Delvin E E, Glorieux F H
Calcif Tissue Int. 1981;33(2):173-5. doi: 10.1007/BF02409431.
Fasting serum 1 alpha, 25-dihydroxyvitamin D [1,25-(OH)2D] levels were measured in 3 groups of hypophosphatemic vitamin D-resistant rickets (VDRR) patients; those untreated; those treated with vitamin D and phosphate; and those treated with 1,25-(OH)2D3 and phosphate. In the untreated patients, the mean 1,25-(OH)2D level was higher than in our age-matched control group. Except for one at 66 pg/ml, individual values were however within normal limits. Long term vitamin D2 therapy was accompanied by a slight but significant decrease in 1,25-(OH)2D concentrations; nonetheless the levels remained within the normal range. In the third group of patients, the concentration of 1,25-(OH)2D rose to supranormal levels when sampling was done 1-3 hours after administration of the hormone, decreasing rapidly to levels below that of normal subjects when the specimens were collected 12-24 hours later. Our data show that an alteration of the vitamin D activation pathway is unlikely to be part of the pathogenic mechanism underlying the VDRR condition.
对三组低磷性维生素D抵抗性佝偻病（VDRR）患者测定了空腹血清1α,25 - 二羟维生素D [1,25-(OH)₂D]水平；未治疗组；维生素D和磷酸盐治疗组；以及1,25-(OH)₂D₃和磷酸盐治疗组。在未治疗的患者中，平均1,25-(OH)₂D水平高于年龄匹配的对照组。然而，除了一名患者为66 pg/ml外，个体值均在正常范围内。长期维生素D₂治疗伴随着1,25-(OH)₂D浓度轻微但显著下降；尽管如此，水平仍保持在正常范围内。在第三组患者中，给药后1 - 3小时采样时，1,25-(OH)₂D浓度升至超正常水平，12 - 24小时后采集标本时迅速降至低于正常受试者的水平。我们的数据表明，维生素D激活途径的改变不太可能是VDRR病症潜在致病机制的一部分。
