Bordier P, Zingraff J, Gueris J, Jungers P, Marie P, Pechet M, Rasmussen H
Am J Med. 1978 Jan;64(1):101-7. doi: 10.1016/0002-9343(78)90184-5.
Six patients with chronic renal disease and variable degrees of renal osteodystrophy were treated for three weeks with either 1alpha,25-dihydroxyvitamin D3 (1alpha25(OH)D3) or 1alpha,hydroxyvitamin D3 (1alpha(OH)D3) and both the biochemical and osseous responses measured. The most consistent changes seen were an increase in serum calcium concentration to normal, a decrease in immunoreactive parathyroid hormone toward normal, an increase in the extent of the calcification front and a decrease in the extent of fibrous dysplasia in the marrow cavity. Two important parameters which did not change significantly were serum alkaline phosphatase activity and the osteoid volume. These data, in conjunction with that from previous studies, indicate that therapy with 1alpha,25(OH)2D3 or 1alpha(OH)D3 does not heal the osteomalacia of renal osteodystrophy, but that it does suppress the secondary hyperparathyroidism, and ameliorate the osteitis fibrosa seen in patients with chronic renal disease. They raise the likelihood that additional factors, such as metabolites of vitamin D other than 1alpha,25(OH)2D3, play a role in regulating bone formation and/or mineralization.
六名患有慢性肾病且伴有不同程度肾性骨营养不良的患者,分别接受了为期三周的1α,25 - 二羟维生素D3(1α25(OH)D3)或1α - 羟维生素D3(1α(OH)D3)治疗,并对生化反应和骨反应进行了测量。观察到的最一致变化包括血清钙浓度升高至正常水平、免疫反应性甲状旁腺激素降至正常水平、钙化前沿范围增加以及骨髓腔内纤维发育异常范围减小。两个未显著变化的重要参数是血清碱性磷酸酶活性和类骨质体积。这些数据与先前研究的数据相结合,表明用1α,25(OH)2D3或1α(OH)D3治疗并不能治愈肾性骨营养不良的骨软化症,但确实能抑制继发性甲状旁腺功能亢进,并改善慢性肾病患者出现的纤维性骨炎。它们增加了其他因素(如1α,25(OH)2D3以外的维生素D代谢产物)在调节骨形成和/或矿化过程中发挥作用的可能性。