Internal Medicine and Rheumatology, Kumamoto Center for Arthritis and Rheumatology, 1-15-7 Kuhonji, Kumamoto 862-0976, Japan.
Clin Exp Rheumatol. 2011 Sep-Oct;29(5):850-7. Epub 2011 Oct 31.
The introduction of biological therapies targeting specific inflammatory mediators revolutionised the treatment of rheumatoid arthritis (RA). Targeting key components of the immune system allows efficient suppression of the pathological inflammatory cascade that leads to RA symptoms and subsequent joint destruction. Reactive amyloid A (AA) amyloidosis, one of the most severe complications of RA, is a serious, potentially life-threatening disorder caused by deposition of AA amyloid fibrils in multiple organs. These AA amyloid fibrils derive from the circulatory acute-phase reactant serum amyloid A protein (SAA), and may be controlled by treatment. New biologics may permit AA amyloidosis secondary to RA to become a treatable, manageable disease. Rheumatologists, when diagnosing and treating patients with AA amyloidosis secondary to RA, must understand the pathophysiology and clinical factors related to development and progression of the disease, including genetic predisposition and biological versatility of SAA.
生物疗法针对特定炎症介质的引入彻底改变了类风湿关节炎（RA）的治疗方法。针对免疫系统的关键组成部分可以有效地抑制导致 RA 症状和随后关节破坏的病理性炎症级联反应。反应性淀粉样蛋白 A (AA) 淀粉样变性是 RA 最严重的并发症之一，是一种严重的、潜在威胁生命的疾病，由 AA 淀粉样纤维在多个器官中的沉积引起。这些 AA 淀粉样纤维来源于循环急性期反应物血清淀粉样蛋白 A 蛋白 (SAA)，并且可能通过治疗进行控制。新型生物制剂可能使继发于 RA 的 AA 淀粉样变性成为一种可治疗、可管理的疾病。在诊断和治疗继发于 RA 的 AA 淀粉样变性患者时，风湿病学家必须了解与疾病的发生和进展相关的病理生理学和临床因素，包括 SAA 的遗传易感性和生物学多样性。
