伴有微血管并发症的胰岛素依赖型糖尿病患者的长期骨质流失

Biørn Mathiassen MD , Søren Nielsen MD , Julia S. Johansen MD , Dorthe Hartwell MD , Jørn Ditzel MD, PhD , Paul Rødbro MD, PhD , Claus Christiansen MD, PhD
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引用次数: 73

摘要

胰岛素依赖型糖尿病患者在临床发病几年后,骨矿物质含量(BMC)下降了约10%。在此之后,没有糖尿病微血管并发症的患者没有或只有很少的进一步骨质流失。本研究的目的是调查是否有任何实质性的长期骨质流失发生在糖尿病患者的微血管并发症。我们研究了19例胰岛素依赖型糖尿病患者,除糖尿病外,这些患者的生理和病理状况均未影响骨代谢。测定BMC 2次,间隔11年。初检无糖尿病微血管病变,终检有糖尿病微血管并发症7例,无糖尿病微血管并发症12例。与性别和年龄匹配的对照组相比,两个亚组在初始检查时BMC均显著降低。在研究期间,有并发症的患者出现了进一步的骨质流失,而没有并发症的亚组BMC下降不变。在最后的检查中,有微血管并发症的患者BMC明显低于无微血管并发症的患者。骨代谢生化指标显示,有并发症的患者空腹尿钙和羟脯氨酸排泄量显著增加,无并发症的患者无显著增加,所有患者血浆骨钙素(骨钙素)与血红蛋白A1c均呈负相关。这些发现表明,除了BMC降低(在糖尿病临床发病之前或之后不久),发生微血管并发症的患者还会发生持续的骨质流失。骨质流失可能是由骨吸收增加引起的,但在糖尿病控制不佳期间骨形成减少也可能涉及到。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Long-term bone loss in insulin-dependent diabetic patients with microvascular complications

Insulin-dependent diabetic patients have an approximately 10% decreased bone mineral content (BMC) when they are studied a few years after clinical onset of diabetes. After that time, patients without diabetic microvascular complications have no, or only very little, further bone loss. The aim of the present study was to investigate if any substantial long-term bone loss occurs in diabetic patients with microvascular complications. We studied 19 insulin-dependent diabetic patients with neither physiologic nor pathologic conditions known to interfere with bone metabolism, other than diabetes. BMC was determined twice, with an interval of 11 years. At initial examination, no patient had diabetic microangiopathy, but at final examination 7 patients had developed diabetic microvascular complications while 12 patients had not. As compared with gender- and age-matched controls, both subgroups had significantly decreased BMC at the initial examination. During the study period, the patients with complications showed further bone loss, whereas the subgroup without complications had unchanged decreased BMC. At final examination, BMC was significantly lower in patients with microvascular complications than in patients without them. The biochemistry of bone metabolism showed a significantly increased fasting urinary excretion of calcium and hydroxyproline in patients with complications, but not in the group without complications, and there was a negative correlation between plasma BGP (osteocalcin) and hemoglobin A1c for all patients. These findings indicate that, in addition to a decreased BMC (before or shortly after clinical onset of diabetes), patients who develop microvascular complications also develop ongoing bone loss. This loss may be caused by an increased bone resorption, but decreased bone formation during periods of poor diabetic control may be involved as well.

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