Ageing: a risk factor for amyloid A amyloidosis in rheumatoid arthritis
Ageing: a risk factor for amyloid A amyloidosis in rheumatoid arthritis
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DOI：
10.3109/13506129.2011.582198
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发表时间：
2011-09-01
影响因子：
5.5
通讯作者：
Goto, Makoto
中科院分区：
文献类型：
--
作者：
Okuda, Yasuaki;Yamada, Toshiyuki;Goto, Makoto
Objective.在类风湿性关节炎（RA）中，尚未对衰老加速淀粉样蛋白A（AA）淀粉样变性诱导进行广泛研究。本研究的目的是在我们的大型队列研究中阐明衰老对RA相关AA淀粉样变性发展的贡献。方法.入选388例成人型RA患者，其RA并发活检证实的AA淀粉样变性。估计每例患者的RA发病年龄和AA淀粉样变性诊断年龄。对144例AA淀粉样变性患者进行了年龄、炎症活动、SAA 1外显子3多态性及性别等因素的多元回归分析。结果老年RA患者发生淀粉样变的时间比年轻RA患者短（p < 0.001）。SAA 1.3阳性组RA发作和AA淀粉样变性诊断之间的间隔显著短于SAA 1.3阴性组（p = 0.001）。多元回归分析表明，从RA发病到诊断AA淀粉样变性的时间间隔由RA发病时的年龄（p < 0.001）、最近的CRP浓度中位数（p = 0.006）和SAA 1.3等位基因（p = 0.058）决定。性别对AA淀粉样变性的发生没有显著影响（p = 0.569）。结论年龄是诱发AA淀粉样变性并发RA的独立危险因素。
Objective. Acceleration of amyloid A (AA) amyloidosis induction by ageing has not been extensively studied in rheumatoid arthritis (RA). The aim of this study is to clarify contribution of ageing to the development of AA amyloidosis associated with RA in our large cohort. Methods. 388 adult-onset RA patients whose RA was complicated by biopsy-proven AA amyloidosis were enrolled. The ages of RA onset and AA amyloidosis diagnosis were estimated in each patient. The contributions of ageing, inflammatory activity, SAA1 exon 3 polymorphism as well as gender to the pathogenesis of AA amyloidosis in 144 cases were also studied by multiple regression analysis. Results. Subjects with RA onset at older age had a shorter period to develop amyloidosis than those with disease onset at younger age (p < 0.001). The interval between RA onset and AA amyloidosis diagnosis was significantly shorter in the SAA1.3 positive group than in the SAA1.3 negative (p = 0.001). Multiple regression analysis indicated that the interval from RA onset to diagnosis of AA amyloidosis is determined by age at RA onset (p < 0.001), the most recent median annual CRP concentration (p = 0.006) and SAA1.3 allele (p = 0.058). Gender did not significantly contribute to the onset of AA amyloidosis (p = 0.569). Conclusion. Ageing is an independent risk factor for the induction of AA amyloidosis complicating RA.