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使用口服钙负荷来表征年轻胰岛素依赖型糖尿病患者的高钙尿症。

Use of oral calcium loading to characterize the hypercalciuria of young insulin-dependent diabetics.

作者信息

Witt M F, White N H, Santiago J V, Seino Y, Avioli L V

出版信息

J Clin Endocrinol Metab. 1983 Jul;57(1):94-100. doi: 10.1210/jcem-57-1-94.

Abstract

To investigate the pathogenesis of the alterations in bone and mineral metabolism that are found in young insulin-dependent diabetics (IDDs), we performed a standard oral calcium load in 26 IDDs, 7-18 yr of age, and in 17 normal children, 9-18 yr of age. Eighty-five percent of the IDDs had second metacarpal cortical bone widths below the mean for matched controls. Calcium excretion in the IDDs fell along a continuous spectrum, ranging from normal to values consistent with renal hypercalciuria. Immunoreactive PTH was significantly (P less than 0.03) lower in the IDDs compared to that in the controls, and 24,25-dihydroxyvitamin D was significantly elevated (P less than 0.001). We were not able to document a significantly lower concentration of 1,25-dihydroxyvitamin D in the IDDs. Serum calcium, phosphate, and PRL levels were normal, as were creatinine (Cr) clearance and 24-hr urinary cortisol excretion. There was no apparent correlation between the fasting and postload urinary Ca to Cr and glucose to Cr concentration ratios. The accumulated data suggest that in many young IDDs, there is a component of intestinal calcium hyperabsorption which results in appropriate feedback responses by the parathyroid gland and vitamin D metabolic pathway(s). This imbalance between circulating PTH and vitamin D metabolites could result in defective bone remodeling and decreased cortical thickness.

摘要

为了研究在年轻的胰岛素依赖型糖尿病患者(IDDs)中发现的骨与矿物质代谢改变的发病机制,我们对26名7至18岁的IDDs患者以及17名9至18岁的正常儿童进行了标准口服钙负荷试验。85%的IDDs患者第二掌骨皮质骨宽度低于匹配对照组的均值。IDDs患者的钙排泄呈连续谱变化,范围从正常到与肾性高钙尿相符的值。与对照组相比,IDDs患者的免疫反应性甲状旁腺激素(PTH)显著降低(P<0.03),而24,25 - 二羟维生素D显著升高(P<0.001)。我们未能证明IDDs患者中1,25 - 二羟维生素D的浓度显著降低。血清钙、磷和催乳素水平正常,肌酐(Cr)清除率和24小时尿皮质醇排泄也正常。空腹和负荷后尿钙与肌酐以及血糖与肌酐浓度比值之间没有明显相关性。累积的数据表明,在许多年轻的IDDs患者中,存在肠道钙吸收过多的情况,这会导致甲状旁腺和维生素D代谢途径产生适当的反馈反应。循环中的PTH与维生素D代谢产物之间的这种失衡可能导致骨重塑缺陷和皮质厚度降低。

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