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Published on: February 19, 2019
Chronic persistent hepatitis and unconjugated hyperbilirubinemia
Gastroenterology
|February 1, 1979
Summary
Chronic persistent hepatitis is linked to reduced hepatic bilirubin UDP-glucuronyltransferase activity, causing unconjugated hyperbilirubinemia. This acquired enzyme defect, distinct from Gilbert's syndrome, is likely related to the hepatitis itself.
Area of Science:
- Hepatology
- Biochemistry
- Gastroenterology
Background:
- Unconjugated hyperbilirubinemia can occur in patients with chronic persistent hepatitis.
- The exact cause of this condition in hepatitis patients is not fully understood.
Purpose of the Study:
- To investigate the activity of hepatic bilirubin UDP-glucuronyltransferase (UGT1A1) in patients with chronic persistent hepatitis and unconjugated hyperbilirubinemia.
- To compare enzyme activity in these patients with normal individuals and those with Gilbert's syndrome.
Main Methods:
- Assayed hepatic bilirubin UDP-glucuronyltransferase activity in 12 patients with chronic persistent hepatitis and mild unconjugated hyperbilirubinemia.
- Compared patient enzyme activity to data from normal subjects, patients with acute hepatitis, and patients with Gilbert's syndrome.
- Examined the incidence of hyperbilirubinemia in first-degree relatives.
Main Results:
- Hepatic bilirubin UDP-glucuronyltransferase activity was significantly lower in patients with chronic persistent hepatitis compared to normal individuals.
- Enzyme activity in chronic persistent hepatitis patients was higher than in patients with Gilbert's syndrome.
- The incidence of hyperbilirubinemia in relatives was lower in chronic persistent hepatitis patients than in Gilbert's syndrome patients.
Conclusions:
- The unconjugated hyperbilirubinemia associated with chronic persistent hepatitis is likely caused by an acquired decrease in hepatic bilirubin UDP-glucuronyltransferase activity.
- This enzyme defect appears to be related to the presence of chronic persistent hepatitis.
- The findings differentiate the mechanism from that of Gilbert's syndrome.
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