Anthropometric and skeletal phenotype in men with idiopathic osteoporosis and their sons is consistent with deficient estrogen action during maturation.
Anthropometric and skeletal phenotype in men with idiopathic osteoporosis and their sons is consistent with deficient estrogen action during maturation.
复制标题
患有特发性骨质疏松症的男性及其儿子的人体测量和骨骼表型与成熟过程中雌激素作用不足一致。
DOI：
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发表时间：
2009
影响因子：
5.8
通讯作者：
J. Kaufman
中科院分区：
文献类型：
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作者：
B. Lapauw;Y. Taes;S. Goemaere;K. Toye;H. Zmierczak;J. Kaufman
上下文
男性特发性骨质疏松症（IO）骨量获得不足的病理生理学仍然知之甚少。
目的
我们的目的是调查IO男性的无骨骨骼的体积和几何参数、生化标志物和人体测量学。
设计、设置和参与者
我们的横断面研究包括107名诊断为特发性低骨量的男性，23名成年儿子和130名年龄匹配的对照。
主要观察指标
评估身体成分和面积骨参数（双能X线吸收法）以及桡骨和胫骨的体积和几何参数（外周定量计算机断层扫描）。血清睾酮、雌二醇（E（2））、SHBG和骨转换标志物水平采用免疫测定法测定。计算游离激素分数。
结果
特发性低骨量的男性体重较低，（-9.6%），躯干高度（-3.3%），以及上/下身体节段比（-2.7%，P均<0.001），主要分布于桡骨和胫骨下骨小梁（分别为-19.0和-23.6%;均P <0.001）和皮质体积骨密度（vBMD）（-2.4和-1.7%;均P <0.001）和较小的皮质区（-9.7和-13.6%; P <0.001）和厚度（-13.5和-14.5%，P <0.001），这是由于骨内膜周长（+11.8和+7.4%，P <0.001）大于对照组。血清游离E（2）降低，SHBG升高（均P <0.01）。他们的儿子有较低的骨小梁vBMD（-10.3%，P = 0.036）和较薄的桡骨皮质（-8.3%，P = 0.024）。
结论
特发性低骨量男性的骨量不足涉及骨小梁和皮质骨，这是由于vBMD较低和皮质骨横截面积和厚度较小所致。至少在他们的部分儿子身上存在类似的骨骼表型。E2值降低，结合上下肢比值降低、骨内膜周长增大和vBMD降低等特征，提示男性IO的发病可能与雌激素有关。
CONTEXT
Pathophysiology of deficient bone mass acquisition in male idiopathic osteoporosis (IO) remains poorly understood.
OBJECTIVE
Our objective was to investigate volumetric and geometric parameters of the appendicular skeleton, biochemical markers, and anthropometrics in men with IO.
DESIGN, SETTING, AND PARTICIPANTS
Our cross-sectional study included 107 men diagnosed with idiopathic low bone mass, 23 of their adult sons, and 130 age-matched controls.
MAIN OUTCOME MEASURES
Body composition and areal bone parameters (dual-energy x-ray absorptiometry) and volumetric and geometric parameters of radius and tibia (peripheral quantitative computed tomography) were assessed. Serum levels of testosterone, estradiol (E(2)), and SHBG, and bone turnover markers were measured using immunoassays. Free hormone fractions were calculated.
RESULTS
Men with idiopathic low bone mass had lower weight (-9.6%), truncal height (-3.3%), and upper/lower body segment ratio (-2.7%; all P < 0.001) and presented at the radius and tibia lower trabecular (-19.0 and -23.6%, respectively; both P < 0.001) and cortical volumetric bone mineral density (vBMD) (-2.4 and -1.7%; both P < 0.001) and smaller cortical areas (-9.7 and -13.6%; both P < 0.001) and thicknesses (-13.5 and -14.5%, both P < 0.001) due to larger endosteal circumferences (+11.8 and +7.4%, both P < 0.001) than controls. Furthermore, (free) E(2) was lower and SHBG higher (both P < 0.01). Their sons had lower trabecular vBMD (-10.3%, P = 0.036) and a thinner cortex (-8.3%, P = 0.024) at the radius.
CONCLUSION
Bone mass deficits in men with idiopathic low bone mass involve trabecular and cortical bone, resulting from lower vBMD and smaller cortical bone cross-sectional areas and thicknesses. A similar bone phenotype is present in at least part of their sons. The lower E(2), together with characteristics as lower upper/lower body segment ratio, larger endosteal circumferences and lower vBMD, may indicate an estrogen-related factor in the pathogenesis of male IO.