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髋部骨折患者可能缺乏维生素B6。血清磷酸吡哆醛-5'-磷酸的对照研究。

Hip fracture patients may be vitamin B6 deficient. Controlled study of serum pyridoxal-5'-phosphate.

作者信息

Reynolds T M, Marshall P D, Brain A M

机构信息

Department of Medical Biochemistry, Cardiff Royal Infirmary, UK.

出版信息

Acta Orthop Scand. 1992 Dec;63(6):635-8. doi: 10.1080/17453679209169725.

Abstract

Deficiency of vitamin B6 in rats may result in defective bone formation, possibly due to decreased activity of the enzyme ornithine decarboxylase which requires pyridoxal-5'-phosphate (PLP) as a co-factor and is responsible for production of intracellular putrescine, a metabolic regulator. We studied 3 groups of patients (62 fit ambulant out-patients, 21 elective arthroplasty patients, and 20 hip fracture patients) and assayed their PLP status by high performance liquid chromatography. The reference range derived from the out-patients was 13-106 nmol/L. 3 of the arthroplasty group and 10 of the fracture group had serum PLP concentrations less than 13 nmol/L (P < 0.01). We conclude that PLP may be an etiologic factor in hip fracture by virtue of its role in the activity of a key regulatory protein.

摘要

大鼠体内维生素B6缺乏可能导致骨形成缺陷,这可能是由于鸟氨酸脱羧酶活性降低所致,该酶需要磷酸吡哆醛(PLP)作为辅因子,并负责产生细胞内腐胺(一种代谢调节物)。我们研究了3组患者(62名健康的门诊患者、21名择期关节置换术患者和20名髋部骨折患者),并通过高效液相色谱法测定了他们的PLP状态。门诊患者的参考范围为13 - 106 nmol/L。关节置换术组中有3名患者和骨折组中有10名患者的血清PLP浓度低于13 nmol/L(P < 0.01)。我们得出结论,PLP可能因其在关键调节蛋白活性中的作用而成为髋部骨折的一个病因。

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