Cuellar Marta Lucia
Section of Allergy, Immunology and Rheumatology, Department of Medicine, Tulane University Medical Center, 1700 Perdido Street-SL57, New Orleans, LA, 70112-2822, USA.
Curr Rheumatol Rep. 2002 Feb;4(1):55-9. doi: 10.1007/s11926-002-0024-y.
Many therapeutic agents, including recently introduced biologic response modifiers, can induce a variety of vasculitic manifestations ranging from small vessel hypersensitivity vasculitis and leukocytoclastic vasculitis to distinct vasculitic syndromes such as Wegener's granulomatosis, polyarteritis nodosa, and Churg Strauss syndrome. The pathogenic mechanisms remain to be defined and appear to be multifactorial, with cell-mediated and humural immune mechanisms playing important roles. Clinical presentation varies in severity from mild to severe and even fatal illness, can be self-limiting, or follows a more chronic protracted course. There are no significant differences in clinical presentation, serologic abnormalities, and pathologic findings with the idiopathic forms of vasculitis. However, it is extremely important to identify the offending drug because the discontinuation of the drug is often followed by a rapid improvement of the underlying vasculitic disorder.
许多治疗药物，包括最近引入的生物反应调节剂，可诱发多种血管炎表现，从小血管超敏性血管炎和白细胞破碎性血管炎到诸如韦格纳肉芽肿、结节性多动脉炎和变应性肉芽肿性血管炎等独特的血管炎综合征。其致病机制仍有待确定，似乎是多因素的，细胞介导和体液免疫机制发挥着重要作用。临床表现的严重程度各不相同，从轻度到重度甚至致命性疾病，可为自限性，或呈更慢性的迁延病程。与特发性血管炎形式相比，临床表现、血清学异常和病理发现并无显著差异。然而，识别出致病药物极其重要，因为停用该药物后，潜在的血管炎疾病通常会迅速改善。
