Kobayashi A, Kawai S, Ohkubo M, Ohbe Y
Arch Dis Child. 1979 May;54(5):367-70. doi: 10.1136/adc.54.5.367.
Serum 25-hydroxy-vitamin D (25-OHD) concentrations were measured in 49 patients with hepatobiliary disease in infancy. Low mean values were found in groups of patients with biliary atresia, neonatal hepatitis, choledochal cyst, and chronic intrahepatic cholestatic syndrome. In the group of patients with surgically repaired biliary atresia, the mean value did not differ from normal. Parenteral vitamin D increased 25-OHD in serum in patients with biliary atresia, but did not do so in one patient with neonatal hepatitis. In contrast, oral vitamin D did not increase serum 25-OHD concentrations in patients with biliary atresia. It is concluded that the reduction of serum 25-OHD seen in biliary atresia was largely due to the malabsorption of vitamin D, while in neonatal hepatitis it was due to impairment of 25-hydroxylation of the vitamin.
对49例婴儿期肝胆疾病患者的血清25-羟维生素D（25-OHD）浓度进行了测定。在患有胆道闭锁、新生儿肝炎、胆总管囊肿和慢性肝内胆汁淤积综合征的患者组中发现平均水平较低。在接受手术修复的胆道闭锁患者组中，平均值与正常水平无差异。肠外维生素D可使胆道闭锁患者血清中的25-OHD升高，但1例新生儿肝炎患者未出现这种情况。相比之下，口服维生素D并不能使胆道闭锁患者的血清25-OHD浓度升高。得出的结论是，胆道闭锁中所见血清25-OHD的降低主要是由于维生素D吸收不良，而在新生儿肝炎中则是由于维生素25-羟化受损。
