Cunnane G
Division of Rheumatology, University of California, San Francisco, Veterans Affairs Medical Center, San Francisco, California 94121, USA.
Curr Opin Rheumatol. 2001 Jan;13(1):67-73. doi: 10.1097/00002281-200101000-00011.
Recent data demonstrating the multifunctional role of serum amyloid A (SAA) in the pathogenesis of amyloidosis have yielded important insights into this potentially fatal consequence of chronic inflammation. SAA has been shown to participate in chemotaxis, cellular adhesion, cytokine production, and metalloproteinase secretion and is thus integrally involved in the disease process. In addition to its production by the liver as part of the acute phase response, SAA is also expressed by several pathologic tissues such atherosclerotic plaques, rheumatoid synovitis and in the brains of patients with Alzheimer disease. Its constitutive production in normal tissue suggests a role for SAA in host defense and tissue turnover. Many pathways are involved in the regulation of SAA, and as more becomes known about these, potential therapeutic targets may be identified. However, the prevention of secondary amyloidosis is best achieved by early and adequate treatment of patients with chronic inflammatory disorders. Suppression of the acute phase response and normalization of SAA levels are likely to significantly impact on the incidence of amyloidosis in inflammatory arthritis.
近期数据表明血清淀粉样蛋白A（SAA）在淀粉样变性病发病机制中具有多功能作用，这为慢性炎症这一潜在致命后果提供了重要见解。SAA已被证明参与趋化作用、细胞黏附、细胞因子产生和金属蛋白酶分泌，因此在疾病过程中起着不可或缺的作用。除了作为急性期反应的一部分由肝脏产生外，SAA还在一些病理组织中表达，如动脉粥样硬化斑块、类风湿性滑膜炎以及阿尔茨海默病患者的大脑中。其在正常组织中的组成性产生表明SAA在宿主防御和组织更新中发挥作用。许多途径参与SAA的调节，随着对这些途径了解的增多，可能会确定潜在的治疗靶点。然而，预防继发性淀粉样变性病的最佳方法是对慢性炎症性疾病患者进行早期和充分治疗。抑制急性期反应和使SAA水平正常化可能会显著影响炎性关节炎中淀粉样变性病的发病率。
