Production, degradation, and circulating levels of 1,25-dihydroxyvitamin D in health and in chronic glucocorticoid excess.
Production, degradation, and circulating levels of 1,25-dihydroxyvitamin D in health and in chronic glucocorticoid excess.
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健康和慢性糖皮质激素过量时 1,25-二羟基维生素 D 的产生、降解和循环水平。
DOI：
10.1172/jci109902
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发表时间：
1980
期刊：
影响因子：
--
通讯作者：
Riggs,BL
中科院分区：
文献类型：
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作者：
Seeman,E;Kumar,R;Hunder,GG;Scott,M;Heath3rd,H;Riggs,BL
与慢性糖皮质激素过量相关的钙的肠吸收减少和骨丢失加速可能由维生素D代谢的变化介导，导致循环1，25-二羟维生素D的可用性降低。在14例内源性或外源性糖皮质激素过量的患者中检查了这一假设。配对血清样本分析13名患者在糖皮质激素正常和糖皮质激素过多期间的平均值（± SE）显示，糖皮质激素过量导致血浆25-羟基维生素D浓度小幅下降（22 +/- 2- 18 +/- 2 ng/ml; P < 0.05），但血浆1，25-二羟维生素D（32 +/- 8- 23 +/- 6 pg/ml）或血清免疫反应性甲状旁腺激素（21 +/- 2- 18 +/- 2 muleq/ml）。此外，我们还研究了10名糖皮质激素过多患者和14名正常对照者静脉推注给药后[3 H] 1，25-二羟维生素D3的血浆动力学。三房室模型评估显示生产率无显著异常（高糖皮质激素患者1.2 +/- 0.3微克/天，对照组1.5 +/- 0.2微克/天）或代谢清除率（糖皮质激素过多患者，18 +/- 2%;对照组，14 +/- 2%）或粪便（糖皮质激素过多患者，60 +/-9%，对照组，54 +/- 6%）。我们的结论是，糖皮质激素过量不会影响血浆水平，生产，或降解的1，25（OH）2D在人类。因此，必须假设其他机制，以圆满地解释骨结构和肠道钙吸收的异常，可能会发生慢性糖皮质激素治疗后。
The decreased intestinal absorption of calcium and accelerated bone loss associated with chronic glucocorticoid excess may be mediated by changes in vitamin D metabolism, leading to decreased availability of circulating 1,25-dihydroxyvitamin D. This hypothesis was examined in 14 patients with either endogenous or exogenous glucocorticoid excess. Analysis of paired serum samples (mean +/- SE) in 13 patients during euglucocorticoidism and during hyperglucocorticoidism showed that glucocorticoid excess resulted in small decreases of plasma 25-hydroxy-vitamin D concentrations (22 +/- 2- 18 +/- 2 ng/ml; P < 0.05) but no significant changes in plasma 1,25-dihydroxyvitamin D (32 +/- 8- 23 +/- 6 pg/ml) or serum immunoreactive parathyroid hormone (21 +/- 2- 18 +/- 2 muleq/ml). Additionally, we studied plasma kinetics of [3H]1,25-dihydroxyvitamin D3 after intravenous bolus administration in 10 hyperglucocorticoid patients and in 14 normal controls. Assessment with a three-compartment model showed no significant abnormalities in production rates (hyperglucocorticoid patients 1.2 +/- 0.3 micrograms/d, controls 1.5 +/- 0.2 micrograms/d) or metabolic clearance rates (hyperglucocorticoid patients, 18 +/- 2%; controls, 14 +/- 2%) or feces (hyperglucocorticoid patients, 60 +/- 9%, controls, 54 +/- 6%). We conclude that glucocorticoid excess does not effect plasma levels, production, or degradation of 1,25(OH)2D in humans. Thus, other mechanisms must be postulated to explain satisfactorily the abnormalities of bone structure and intestinal calcium absorption that may occur after chronic glucocorticoid therapy.