Gladman D D, Brockbank J
University of Toronto Psoriatic Arthritis Clinic and Psoriatic Arthritis Program, Centre for Prognosis Studies in The Rheumatic Diseases, Toronto Western Hospital, Toronto, Ontario, Canada.
Expert Opin Investig Drugs. 2000 Jul;9(7):1511-22. doi: 10.1517/13543784.9.7.1511.
Psoriatic arthritis occurs in 5 - 42% of patients with psoriasis. It is an inflammatory arthritis distinct from rheumatoid, being usually sero-negative, asymmetrical and often affecting the spine, sacro-iliac and distal interphalangeal joints. It runs a very variable course, from a mild non-destructive disease to a severe rapidly progressive erosive arthropathy, producing an 'arthritis mutilans' with a combination of bone lysis and joint ankylosis. Its pathogenesis is not as well understood as rheumatoid arthritis, but is thought to be similarly immune driven, with a qualitatively similar immunomodulatory cascade and cytokine profile. Quantitatively, however, there are distinct differences in cell ratios and cytokine levels that may well impact on therapeutic strategies. Current therapies, such as methotrexate and sulphasalazine, have yet to be shown to be significantly more effective than placebo in delaying damage and produce only marginal improvements in symptoms. The newer specific biological agents, such as the anticytokine antibodies, interleukins and more specific anti-T-cell therapies, are starting to be studied in psoriatic arthritis. The rationale for their use comes mostly from extrapolation of their efficacy in rheumatoid arthritis. It has yet to be seen whether they will be efficacious in treating the osteolysis, fibrosis and new bone formation particular to psoriatic arthritis. Any treatment for the arthritis must also help the skin. Greater understanding of psoriatic arthritis, its pathogenesis and natural history is required if we are to target these exciting but expensive therapies effectively.
银屑病关节炎发生于5% - 42%的银屑病患者中。它是一种与类风湿关节炎不同的炎性关节炎，通常为血清阴性、不对称，且常累及脊柱、骶髂关节和远端指间关节。其病程变化很大，从轻度非破坏性疾病到严重的快速进展性侵蚀性关节病，可导致“毁形性关节炎”，伴有骨溶解和关节强直。其发病机制不像类风湿关节炎那样被充分了解，但被认为同样由免疫驱动，具有定性相似的免疫调节级联反应和细胞因子谱。然而，在细胞比例和细胞因子水平上存在明显差异，这可能对治疗策略产生重大影响。目前的治疗方法，如甲氨蝶呤和柳氮磺胺吡啶，在延缓损伤方面尚未显示出比安慰剂显著更有效，且仅能使症状有轻微改善。新型特异性生物制剂，如抗细胞因子抗体、白细胞介素和更具特异性的抗T细胞疗法，已开始在银屑病关节炎中进行研究。使用它们的理论依据大多来自于对其在类风湿关节炎中疗效的推断。它们是否能有效治疗银屑病关节炎特有的骨溶解、纤维化和新骨形成还有待观察。关节炎的任何治疗方法都必须对皮肤有益。如果我们要有效地针对这些令人兴奋但昂贵的疗法，就需要对银屑病关节炎及其发病机制和自然史有更深入的了解。
