普雷迪尼索隆会损害21-基酶缺乏症的青少年的脊椎骨评分变化
Pattara Wiromrat1, Yutapong Raruenrom2, Phanpaphorn Namphaisan1
1Division of Endocrinology, Department of Pediatrics, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Clinical and experimental pediatrics
|November 13, 2024
概括
患有21-基酶缺乏症 (21OHD) 的青少年通常具有受损的骨微型架构. 普雷迪尼索隆疗法对骨发育产生负面影响,这表明皮可能是保护骨健康的更好的一线治疗方法.
科学领域:
- 内分泌学 在内分泌学.
- 骨的新陈代谢 骨的新陈代谢
- 儿科内分泌学 儿科内分泌学
背景情况:
- 对21-基酶缺乏症 (21OHD) 的终身葡萄糖皮质激素 (GC) 治疗会增加骨折的风险.
- 尽管正常的骨矿物质密度 (BMD),但GC治疗个体的骨折可能会发生,这表明微观结构的变化.
研究的目的:
- 为了评估 21OHD.OHD 的青少年的脊椎骨微架构及其变化.
- 评估不同类型的皮质糖类药物治疗对这一群体骨微型架构的影响.
主要方法:
- 38名患有21OHD的青少年在1.5年内进行了基线和随访的腰椎骨髓 BMD (LSBMD) 的评估.
- 使用iNsight软件分析了骨微架构的间接测量 - - 轨道骨评分 (TBS).
- 损伤的BMD和TBS被定义为z分数≤-1.5.5.
主要成果:
- 在基线时,18%的参与者TBS受损,5%的BMD受损.
- 服用普雷迪尼索隆的青少年与服用皮的青少年相比,TBS的年增幅较小 (P=0.028).
- 体重指数百分位和丸激素度预测了较高的基线TBSz分数,而普雷尼索隆使用预测了较低的年度TBS变化.
结论:
- 患有21OHD的青少年表现出受损骨微型架构的高患病率.
- 普雷尼索隆治疗与较差的骨微型架构发展有关.
- 在21岁OHD的青少年中,皮可能更适合保存骨微型架构.
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