Journal of Okayama Medical Association
Published by Okayama Medical Association

Full-text articles are available 3 years after publication.

硫酸抱合型bilirubinに関する研究 第2編 各種肝疾患患者の胆汁中bilirubin sulfate分画の臨床的意義

渡部 寛 岡山大学医学部第一内科教室
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Clinical significance of the components of direct bilirubin in bile was investigated on the basis of the relation between bilirubin sulfate fraction in bile and serological liver function tests in various liver diseases. Forty-three examined cases were consisted of eight cases with cholecystopathy, seven cases with acute hepatitis, nine cases with chronic hepatitis, seven cases with cirrhosis of the liver, four cases with Gilbert's syndrome and eight normal subjects, and their bile were collected with duodenal tube. The sulfate radical in direct bilirubin was quantitatively determined by Weber & Schalm's method and the molar ratio of sulfate radical to bilirubin was calculated. The following results were obtained. 1) No difference was observed between male and female, and among the age of patients on the molar ratios of sulfate to bilirubin. 2) The molar ratio of glucuronic acid to ester-form bilirubin was inversely proportional to that of sulfate radical to direct bilirubin. 3) The mean molar ratio of sulfate radical to direct bilirubin was found to be 0.10 in normal subjects, 0.08 in the cases with cholecystopathy, 0.27 in chronic hepatitis, 0.39 in acute hepatitis, 0.51 in liver cirrhosis and 0.48 in Gilbert's syndrome. The each values of liver diseases was significantly higher than normal subjects, and no difference between normal subjects and the cases with cholecystopathy. 4) Significant correlation was observed between the molar ratio of sulfate radical to direct bilirubin and following items, that is, ZnTT, TTT and γ-globulin; but no correlation between the molar ratio of sulfate radical to direct bilirubin and S-GOT, S-GPT, serum alkaline phosphatase, serum bilirubin and BSP retention test. These results suggest that the sulfate conjugation of bilirubin was compensated as compared to the disturbance of glucuronide formation of bilirubin in liver parenchymal damage.