Yamaguchi Yumi, Yamamoto Kazuhiko
The University of Tokyo, Graduate School of Medicine, Department of Allergy and Rheumatology.
Clin Calcium. 2007 Apr;17(4):463-73.
Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic synovitis and bone damages, which consist of joint destruction. The pathogenesis of RA is not well understood, but molecular events leading to tissue inflammation with cartilage and bone destruction are now defined in more detail. Previous therapy, slow acting disease-modifying antirheumatic drugs (DMARDs) as with low-dose methotrexate (MTX) were accepted for RA and lead to a significant improvement of disease symptoms, however were unable to stop joint destruction. Recently therapeutic strategies using biologics including infliximab and etaner-cept are effective for treating RA disease activity and reduce joint destruction. Moreover it has been shown that disability and joint destruction occur early in the course of RA and progress rapidly. These findings support the hypothesis "window of opportunity for therapeutic intervention in RA" , and the aggressive therapy early in the course of RA is expected to result in the induction of remission or, perhaps most important, a chance of cure.
类风湿性关节炎(RA)是一种全身性自身免疫性疾病,其特征为慢性滑膜炎和骨损伤,包括关节破坏。RA的发病机制尚不完全清楚,但导致伴有软骨和骨破坏的组织炎症的分子事件现在已得到更详细的界定。以前的治疗方法,如使用低剂量甲氨蝶呤(MTX)的慢作用抗风湿药物(DMARDs)被用于治疗RA,并能显著改善疾病症状,然而却无法阻止关节破坏。最近,使用包括英夫利昔单抗和依那西普在内的生物制剂的治疗策略对治疗RA疾病活动有效,并减少关节破坏。此外,研究表明,残疾和关节破坏在RA病程早期就会出现并迅速进展。这些发现支持了“RA治疗干预机会窗”这一假说,并且预计在RA病程早期进行积极治疗会诱导病情缓解,或者也许最重要的是,带来治愈的机会。