Mawer E B, Klass H J, Warnes T W, Berry J L
Clin Sci (Lond). 1985 Nov;69(5):561-70. doi: 10.1042/cs0690561.
The metabolism of isotopically labelled vitamin D2 and D3 has been investigated in eight patients with primary biliary cirrhosis and in five controls. The concentration of labelled vitamin D2 was lower than that of vitamin D3 in serum of patients with primary biliary cirrhosis on days 1 and 2 after intravenous injection (P less than 0.005 and P less than 0.05, respectively) but no difference was seen in controls. Similar amounts of labelled 25-hydroxyvitamin D2 and D3 were seen in serum of the control group; the same pattern was observed in the primary biliary cirrhosis group, and no significant differences were observed between the two groups. In both control and primary biliary cirrhosis groups, the serum concentration of labelled 24,25-dihydroxyvitamin D2 exceeded that of 24,25-dihydroxyvitamin D3 (significant for controls on day 2, P less than 0.02) but concentrations in the two groups were not different. Concentrations of labelled 25,26-dihydroxyvitamin D3 were significantly higher than those of 25,26-dihydroxyvitamin D2 in the primary biliary cirrhosis group at all times and in the control group on days 2 and 3. Both 25,26-dihydroxyvitamin D2 and D3 were higher in the serum of patients with primary biliary cirrhosis than in controls (significant on day 1; P less than 0.05). Urinary excretion over days 0-3 of radioactivity from both vitamins D2 and D3 was significantly higher in the primary biliary cirrhosis group than in controls: 12.03 vs 1.80% for vitamin D2 and 8.98 vs 1.76% for vitamin D3 (P less than 0.005). Vitamin D2-derived urinary radioactivity in primary biliary cirrhosis correlated strongly with serum bilirubin (P = 0.005). The metabolism of labelled vitamin D3 was studied in seven patients with alcoholic liver disease, three of whom showed low serum concentrations of labelled 25-hydroxyvitamin D3 suggesting impaired hepatic synthesis. The 25-hydroxylation response was quantified as the relative index of 25-hydroxylation and was significantly related to two other indices of liver function. It is concluded that impaired 25-hydroxylation of vitamin D may occur in alcoholic liver disease and results from hepatocellular dysfunction. Less than the predicted amounts of 1,25-dihydroxyvitamin D3 were produced in four of the seven patients with alcoholic liver disease; this defect may be attributable in part to decreased precursor 25-hydroxyvitamin D and to poor renal function.
对8例原发性胆汁性肝硬化患者和5名对照者进行了同位素标记维生素D2和D3代谢的研究。静脉注射后第1天和第2天，原发性胆汁性肝硬化患者血清中标记维生素D2的浓度低于维生素D3（分别为P<0.005和P<0.05），但对照者未见差异。对照组血清中标记的25-羟基维生素D2和D3含量相似；原发性胆汁性肝硬化组也观察到相同模式，两组之间未观察到显著差异。在对照组和原发性胆汁性肝硬化组中，标记的24,25-二羟基维生素D2的血清浓度均超过24,25-二羟基维生素D3（第2天对照组差异显著，P<0.02），但两组浓度无差异。在原发性胆汁性肝硬化组所有时间以及对照组第2天和第3天，标记的25,26-二羟基维生素D3的浓度均显著高于25,26-二羟基维生素D2。原发性胆汁性肝硬化患者血清中25,26-二羟基维生素D2和D3均高于对照组（第1天差异显著；P<0.05）。原发性胆汁性肝硬化组维生素D2和D3在0 - 3天的放射性尿排泄均显著高于对照组：维生素D2为12.03%对1.80%，维生素D3为8.98%对1.76%（P<0.005）。原发性胆汁性肝硬化中维生素D2来源的尿放射性与血清胆红素密切相关（P = 0.005）。对7例酒精性肝病患者的标记维生素D3代谢进行了研究，其中3例血清中标记的25-羟基维生素D3浓度较低，提示肝脏合成受损。将25-羟化反应量化为25-羟化的相对指数，其与肝功能的另外两个指标显著相关。结论是酒精性肝病中可能发生维生素D的25-羟化受损，这是由肝细胞功能障碍引起的。7例酒精性肝病患者中有4例产生的1,25-二羟基维生素D3量低于预期；这种缺陷可能部分归因于前体25-羟基维生素D减少和肾功能不良。
