目的　糖皮质激素是治疗肾病综合征的首选药物。但糖皮质激素可抑制成骨细胞功能,导致骨质疏松。该研究通过检测成骨细胞不同分化阶段的生化指标:I型前胶原羧基端前肽(PICP)、骨钙素(BGP)和总碱性磷酸酶(AKP),探讨糖皮质激素对肾病综合征(NS)患儿成骨细胞功能的影响。方法　测定正常对照组(n=30),未治NS患儿(n=30)和激素治疗后NS患儿(每日泼尼松2mg/kg治疗4 ~8周,n=30)血清PICP、BGP及AKP水平。结果　未治NS患儿血清PICP165 ±56μg/L,BGP15 ±9ng/L水平明显低于正常对照组205 ±81μg/L, 19 ±12ng/L(均P<0. 05),而血清总AKP198 ±71U/L与正常对照组202 ±46U/L比较差异无显著性。激素治疗后NS患儿血清PICP85 ±56μg/L、BGP8±5ng/L、AKP104 ±59 U/L均明显低于未治NS患儿(P<0. 01)。结论　NS患儿本身存在骨合成障碍,大剂量糖皮质激素治疗可进一步抑制NS患儿的成骨细胞合成功能。

ObjectiveGlucocorticoid is a first-selected medicine for the treatment of nephrotic syndrome (NS). But glucocorticoid can repress ossification and result in osteoporosis. This research examined the concentrations of biochemical markers of osteoblasts at different differentiation stages to explore the effects of glucocorticoid on osteoblast function in children with NS.Methods Serum procollagen type I c-terminal propeptide (PICP), bone Gla protein (BGP) and total alkaline phosphatase (AKP) were detected in 30 healthy children, 30 prednisone-treated NS children (2 mg/kg·d for 4-8 weeks) and 30 untreated NS children.Results Serum concentrations of PICP (165 ±56 μg/L vs 205 ±81 μg/L)and BGP (15±9 ng/L vs 19±12 ng/L)were significantly lower in untreated NS children than those in healthy controls (P<0.05). There was no significant difference in serum total AKP between the two groups. As compared with the untreated NS children, PICP (85 ±56 μg/L), BGP (8±5 ng/L) and AKP (104 ±59 U/L) in the prednisone-treated NS children were significantly lower (P<0.01). Conclusions There is a decreased bone composition in NS children. High-dose of glucocorticoid treatment for NS can further inhibit osteoblast composition.