Reynolds T M, Marshall P D, Brain A M
Department of Medical Biochemistry, Cardiff Royal Infirmary, UK.
Acta Orthop Scand. 1992 Dec;63(6):635-8. doi: 10.1080/17453679209169725.
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.
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。
