Jung R T, Davie M, Siklos P, Chalmers T M, Hunter J O, Lawson D E
Gut. 1979 Oct;20(10):840-7. doi: 10.1136/gut.20.10.840.
To study the effects of acute and chronic cholestasis on vitamin D metabolism we investigated six cases of acute extrahepatic obstructive jaundice and eight cases of primary biliary cirrhosis (PBC) (three supplemented with vitamin D). Plasma 25-hydroxyvitamin D (25OHD) was low in the patients with PBC unsupplemented with vitamin D but normal in obstructive jaundice. None of the patients with PBC showed radiological or histological evidence of osteomalacia. In PBC, dietary intake of vitamin D was low but response to ultra-violet irradiation of the skin was normal even in those with a considerably raised serum bilirubin. Patients with PBC or obstructive jaundice had low levels of 25 hydroxyvitamin D binding protein which correlated with the serum albumin. The half-life of intravenously injected (3)H vitamin D(3) ((3)HD(3)) and the subsequent production of (3)H 25OHD were normal in all the patients with obstructive jaundice and in most with PBC. The two patients with PBC who produced less (3)H 25OHD than expected were receiving vitamin D supplements. The urinary tritium ((3)H) excretion after the injection of (3)HD(3) correlated with the serum bilirubin. After the injection of (3)H 25OHD(3) the urinary excretion of (3)H was minimal and did not correlate with the serum bilirubin, suggesting that the radioactivity appearing in the urine after the (3)H vitamin D(3) injection was associated with vitamin D metabolites other than 25OHD. Factors contributing to the low plasma 25OHD in primary biliary cirrhosis may be a low dietary intake of vitamin D, inadequate exposure to ultra-violet light, and a tendency to urinary wastage of vitamin D metabolites.
为研究急慢性胆汁淤积对维生素D代谢的影响，我们调查了6例急性肝外阻塞性黄疸患者和8例原发性胆汁性肝硬化（PBC）患者（其中3例补充了维生素D）。未补充维生素D的PBC患者血浆25-羟维生素D（25OHD）水平较低，但阻塞性黄疸患者的该水平正常。PBC患者均未显示出骨软化症的影像学或组织学证据。在PBC中，维生素D的饮食摄入量较低，但即使是血清胆红素大幅升高的患者，其皮肤对紫外线照射的反应仍正常。PBC或阻塞性黄疸患者的25羟维生素D结合蛋白水平较低，且与血清白蛋白相关。在所有阻塞性黄疸患者及大多数PBC患者中，静脉注射（3）H维生素D3（（3）HD3）的半衰期及随后（3）H 25OHD的生成均正常。两名产生的（3）H 25OHD低于预期的PBC患者正在接受维生素D补充剂治疗。注射（3）HD3后尿氚（（3）H）排泄与血清胆红素相关。注射（3）H 25OHD3后，尿（3）H排泄极少，且与血清胆红素无关，这表明注射（3）H维生素D3后尿中出现的放射性与25OHD以外的维生素D代谢产物有关。原发性胆汁性肝硬化患者血浆25OHD水平低的因素可能包括维生素D饮食摄入量低、紫外线暴露不足以及维生素D代谢产物经尿液浪费的倾向。
