Chesney R W, Mazess R B, Hamstra A J, DeLuca H F, O'Reagan S
Lancet. 1978 Nov 25;2(8100):1123-5. doi: 10.1016/s0140-6736(78)92277-8.
Serum-1,25-dihydroxyvitamin-D3 (1,25-[OH]2D3) was subnormal in children receiving long-term glucocorticoid treatment for various glomerular diseases, including nephrotic syndrome. In children with chronic glomerulonephritis not treated with glucocorticoids who had similar serum-creatinine with glucocorticoids who had similar serum-creatinine concentrations, serum-1,25-dihydroxyvitamin-D3 concentrations resembled those in healthy controls, indicating that glomerular renal disease per se does not account for reduced serum-1,25(OH)2DE concentrations in steroid-treated patients. The reduction in concentration of this most active vitamin-D metabolite correlated with the dose of steroid administered and with reduction in forearm bone mineral content measured by the photon absorption technique. Reduced serum-1,25-(OH)2D3 concentration may be important in the pathogenesis of steroid-induced osteopenia.
在因各种肾小球疾病（包括肾病综合征）接受长期糖皮质激素治疗的儿童中，血清1,25 - 二羟基维生素D3（1,25 - [OH]2D3）水平低于正常。在未接受糖皮质激素治疗、血清肌酐浓度与接受糖皮质激素治疗的儿童相似的慢性肾小球肾炎儿童中，血清1,25 - 二羟基维生素D3浓度与健康对照相似，这表明肾小球疾病本身并不能解释接受类固醇治疗患者血清1,25(OH)2D3浓度降低的原因。这种最具活性的维生素D代谢产物浓度的降低与所给予的类固醇剂量以及通过光子吸收技术测量的前臂骨矿物质含量的降低相关。血清1,25 - (OH)2D3浓度降低可能在类固醇诱导的骨质减少的发病机制中起重要作用。
