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2型糖尿病老年人的骨转换与骨密度

Bone turnover and bone mineral density in old persons with type 2 diabetes.

作者信息

Martins João Martin, Aranha Patrícia

机构信息

Endocrine Department, Hospital Santa Maria, 6th Floor, Avenida Professor Egas Moniz, 1649-028 Lisboa, Portugal.

Endocrine University Clinic, Lisbon Medical School, Avenida Professor Egas Moniz, 1649-028 Lisboa, Portugal.

出版信息

J Clin Transl Endocrinol. 2018 Sep 24;14:12-18. doi: 10.1016/j.jcte.2018.09.002. eCollection 2018 Dec.

Abstract

AIMS

To understand the paradox of an increased fracture risk despite increased bone mineral density (BMD) in persons with type 2 diabetes (DM2).

PATIENTS AND METHODS

We studied 80 old persons with DM2. Mineral metabolism, parathyroid hormone (PTH), 25-hydroxyvitamin D (25OHD), bone turnover - osteocalcin, procollagen type 1 N-terminal propeptide (P1NP) and C-terminal telopeptide of type 1 collagen (CTX) - were measured and BMD was assessed at the lumbar spine (LS) and femoral neck (FN). Data was analyzed with the Statistical Package for the Social Sciences Program.

RESULTS

Low levels of 25OHD (84%) and high values of PTH (20%) were found. Osteocalcin was directly related to CTX, p < 0.001, with increased bone formation and increased BMD (z-score) at LS and FN. PTH was directly related to osteocalcin and CTX and inversely related to BMD at the FN, p < 0.05. Patients with dyslipidemia presented higher P1NP, p < 0.05 and patients with hypertension presented higher BMD at LS and FN, p < 0.01.

CONCLUSION

Old type 2 diabetics present increased bone formation, PTH-driven. Low grade secondary hyperparathyroidism may explain the paradox of an increased fracture risk despite increased BMD.

摘要

目的

了解2型糖尿病(DM2)患者骨矿物质密度(BMD)增加但骨折风险却升高这一矛盾现象。

患者与方法

我们研究了80例老年DM2患者。检测了矿物质代谢、甲状旁腺激素(PTH)、25-羟基维生素D(25OHD)、骨转换指标——骨钙素、1型前胶原N端前肽(P1NP)和1型胶原C端肽(CTX),并评估了腰椎(LS)和股骨颈(FN)的骨密度。数据采用社会科学统计软件包进行分析。

结果

发现25OHD水平低(84%)和PTH值高(20%)。骨钙素与CTX直接相关,p<0.001,同时腰椎和股骨颈的骨形成增加且骨密度(z评分)升高。PTH与骨钙素和CTX直接相关,与股骨颈骨密度呈负相关,p<0.05。血脂异常患者的P1NP较高,p<0.05,高血压患者腰椎和股骨颈的骨密度较高,p<0.01。

结论

老年2型糖尿病患者存在由PTH驱动的骨形成增加。轻度继发性甲状旁腺功能亢进可能解释了骨密度增加但骨折风险却升高这一矛盾现象。

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