Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: The use of glucocorticoids in rheumatoid arthritis no ‘rational’ approach yet. | Desai and Solomon Arthritis Research Therapy 2010 12 127 http content 12 3 127 EDITORIAL L_ The use of glucocorticoids in rheumatoid arthritis -no rational approach yet Sonali P Desai and Daniel H Solomon See related research by Ibanez etal. http content 12 2 R50 Abstract The relationship between glucocorticoids and bone mineral density in rheumatoid arthritis is complex. Further study into the optimal dosing timing and duration of glucocorticoid use in rheumatoid arthritis is necessary. In the previous issue of Arthritis Research and Therapy Ibanez and colleagues 1 report on the rational use of glucocorticoids GCs in the management of early arthritis. This article concludes that GCs cause minimal variation in bone mineral density BMD at multiple skeletal sites and in fact may increase BMD at the ultradistal forearm a juxta-articular site. Although this article is notable for examining the effect of GCs on BMD at five anatomic sites a rational use of GCs for rheumatoid arthritis RA is still elusive. To grasp the complex relationship between GCs and both localized juxta-articular bony erosions and systemic osteoporosis bone loss in RA we need to first step back and appreciate the interplay of the immune system and bone metabolism. The osteoclast plays a central role at the site of inflamed joints and is critical in the pathogenesis of joint erosions in RA 2 . Receptor activator of nuclear factor-kappa B ligand RANKL expressed by TH1 and TH17 T cell subsets is a potent inducer of osteoclast differentiation. Additionally an array of pro-inflammatory cytokines such as TNF IL-1 IL-6 and IL-17 can stimulate RANKL expression 3 Figure 1 . GCs in turn directly affect both osteoblast and osteoclast activity and indirectly exert many effects on bone metabolism leading to an increased fracture risk 4 Figure 2 . How should the relationship between the bone biology in RA and the effects of GCs translate into the use of GCs .
