Decreased axial and peripheral bone density in patients taking long-term warfarin.
Decreased axial and peripheral bone density in patients taking long-term warfarin.
复制标题
长期服用华法林的患者的轴骨和周围骨密度降低。
DOI：
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发表时间：
1995
期刊：
影响因子：
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通讯作者：
A. S. Douglas
中科院分区：
文献类型：
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作者：
W.J.U. Philip;J. Martin;J. Richardson;David M. Reid;John Webster;A. S. Douglas
维生素K代谢受损与非胶原骨基质蛋白骨钙素的羧化不足有关，骨钙素在其完全羧化状态下是正常骨形成所需的。绝经后妇女的骨钙素羧化不足，随着年龄的增长而增加，在老年人中尤为明显。在香豆素治疗过程中也会出现类似程度的羧化受损，关键问题是这是否会导致骨量加速丢失，这在临床上很重要。我们测量了40名服用华法林的男性患者和40名年龄、疾病和其他药物治疗相匹配的对照组的轴向和外周骨密度（BMD）。在华法林治疗的患者中观察到所有部位BMD降低的一致趋势。这在桡骨远端的松质骨（减少9%，p = 0.023）和富含松质骨的腰椎部位（减少10.4%，p < 0.004）中尤其明显。未观察到华法林剂量、国际标准化比值（INR）或治疗持续时间与骨密度之间存在显著相关性。由于生物化学的相似性，这项研究提供了一个新的线索绝经后骨质疏松症，并支持这一假设，即受损的羧化骨钙素通过维生素K代谢的缺乏在老年人骨丢失的发病机制中发挥作用。
Impaired vitamin K metabolism is associated with under-carboxylation of the non-collagenous bone-matrix protein osteocalcin, which is required in its fully carboxylated state for normal bone formation. Post-menopausal women have under-carboxylation of osteocalcin which increases with age and is marked in the elderly. A similarly marked degree of impaired carboxylation occurs during coumarin therapy, and a key question is whether this may lead to accelerated loss of bone mass which is clinically important. We measured axial and peripheral bone mineral density (BMD) in 40 male patients on warfarin and 40 controls individually matched for age, disease and other drug therapy. A consistent trend for reduced BMD at all sites was observed in the warfarin-treated patients. This was particularly marked in the cancellous bone at the distal radius (9% reduction, p = 0.023) and at the cancellous rich lumbar spine site (10.4% reduction, p < 0.004). No significant relationship was observed between warfarin dose, International Normalized Ratio (INR) or duration of therapy and bone density. Because of the biochemical similarity, this study provides a new lead on post-menopausal osteoporosis, and supports the hypothesis that impaired carboxylation of osteocalcin plays a role in the pathogenesis of bone loss in the elderly through deficiency in vitamin K metabolism.