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类风湿关节炎的全身表现和关节外表现概述

Authors
Peter H Schur, MD
Eric L Matteson, MD, MPH
Carl Turesson, MD, PhD
Section Editor
Ravinder N Maini, BA, MB BChir, FRCP, FMedSci, FRS
Deputy Editor
Paul L Romain, MD
Translators
陈华, 主治医师

引言

尽管类风湿关节炎(rheumatoid arthritis, RA)的主要病理改变发生于可动关节的滑膜内，但也可累及各种非关节性器官，尤其是在严重关节病变的患者。虽然关节与关节外组织(例如骨髓)之间正常形态和功能存在差异，但是日渐明确的是，导致滑膜病变的细胞因子也会导致关节外组织病变。 (参见“类风湿关节炎的发病机制”)

约40%的RA患者在病程中会出现关节外的肌肉骨骼系统(如骨骼和肌肉)和非肌肉骨骼系统的器官(如皮肤、眼、肺部、心脏、肾脏、血管、唾液腺、中枢与周围神经系统，以及骨髓)受累[1,2]。这些表现将总结在此。关节表现将会单独详细讨论。 (参见“类风湿关节炎的临床表现”)

全身性关节外病变的危险因素包括类风湿因子(rheumatoid factor, RF)阳性和吸烟[3]。重症关节外RA患者在出现全身表现时，RF水平通常较高，且与没有关节外病变的RA患者相比，前者的血清抗瓜氨酸化蛋白抗体的阳性率更高[4]。

RA的关节外表现是病情严重的标志，并且与总体并发症发生率和早期死亡率升高相关[5,6]。成功治疗RA全身表现的基础是控制潜在关节病变，常需要糖皮质激素和免疫抑制治疗[7]。

骨质减少

RA患者的骨质减少可能是全身性的，由不活动、炎症进程和糖皮质激素治疗的影响导致；骨质减少也包括RA典型性关节周围去矿化。这是前列腺素、多种细胞因子和正常水平甲状旁腺激素的共同作用结果。如果不使用抗骨吸收治疗，预计所有RA患者都会出现骨矿物质损失[8]。继发于疾病自身的骨减少与糖皮质激素诱发的骨质减少不同；但是对于某些患者，疾病和糖皮质激素治疗的作用相加，导致并发症发病率高。这些患者尤其容易出现身高缩减、症状性脊椎压缩骨折，以及跖骨或腿部长骨的应力性骨折。发生骨折的患者通常长时间不活动，缺乏正常负重，导致骨吸收加速并减少新骨形成而加重骨丢失。

                                             

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Literature review current through: 2017-06 . | This topic last updated: 2016-10-28.
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