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本文引用的文献

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Suppression of bone turnover by B-cell depletion in patients with rheumatoid arthritis.B 细胞耗竭抑制类风湿关节炎患者的骨转换。
Osteoporos Int. 2011 Dec;22(12):3067-72. doi: 10.1007/s00198-011-1607-0. Epub 2011 Apr 6.
2
The change of bone mineral density according to treatment agents in patients with ankylosing spondylitis.强直性脊柱炎患者的骨密度随治疗药物的变化。
Joint Bone Spine. 2011 Mar;78(2):188-93. doi: 10.1016/j.jbspin.2010.05.010.
3
Stable bone mineral density in lumbar spine and hip in contrast to bone loss in the hands during long-term treatment with infliximab in patients with rheumatoid arthritis.类风湿关节炎患者长期使用英夫利昔单抗治疗期间,腰椎和髋部骨矿物质密度稳定,而手部出现骨质流失。
Ann Rheum Dis. 2011 Feb;70(2):389-90. doi: 10.1136/ard.2009.127787. Epub 2010 May 6.
4
Bone remodeling in rheumatic disease: a question of balance.风湿性疾病中的骨重建:平衡问题。
Immunol Rev. 2010 Jan;233(1):301-12. doi: 10.1111/j.0105-2896.2009.00857.x.
5
How antirheumatic drugs protect joints from damage in rheumatoid arthritis.抗风湿药物如何在类风湿关节炎中保护关节免受损伤。
Arthritis Rheum. 2008 Oct;58(10):2936-48. doi: 10.1002/art.23951.
6
Bone mineral density in rheumatoid arthritis patients 1 year after adalimumab therapy: arrest of bone loss.类风湿关节炎患者接受阿达木单抗治疗1年后的骨密度:骨质流失停止。
Ann Rheum Dis. 2009 Mar;68(3):373-6. doi: 10.1136/ard.2008.091611. Epub 2008 Apr 13.
7
Clinical assessment of the long-term risk of fracture in patients with rheumatoid arthritis.类风湿关节炎患者骨折长期风险的临床评估
Arthritis Rheum. 2006 Oct;54(10):3104-12. doi: 10.1002/art.22117.
8
Evaluation of bone mineral density, bone metabolism, osteoprotegerin and receptor activator of the NFkappaB ligand serum levels during treatment with infliximab in patients with rheumatoid arthritis.类风湿关节炎患者接受英夫利昔单抗治疗期间骨密度、骨代谢、骨保护素及核因子κB受体活化因子配体血清水平的评估
Ann Rheum Dis. 2006 Nov;65(11):1495-9. doi: 10.1136/ard.2005.044198. Epub 2006 Apr 10.
9
Vertebral deformities in rheumatoid arthritis: a comparison with population-based controls.类风湿关节炎中的椎体畸形:与基于人群的对照的比较。
Arch Intern Med. 2004 Feb 23;164(4):420-5. doi: 10.1001/archinte.164.4.420.
10
Osteoclast differentiation and activation.破骨细胞的分化与激活。
Nature. 2003 May 15;423(6937):337-42. doi: 10.1038/nature01658.

生物制剂与骨质流失

Biologicals and bone loss.

机构信息

Department of Rheumatology, Jan van Breemen Research Institute/Reade, Amsterdam, The Netherlands.

出版信息

Ther Adv Musculoskelet Dis. 2012 Aug;4(4):245-7. doi: 10.1177/1759720X12441275.

DOI:10.1177/1759720X12441275
PMID:22859923
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3403251/
Abstract

Inflammatory joint diseases are associated with extra-articular side effects including bone involvement.There is an increased risk of osteoporotic fractures. The pathogeneses of local and generalized bone loss share a common pathway. Early and active rheumatoid arthritis is associated with longitudinal observed bone loss and fracture rate is of vertebral and nonvertebral fractures is doubled compared with matched healthy controls. Lowering disease activity with TNF inhibitors or is associated with stabilisation of bone mineral density by counteracting elevated bone resorption.

摘要

炎性关节病与包括骨骼受累在内的关节外副作用相关。存在骨质疏松性骨折风险增加。局部和全身性骨质流失的发病机制具有共同途径。早期和活跃的类风湿关节炎与纵向观察到的骨质流失有关,与匹配的健康对照组相比,椎体和非椎体骨折的发生率增加了一倍。使用 TNF 抑制剂降低疾病活动度与通过对抗骨吸收增加来稳定骨矿物质密度有关。