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口服抗凝治疗对钙和骨代谢标志物的影响。

Effect of oral anticoagulant treatment on markers for calcium and bone metabolism.

作者信息

Knapen M H, Hellemons-Boode B S, Langenberg-Ledeboer M, Knottnerus J A, Hamulyák K, Price P A, Vermeer C

机构信息

Department of Biochemistry, University of Maastricht, Maastricht, The Netherlands.

出版信息

Haemostasis. 2000 Nov-Dec;30(6):290-7. doi: 10.1159/000054146.

Abstract

Vitamin K-dependent proteins regulate blood coagulation as well as bone growth and calcification. Here, we have compared the effects of oral anticoagulants on circulating vitamin K-dependent proteins and on markers for calcium and bone metabolism. Patients with a clinical indication for antithrombotic therapy were randomized into three groups and treated with either aspirin, regular-intensity anticoagulation [target international normalized ratio (INR) values: 2.5-3.5] or low-intensity anticoagulation (target INR values: 1.1-1.6). At the start and after 1 year of treatment, various biochemical markers were assessed. Both the circulating levels and the degree of carboxylation of the various gamma-carboxyglutamate (Gla)-containing proteins were affected differently by oral anticoagulant treatment. Circulating osteocalcin was more sensitive to poor vitamin K status than other Gla proteins. From the fact that - except for osteocalcin - neither markers for osteoblast nor osteoclast function were affected by oral anticoagulant treatment, we conclude that bone turnover remained unaltered, which is indicative of an unchanged rate of bone loss. Whether the long-term production of undercarboxylated bone Gla proteins may have a negative effect on the quality of bone (e.g. bone strength) cannot be concluded from this study.

摘要

维生素K依赖蛋白调节血液凝固以及骨骼生长和钙化。在此,我们比较了口服抗凝剂对循环中维生素K依赖蛋白以及钙和骨代谢标志物的影响。有抗血栓治疗临床指征的患者被随机分为三组,分别接受阿司匹林、常规强度抗凝治疗(目标国际标准化比值[INR]值:2.5 - 3.5)或低强度抗凝治疗(目标INR值:1.1 - 1.6)。在治疗开始时和治疗1年后,评估了各种生化标志物。口服抗凝剂治疗对各种含γ-羧基谷氨酸(Gla)蛋白的循环水平和羧化程度的影响各不相同。循环中的骨钙素比其他Gla蛋白对维生素K状态不佳更敏感。鉴于除骨钙素外,口服抗凝剂治疗对成骨细胞或破骨细胞功能的标志物均无影响,我们得出结论,骨转换保持不变,这表明骨丢失率未变。本研究无法得出骨Gla蛋白羧化不足的长期产生是否会对骨质量(如骨强度)产生负面影响的结论。

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