期刊文献+

儿童骨质疏松的诊疗进展 被引量:6

Progress on the diagnosis and treatment of osteoporosis in children
下载PDF
导出
摘要 骨质疏松症属代谢性骨病范畴,常见于老年人,儿童骨质疏松相对少见但更值得关注。在病因学上同样分为原发性和继发性,原发性主要见于潜在遗传性疾病的儿童,而继发性主要起因于慢性病及其相关治疗。既往骨折史以及后背痛常提示骨质疏松的存在,而在影像学上骨皮质变薄或低骨密度同样预示着骨折的风险。儿童骨质疏松的诊断工具优选双能X线骨密度仪,对于那些处于继发性骨质疏松风险的儿童,要保持高度警惕,而对于那些已经罹患骨质疏松的儿童,应尽量避免或减少可能进一步损伤骨骼的因素,以及尽早给予充足的钙及维生素D。治疗重点应侧重于改善功能结局,同时也应认识到生长发育期本身椎体重塑或症状自发缓解的可能性,因此应尽量避免不必要的治疗。双膦酸盐目前为治疗首选,但在儿童骨质疏松中证据有限,长期应用的时间及剂量仍有争议。尽管目前抗骨吸收的药物有很多种,但仍缺乏促进骨形成药物的研究,希望未来有更多适合儿童骨质疏松治疗的证据来填补这个空缺。 Osteoporosis is a metabolic bone disease particularly common in the elderly. Osteoporosis in children is relatively rare,but is of great concern. Osteoporosis in children can be etiologically primary or secondary due to chronic disease. Primary osteoporosis mainly result from underlying genetic disease,whereas secondary osteoporosis is caused by chronic diseases and the associated treatment. Previous fractures and backaches are clinical predictors,and low cortical thickness and low bone density are radiological predictors of fractures. Dual energy X-ray absorptiometry( DXA) is the first choice for osteoporosis diagnosis in children. We should pay more attention to children who are at risk for secondary osteoporosis,and in affected children,further weakening of the bones should be avoided through minimizing exposure to osteotoxic medication and optimizing nutrition including calcium and vitamin D. Treatment should focus on improving functional outcomes. It is important to identify patient groups in whom spontaneous vertebral reshaping and resolution of symptoms occur during growth to avoid unnecessary treatment. Bisphosphonate therapy remains the first choice of pharmacological treatment of osteoporosis in children,despite there are limited evidence for its usefulness in the pediatric population. The duration and dose of treatment remain a concern for long-term safety. Various new potent antiresorptive agents are being studied,but more urgently required are studies using anabolic medications that stimulate bone formation.
作者 胡咏新 曹雯 褚晓秋 刘洲君 刘超 HU Yongxin;CAO Wen;CHU Xiaoqiu;LIU Zhoujun;LIU Chao(Endocrine and Diabetes Center, Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Traditional Chinese Medicine, Jiangsu Province Academy of Traditional Chinese Medicine, Nanjing 210028, China)
出处 《中国骨质疏松杂志》 CAS CSCD 北大核心 2018年第4期530-533,共4页 Chinese Journal of Osteoporosis
基金 江苏省科技计划项目(BM2012064)
关键词 儿童骨质疏松 诊断 治疗 Osteoporosis in children Diagnosis Treatment
  • 相关文献

参考文献1

二级参考文献41

  • 11, Bianchi ML, Balm S, Bishop N], Gordon CM, Hans D et al. OffMal positions of the International Society for Clinical Densitometry on DXA evaluation in children and adolescents. Pediatr Nephrol 2010; 25: 37-47.
  • 2Marini JC, Forlino A, Cabral WA, Barnes AM, San Antonio JD et al. Consortium for osteogenesis imperfecta mutations in the helical domain of type I collagen : regions rich in lethal mutations align with collagen binding sites for integrins and proteoglycans. H,,man Mutat 2007 : 28 : 209-21.
  • 3Carpenter TO. The expanding family of hypophosphatemic syndromes J Bone Miner Metab 2012 ; 30 : 1-9.
  • 4Juarez Jiminez HG, Mier Cisneros R, Peralta Cruz S. Mid-third femoral shaft fracture in a patient with hypophosphatemic rickets with a locking centromedullary nail. Acta Ortop Mex 2009; 23 : 193-6.
  • 5Jonas J, Burns J, Abel EW, Cresswell M J, Strain JJ, Paterson CR. Impaired mechanical strength of bone in experimental copper deficiency. Ann Nutr Metab 1993 ; 37 : 245-52.
  • 6Glorieux FH. Treatment of osteogenesis imperfecta: Who? Why? What? Horm Res 2007; 65 Suppl 5: 8-11.
  • 7Deng HW, Reeker RR. Gene mapping and identification for osteoporosis. J Musculoskelet Neuronal Interact 2004; 4: 91- 100.
  • 8Haussler M, Whitfield GK, Haussler CA, Hsieh JC, Thompson PD et al. The nuclear vitamin D receptor: biological and molecular regulatory proteins revealed. J Bone Miner Res 1998; 13 : 325-49.
  • 9Boyan BD, Sylvia VL, McKinney N, Schwartz Z. Membrane action of vitamin D metabolites 1-alpha, 25 (OH) 2D3 and 24R, 25(OH)2D3 are retained in growth plate cartilage ceils from vitamin D receptor knockout mice. J Cel Biochem 2003; 90: 1207-23.
  • 10Kristjansson K, Rut AR, Hewison M, O' Riordan JL, Hughes MR. Two mutations in the hormone binding domain of the vitamin D receptor cause tissue resistance to 1, 25 dihydroxyvitamin D3. J Clin Invest 1993; 92: 12-6.

共引文献7

同被引文献70

引证文献6

二级引证文献9

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部