, imbalances in T-cell subtypes, and/or cytokine - chemokine networks. The role of the alternative complement pathway was established more recently, and studies of the antagonist of human C5a receptor (avacopan) in AAV have just been completed, with promising results. The current standard management of severe AAV still consists of remission induction therapy with glucocorticoids combined with rituximab or, less often now, cyclophosphamide. Several studies showed that reduced-dose regimens of glucocorticoids are noninferior to the previously used heavier regimens, for therefore less cumulative exposure to glucocorticoids. Avacopan use may even lead to new steroid-free therapeutic approaches, at least for some selected patients. Several trials and studies have now shown the superiority of rituximab over azathioprine or methotrexate as maintenance therapy. However, the optimal dosing regimen and duration for maintenance remain to be better defined, at the individual patient level. Many changes have occurred in the standard of care for AAV over the past decades, and more are expected soon, including with use of avacopan, but also, likely, a few other agents under investigation or development.

摘要

抗中性粒细胞胞浆抗体 (ANCA)-相关性血管炎 (AAV) 是小血管血管炎,包括肉芽肿性多血管炎(以前称为韦格纳肉芽肿病)、显微镜下多血管炎和嗜酸性肉芽肿性多血管炎(Churg-Strauss 综合征)。肾局限性 AAV 可被视为第四种实体。尽管它们罕见且病因仍不清楚,但过去几十年来,对 AAV 的研究非常活跃,并开发了新的治疗方案。发病机制是一个复杂的免疫失调过程,受到遗传和环境因素的影响。最近的全基因组关联研究确定了多个遗传易感性变体,特别是在主要组织相容性复合体区域。几种动物模型很好地支持抗髓过氧化物酶 ANCA (MPO-ANCA) 的致病性作用,但抗蛋白酶 3 ANCA (PR3-ANCA) 的作用则没有得到充分证明。B 细胞可能在发病机制中起主要作用,因为它们产生 ANCAs,同时也存在中性粒细胞异常、T 细胞亚型失衡和/或细胞因子-趋化因子网络失衡。补体替代途径的作用是最近才确定的,并且对 AAV 中人类 C5a 受体拮抗剂(avacopan)的研究刚刚完成,结果很有前景。目前严重 AAV 的标准治疗仍包括使用糖皮质激素联合利妥昔单抗或现在较少使用的环磷酰胺进行缓解诱导治疗。几项研究表明,与以前使用的较重方案相比,糖皮质激素的低剂量方案不劣效,因此糖皮质激素的累积暴露量更少。阿伐考帕可能会导致新的无类固醇治疗方法,至少对一些选定的患者如此。现在有几项试验和研究表明,利妥昔单抗作为维持治疗优于硫唑嘌呤或甲氨蝶呤。然而,在个体患者层面上,维持治疗的最佳剂量方案和持续时间仍有待更好地确定。过去几十年,AAV 的治疗标准发生了许多变化,预计很快还会有更多变化,包括使用阿伐考帕,但也可能包括一些正在研究或开发的其他药物。

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