首页> 外文期刊>Bone >Vu, T.D.T.a , Wang, X.F.a , Wang, Q.a , Cusano, N.E.b , Irani, D.b , Silva, B.C.b , Ghasem-Zadeh, A.a , Udesky, J.b , Romano, M.E.b , Zebaze, R.a , Jerums, G.a , Boutroy, S.b , Bilezikian, J.P.b , Seeman, E.a New insights into the effects of primary hyperparathyroidism on the cortical and trabecular compartments of bone
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Vu, T.D.T.a , Wang, X.F.a , Wang, Q.a , Cusano, N.E.b , Irani, D.b , Silva, B.C.b , Ghasem-Zadeh, A.a , Udesky, J.b , Romano, M.E.b , Zebaze, R.a , Jerums, G.a , Boutroy, S.b , Bilezikian, J.P.b , Seeman, E.a New insights into the effects of primary hyperparathyroidism on the cortical and trabecular compartments of bone

机译:Vu,TDTa,Wang,XFa,Wang,Qa,Cusano,NEb,伊朗语,Db,Silva,BCb,Ghasem-Zadeh,AA,Udesky,Jb,Romano,MEb,Zebaze,Ra,Jerums,Ga,Boutroy,Sb, Bilezikian,JPb,Seeman,Ea对原发性甲状旁腺功能亢进症对骨皮质和小梁腔的影响的新见解

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摘要

In primary hyperparathyroidism (PHPT), protracted elevation of serum parathyroid hormone (PTH) is held to be associated with cortical, but not trabecular, bone loss. However, an alternative explanation for the apparent preservation of trabecular bone is fragmentation of the cortex by intracortical remodeling. The cortical fragments resemble trabeculae and so may be erroneously included in the quantification of 'trabecular' bone density.To test this hypothesis, we compared bone microarchitecture in 43 patients with untreated PHPT (mean 62.9. years, range 31-84) with 47 healthy age-matched controls and 25 patients with surgically treated PHPT (63.6. years, 30-82). Images of the distal radius and tibia were acquired using high-resolution peripheral quantitative CT and analysed using StrAx1.0, a new software program that quantifies bone morphology in-vivo. Results were expressed as the mean number of standardized deviations (SD) from the age-specific mean (Z scores, mean ± SEM).In subjects with PHPT, total tibial cortical area was reduced - 0.26 ± 0.08 SD; p = 0.002). Cortical volumetric bone mineral density (vBMD) was reduced (- 0.29 ± 0.06 SD; p < 0.001) due to higher cortical porosity (0.32 ± 0.06 SD; p < 0.001) and lower tissue mineralization density (- 0.21 ± 0.06 SD; p = 0.002). Medullary area was increased (0.26 ± 0.08 SD; p = 0.002) and trabecular vBMD was reduced (- 0.14 ± 0.04 SD; p < 0.001).In subjects who underwent successful parathyroidectomy, cortical area (- 0.18 ± 0.10 SD; NS) and medullary area (0.18 ± 0.10 SD; NS) did not differ from controls. Cortical vBMD was reduced (- 0.15 ± 0.05 SD; p = 0.003) due to high porosity (0.15 ± 0.05 SD; p = 0.006), values numerically lower than in untreated PHPT. Tissue mineralization density (- 0.26 ± 0.04 SD; p < 0.001) and trabecular vBMD were reduced (- 0.16 ± 0.04 SD, p < 0.001). The results were similar in the distal radius.In PHPT, chronically elevated endogenous PTH does not spare trabecular bone; it causes bone loss and microarchitectural deterioration in both cortical and trabecular compartments of bone.
机译:在原发性甲状旁腺功能亢进症(PHPT)中,血清甲状旁腺激素(PTH)持续升高被认为与皮质骨损失有关,但与小梁骨损失无关。然而,对于小梁骨的明显保存的另一种解释是通过皮层内重塑使皮质碎裂。皮质碎片类似于小梁,因此可能被错误地包括在“小梁”骨密度的量化中。为了验证这一假设,我们比较了43例未经治疗的PHPT患者(平均年龄62.9。岁,范围31-84)与47例健康的PHP患者的骨微结构。年龄匹配的对照组和25例接受过PHPT手术治疗的患者(63.6岁,30-82岁)。远端radius骨和胫骨的图像是使用高分辨率的外周定量CT采集的,并使用StrAx1.0(一种可对体内骨骼形态进行定量的新软件程序)进行分析。结果表示为与特定年龄段的平均值的标准偏差的平均值(SD)(Z评分,平均值±SEM)。PHPT患者的胫骨总皮质面积减少了-0.26±0.08 SD; p = 0.002)。由于较高的皮质孔隙率(0.32±0.06 SD; p <0.001)和较低的组织矿化密度(-0.21±0.06 SD; p =),皮质骨的骨矿物质密度(vBMD)降低(-0.29±0.06 SD; p <0.001) 0.002)。髓样面积增加(0.26±0.08 SD; p = 0.002)和小梁vBMD减少(-0.14±0.04 SD; p <0.001)在成功进行甲状旁腺切除术的受试者中,皮质区域(-0.18±0.10 SD; NS)和延髓面积(0.18±0.10 SD; NS)与对照无差异。由于孔隙率高(0.15±0.05 SD; p = 0.006),皮质vBMD降低了(-0.15±0.05 SD; p = 0.003),该值在数值上低于未处理的PHPT。组织矿化密度(-0.26±0.04 SD; p <0.001)和小梁vBMD降低(-0.16±0.04 SD,p <0.001)。在远端radius骨中,结果相似。在PHPT中,内源性PTH的慢性升高不能保留小梁骨。它会在骨骼的皮质和小梁腔内造成骨质流失和微结构性退化。

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