Guilpain P, Maldini C, Guillevin L
Pôle de médecine interne, Centre national de référence maladies auto-immunes et systémiques rares (vascularites et sclérodermie), hôpital Cochin, AP-HP, faculté de médecine, université Paris Descartes, 27, rue du Faubourg, Saint-Jacques, 75679 Paris cedex 14, France.
Rev Med Interne. 2011 Jul;32(7):411-5. doi: 10.1016/j.revmed.2010.05.005. Epub 2010 Jul 14.
Antimyeloperoxidase antibodies are a variety of antineutrophil cytoplasm antibodies (Anca), which can be detected in systemic small-sized vessel vasculitides such as microscopic polyangiitis, Wegener's granulomatosis and Churg-Strauss syndrome. Antimyeloperoxidase antibodies have been also associated with the development of lung fibrosis. Their pathogenic role has been well established, both in vitro and in vivo. These autoantibodies can activate neutrophils and trigger their oxidative burst leading to the release of free oxygen species and cytotoxic proteins. The oxidative burst is deleterious for the endothelium. Another mechanism by which antimyeloperoxidase may act is the activation of myeloperoxydase leading to an increased production of hypochlorous acid, which is highly toxic for the endothelial cells. These mechanisms contribute to the development of vasculitis.
抗髓过氧化物酶抗体是抗中性粒细胞胞浆抗体（ANCA）的一种，可在系统性小血管血管炎中检测到，如显微镜下多血管炎、韦格纳肉芽肿和变应性肉芽肿性血管炎。抗髓过氧化物酶抗体也与肺纤维化的发生有关。其致病作用在体外和体内均已得到充分证实。这些自身抗体可激活中性粒细胞并引发其氧化爆发，导致释放游离氧和细胞毒性蛋白。氧化爆发对内皮细胞有害。抗髓过氧化物酶可能起作用的另一种机制是激活髓过氧化物酶，导致次氯酸生成增加，而次氯酸对内皮细胞具有高毒性。这些机制促成了血管炎的发展。
