Acott Philip D, Wong Jaime A, Lang Bianca A, Crocker John F S
Department of Pediatrics, Dalhousie University, 5850 University Avenue, Halifax, Nova Scotia, B3J 3G9, Canada.
Pediatr Nephrol. 2005 Mar;20(3):368-73. doi: 10.1007/s00467-004-1790-8. Epub 2005 Feb 3.
Pediatric nephrology and rheumatology patients with steroid-induced osteopenia are at risk of skeletal fracture. Bisphosphonate therapy has not been routinely advocated as a primary or secondary intervention for steroid-associated fractures in this population. This case control study evaluates the role of pamidronate therapy as a secondary fracture intervention. Children with symptomatic pathological fractures of the axial spine or ribs were treated with pamidronate 1 mg/kg/dose (n=17) IV at 60-day intervals for 1 yr (n=15) or 2 yr (n=2). Bone mineral density of L1-L4 (BMD) was assessed prior to treatment and at six-month intervals, and compared to 17 disease-age-gender-steroid dose-matched control patients. Alkaline phosphatase, calcium, phosphate, PTH, renal biochemistry, and 24-hr urine collections for CrCl, N-telopeptide/creatinine ratio, phosphate excretion, and calcium excretion were obtained every two months in the pamidronate population. Pamidronate caused a first exposure transient flu-like illness lasting <24 h in three patients and one patient had a new pathological fracture. No adverse events of hypocalcemia, allergic reaction or thrombophlebitis were noted. All patients reported improvement of skeletal pain. Despite ongoing steroid treatment, pamidronate significantly increased L1-L4 BMD Z-scores (mean+/-SE) relative to baseline (pamidronate vs control: 0-6 months: 0.27+/-0.14 vs -0.82+/-0.31; 0-12 months: 0.63+/-0.17 vs -0.46+/-0.27; 0-18 months: 0.55+/-0.32 vs 0.17+/-0.27; 0-24 months: 0.15+/-0.21 vs -0.23+/-0.22; 0-30 or 36 months: 0.77+/-0.71 vs -0.68+/-0.25) with repeated measures ANOVA assessment (F=11.27, p=0.0057). This study supports the safety and efficacy of pamidronate in steroid-induced fractures in pediatric nephrology and rheumatology patients.
患有类固醇诱导性骨质减少的儿科肾脏病和风湿病患者存在骨骼骨折风险。双膦酸盐疗法尚未被常规推荐作为该人群中类固醇相关骨折的一级或二级干预措施。本病例对照研究评估了帕米膦酸疗法作为骨折二级干预措施的作用。患有有症状的脊柱或肋骨病理性骨折的儿童,以1mg/kg/剂量静脉注射帕米膦酸,每60天一次,持续1年(n = 15)或2年(n = 2)。在治疗前及每6个月评估一次L1-L4的骨密度(BMD),并与17名疾病、年龄、性别、类固醇剂量匹配的对照患者进行比较。在接受帕米膦酸治疗的人群中,每两个月检测一次碱性磷酸酶、钙、磷、甲状旁腺激素、肾脏生化指标,以及收集24小时尿液检测肌酐清除率、N-端肽/肌酐比值、磷排泄和钙排泄。三名患者首次接触帕米膦酸后出现持续<24小时的短暂流感样疾病,一名患者出现新的病理性骨折。未观察到低钙血症、过敏反应或血栓性静脉炎等不良事件。所有患者均报告骨骼疼痛有所改善。尽管持续使用类固醇治疗,但与基线相比,帕米膦酸显著提高了L1-L4的骨密度Z评分(均值±标准误)(帕米膦酸组与对照组比较:0 - 6个月:0.27±0.14对 -0.82±0.31;0 - 12个月:0.63±0.17对 -0.46±0.27;0 - 18个月:0.55±0.32对0.17±0.27;0 - 24个月:0.15±0.21对 -0.23±0.22;0 - 30或36个月:0.77±0.71对 -0.68±0.25),采用重复测量方差分析评估(F = 11.27,p = 0.0057)。本研究支持帕米膦酸在儿科肾脏病和风湿病患者类固醇诱导性骨折中的安全性和有效性。