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男性特发性骨质疏松症患者血清骨硬化蛋白水平。

Serum sclerostin levels in men with idiopathic osteoporosis.

机构信息

Department of Endocrinology, Ghent University Hospital, Ghent, Belgium.

出版信息

Eur J Endocrinol. 2013 Mar 15;168(4):615-20. doi: 10.1530/EJE-12-1074. Print 2013 Apr.

DOI:10.1530/EJE-12-1074
PMID:23389587
Abstract

OBJECTIVE

Sclerostin inhibits osteoblast differentiation and bone formation. If aberrant sclerostin action is involved in less efficient bone acquisition in men with idiopathic low bone mass, this might be reflected in higher serum sclerostin levels.

METHODS

In 116 men with idiopathic osteoporosis (≤65 years old), 40 of their sons and healthy controls, areal bone parameters were measured using dual-energy X-ray absorptiometry, and volumetric and geometric bone parameters were measured using peripheral quantitative computed tomography. Serum analytes were measured using immunoassays and estradiol (E2) levels using liquid chromatography-tandem mass spectrometry.

RESULTS

Men with idiopathic low bone mass had lower levels of sclerostin than the controls (0.54±0.17 vs 0.66±0.23 ng/ml; P<0.001). In both groups, sclerostin levels were strongly associated with age; when adjusting for age, no associations with anthropometrics were observed (P>0.14). In multivariate analyses, sclerostin levels displayed a positive association with whole-body bone mineral content (BMC) and areal BMD (aBMD), as well as with trabecular and cortical volumetric bone mineral density (vBMD) at the tibia in the probands. No clear associations were observed in the control group, neither were sclerostin levels associated with BMC at the radius or lumbar spine (all P>0.11). Testosterone, but not E2, was inversely related to sclerostin levels in the probands. No difference in sclerostin levels was found in their sons when compared with their controls.

CONCLUSION

Lower rather than higher serum sclerostin levels in the probands with idiopathic low bone mass suggest that aberrant sclerostin secretion is not involved in the pathogenesis of low bone mass in these subjects.

摘要

目的

骨硬化蛋白可抑制成骨细胞分化和骨形成。如果异常的骨硬化蛋白作用参与了男性特发性低骨量人群中骨量获取效率降低的过程,那么这可能反映在更高的血清骨硬化蛋白水平上。

方法

在 116 名患有特发性骨质疏松症(≤65 岁)的男性、其中 40 名的儿子以及健康对照者中,使用双能 X 射线吸收法测量骨面积参数,使用外周定量计算机断层扫描法测量骨体积和几何参数。使用免疫分析法测量血清分析物,使用液相色谱-串联质谱法测量雌二醇(E2)水平。

结果

与对照组相比,患有特发性低骨量的男性的骨硬化蛋白水平较低(0.54±0.17 对 0.66±0.23 ng/ml;P<0.001)。在这两个组中,骨硬化蛋白水平与年龄密切相关;当调整年龄因素后,与人体测量学指标没有关联(P>0.14)。在多元分析中,骨硬化蛋白水平与全身骨矿物质含量(BMC)和面积骨密度(aBMD)以及胫骨的小梁和皮质体积骨密度(vBMD)呈正相关。在对照组中没有观察到明确的关联,骨硬化蛋白水平与桡骨或腰椎的 BMC 也没有关联(所有 P>0.11)。在患者中,睾酮而不是 E2 与骨硬化蛋白水平呈负相关。与对照组相比,他们的儿子的骨硬化蛋白水平没有差异。

结论

在患有特发性低骨量的患者中,骨硬化蛋白水平较低而不是较高,表明异常的骨硬化蛋白分泌并未参与这些患者低骨量的发病机制。

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