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山东大学学报(医学版) ›› 2017, Vol. 55 ›› Issue (5): 103-107.doi: 10.6040/j.issn.1671-7554.0.2016.1681

• 临床医学 • 上一篇    下一篇

糖皮质激素性骨质疏松症骨代谢与糖皮质激素用药时间的相关性

徐大霞1,侯楠2,李晓峰1,王闯1,孔猛1,焦广俊1,陈允震1   

  1. 1.山东大学齐鲁医院骨外科, 山东 济南 250012;2.山东大学齐鲁医院风湿科, 山东 济南 250012
  • 收稿日期:2016-12-20 出版日期:2017-05-10 发布日期:2017-05-10
  • 通讯作者: 陈允震. E-mail:qilucyz@yeah.net E-mail:qilucyz@yeah.net
  • 基金资助:
    山东省科技计划(2014GSF118097)

Relevance between bone metabolism of glucocorticoid-induced osteoporosis and duration of glucocorticoid treatment

XU Daxia1, HOU Nan2, LI Xiaofeng1, WANG Chuang1, KONG Meng1, JIAO Guangjun1, CHEN Yunzhen1   

  1. 1. Department of Orthopedics, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China;
    2. Department of Rheumatism, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China
  • Received:2016-12-20 Online:2017-05-10 Published:2017-05-10

摘要: 目的 观察骨代谢在糖皮质激素性骨质疏松症(GIOP)进展过程中与糖皮质激素用药时间的关系及变化规律,并依据骨代谢变化趋势探讨GIOP的防治策略。 方法 检测应用GC控制病情的系统红斑狼疮患者117例和健康人群21例骨代谢标志物(β-CTX、T-P1NT、N-MIDOs),测定L1-4椎体骨密度。依据GC使用时间将患者分为7个亚组:Ⅰ组用药1~6个月,Ⅱ组用药7~12个月,Ⅲ组用药13~18个月,Ⅳ组用药19~24个月,Ⅴ组用药25~30个月,Ⅵ组用药31~36个月,Ⅶ组用药>36个月。 结果 Ⅰ组、Ⅱ组和Ⅲ组β-CTX较正常对照组明显升高,差异有统计学意义(P<0.05);Ⅵ组和Ⅶ组β-CTX较正常对照组明显减低,差异有统计学意义(P<0.05);Ⅳ组和Ⅴ组β-CTX较正常对照组无明显差异(P>0.05);应用GC的各亚组T-P1NT、N-MIDOs均较正常对照组明显减低,差异有统计学意义(P<0.05);Ⅱ~Ⅶ组骨密度较正常对照组明显减低,差异有统计学意义(P<0.05)。 结论 GIOP形成过程中,骨代谢是由高分解状态向低分解低成骨低转换状态转变。应用GC 1~18个月的SLE患者骨代谢状态处于高分解低成骨,应用GC 30个月以上的患者骨代谢状态处于低分解低成骨低转换状态。

关键词: 糖皮质激素性骨质疏松症, 系统性红斑狼疮, 糖皮质激素, 骨代谢标志物, 骨密度

Abstract: Objective To investigate the changes of bone metabolism in different durations of glucocorticoid(GC)treatment of systemtic lupus erythematosus(SLE), and to explore the therapeutic schedule of glucocorticoid-induced osteoporosis(GIOP). Methods A total of 117 pre-menopausal women with SLE were involved as the observation group and 21 healthy pre-menopausal women served as the control group. According to the duration of GC therapy, the patients were divided into 7 subgroups: group Ⅰ(medication for 1~6 months), group Ⅱ(medication for 7~12 months), group Ⅲ(medication for 13~18 months), group Ⅳ(medication for 19~24 months), group Ⅴ(medication for 25~30 months), group Ⅵ(medication for 31~36 months), and group Ⅶ(medication for >36 months). The contents of amino-terminal-propeptide of type I collagen(T-PINT), amino-terminal of osteocalcin(N-MIDOs), type I collagen cross-linked C-telopeptide degradation fragments(β-CTX)and bone mineral density(BMD)of all subjects were measured. Results The serum β-CTX level was significantly elevated in group Ⅰ, Ⅱ and Ⅲ, and remark- 山 东 大 学 学 报 (医 学 版)55卷5期 -徐大霞,等.糖皮质激素性骨质疏松症骨代谢与糖皮质激素用药时间的相关性 \=-ably reduced in group Ⅵ and Ⅶ compared with the control group(P<0.05), while there was no difference in group Ⅳ and V(P>0.05). The serum levels of T-PINT and N-MIDOs in all subgroups were significantly lower than those in the control group(P<0.05). The BMD of patients receiving more than 6-month GC therapy was significantly lower than that of healthy controls(P<0.05). Conclusion In conclusion, the change of bone metabolism is from high decomposition to low decomposition and low osteogenesis in the process of GIOP formation. In the first 18 months of GC therapy, bone metabolism is in the state of low osteogenesis and high decomposition; after 30 months, it is in the state of low osteogenesis and low decomposition.

Key words: Glucocorticoid-induced osteoporosis, Systemic lupus erythematosus Glucocorticoid, Bone metabolism, Bone mineral density

中图分类号: 

  • R593.24
[1] Weinstein RS.Glucocorticoid-induced Osteoporosis and Osteonecrosis[J].Endocrine Metab Clin North Am, 2012, 41(3):595-611.
[2] Rizzoli R, Adachi JD, Cooper C, et al.Management of glucocorticoid-induced Osteoporosis[J].Calcif TIssue Int, 2012, 91(4):225-243.
[3] 郭惠芳,高丽霞.2014年风湿免疫病学主要临床进展[J].临床荟萃, 2015, 30(2): 167-173.
[4] Grossman JM, Gordon R, Ranganath VK, et al. American College of Rheumatology 2010 recommendations for the prevention and treatment of glucocorticoid-induced Osteoporosis[J].Arthritis Care Res, 2010, 62(11):1515-1526.
[5] Lekamwasam S, Adachi JD, Agnusdei D, et al.A framework for the development of guidelines for the management of glucocorticoid-induced osteoporosis[J].Osteoporos Int, 2012, 23(9):2257-2276.
[6] Zimlichman E, Rothschild J, Shoenfeld Y, et al. Good prognosis for hospitalized SLE patients with non-related disease[J]. Autoimmun Rev, 2014, 13(11): 1090-1093.
[7] Weinstein RS. Clinical practice:Glucocorticoid-induced bone disease[J]. N Engl J Med, 2011, 36(5): 62-70.
[8] Kearns AE, Khosla S, Kostenuik PJ. Receptor activatior of nuclear factor kappaB ligand and oateoprotegerin regulation of bone remodeling in health and disease[J]. Endcor Rev, 2008, 29(2):155-192.
[9] Gifre L, Mongegal A, Peris P, et al.Effect of glucocorticoid treatment on Wnt signalling antagonists(sclerostin and Dkk-1)and their relationship with bone turnover[J]. Bone, 2013, 57(1): 272-276.
[10] Shusuke U, Toru I. Osteocytic cell necrosis is caused by a combination of glucocorticoid-induced Dickkopf-1 and hypoxia[J]. Med Mol Morphol, 2015, 48(2): 69-75.
[11] Qiang YW, Chen Y, Stepens O, et al. Myeloma-derived Dickkopf-1 disrupts Wnt-regulated osteoprotegerin and RANKL production by osteoblasts: a potential mechanism underlying osteolytic bone lesions in multiple myeloma[J]. Blood, 2008, 112(1): 196-207.
[12] Humphrey EL, Williams JH, Davie MW, et al. Effects of dissociated glucocorticoid on OPG and RANKL in osteoblastic cells[J]. Bone, 2006, 38(5): 652-661.
[13] Canalis E, Delany AM. Mechanisms of glucocorticoid action in bone[J]. Ann NY Acad Sci, 2002, 6(966): 73-81.
[14] Robert RC. Mechanisms of impaired growth: effect of steroids on bone and cartilage[J]. Horm Res, 2009, 72(1): 30-35.
[15] 刘海春,张剑锋,陈允震.骨质疏松大鼠股骨生物力学特性与骨胶原质量变化的相关研究[J].山东大学学报(医学版),2009, 47(5): 42-46. LIU Haichun, ZHANG Jianfeng, CHEN Yunzhen. Bone collagen and biomechanical propertyies in the femur of osteoporosis rats[J]. Journal of Shandong University(Health Sciences), 2009, 47(5): 42-46.
[16] Den Uyl D, Bultink IE, Lems WF. Adwances in glucocorticoid-induced osteoporosis[J]. Curr Rheumatol Rep, 2011, 13(3): 233-240.
[17] Seibel MJ, Cooper MS, Zhou H. glucocorticoid-induced osteoporosis: mechanisms,management, and future perspectives[J]. Lancet Diabetes Endocrinol, 2013, 1(1): 59-70.
[18] Reid DM, Devogelaer JP, Saag K, et al. Zoledronic acid and risedronate in the prevention and treatment of glucocorticoid-induced osteoporosis(HORIZON): a multicentre,double-blind, double-dummy, randomised controlled trial[J]. Lancet, 2009, 373(9671): 1253-1263.
[19] Saag KG, Shane E, Boonen S, et al. Teriparatide or alendronate in glucocorticoid-induced osteoporosis[J]. N Engl J Med. 2007, 357(20): 2028-2039.
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