Hordon L D, Peacock M
Department of Rheumatology, General Infirmary, Leeds, England.
Bone Miner. 1987 Aug;2(5):413-26.
Abnormalities in plasma vitamin D metabolites and an increased prevalence of osteomalacia have been described in elderly patients sustaining a fracture of the femoral neck. In order to investigate whether the plasma concentrations of the vitamin D metabolites are normal, and whether vitamin D deficient osteomalacia in patients with femoral fracture can be diagnosed using biochemical criteria alone, we have studied before and after 7 days of 40 micrograms oral 25-hydroxyvitamin D3 elderly patients admitted to hospital with a femoral fracture, elderly patients undergoing elective replacement of the femoral head and elderly control patients in hospital with no clinical evidence of bone disease. Plasma 25-hydroxyvitamin D (25(OH)D) and 24,25-dihydroxyvitamin D increased after 7 days of oral 25-hydroxyvitamin D3 to the same levels in the three groups, but in contrast to the controls there was no significant increase in plasma 1,25-dihydroxyvitamin D or radiocalcium absorption in femoral fracture and hip replacement patients. However, when femoral fracture patients were restudied 6-12 months after fracture, plasma 1,25-dihydroxyvitamin D increased after oral 25-hydroxyvitamin D3 to the same extent as it had in the control patients. We conclude that reduced calcium absorption due to low plasma 25(OH)D levels, i.e., vitamin D insufficiency is common in all elderly patients. Furthermore biochemical criteria for diagnosis of vitamin D-deficient osteomalacia are of very limited use at the time of fracture in elderly patients since there is a failure of production of 1,25 dihydroxyvitamin D which resolves within 6-12 months of the fracture. This failure makes the 1,25-dihydroxyvitamin D response to oral 25(OH)D an unreliable guide to the presence of vitamin D-deficient osteomalacia at the time of fracture. The abnormality in 1,25-dihydroxyvitamin D is also present in patients undergoing hip replacement surgery, and is therefore unlikely to be involved in the aetiology of femoral neck fracture. It may, however, contribute to the morbidity after fracture.
股骨颈骨折的老年患者存在血浆维生素D代谢物异常及骨软化症患病率增加的情况。为了研究维生素D代谢物的血浆浓度是否正常,以及单纯使用生化标准能否诊断股骨骨折患者的维生素D缺乏性骨软化症,我们对40微克口服25 - 羟基维生素D3治疗7天前后的股骨骨折老年住院患者、接受股骨头择期置换术的老年患者以及无骨病临床证据的老年对照住院患者进行了研究。口服25 - 羟基维生素D3 7天后,三组患者的血浆25 - 羟基维生素D(25(OH)D)和24,25 - 二羟基维生素D均升高至相同水平,但与对照组相比,股骨骨折和髋关节置换患者的血浆1,25 - 二羟基维生素D或放射性钙吸收无显著增加。然而,当股骨骨折患者在骨折后6 - 12个月重新进行研究时,口服25 - 羟基维生素D3后血浆1,25 - 二羟基维生素D升高的程度与对照患者相同。我们得出结论,由于血浆25(OH)D水平低导致的钙吸收减少,即维生素D不足在所有老年患者中都很常见。此外,在老年患者骨折时,诊断维生素D缺乏性骨软化症的生化标准用途非常有限,因为存在1,25 - 二羟基维生素D生成障碍,而这种障碍在骨折后6 - 12个月内会消失。这种障碍使得1,25 - 二羟基维生素D对口服25(OH)D的反应在骨折时不能可靠地指导维生素D缺乏性骨软化症的存在。1,25 - 二羟基维生素D的异常在接受髋关节置换手术的患者中也存在,因此不太可能参与股骨颈骨折的病因。然而,它可能导致骨折后的发病率增加。