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Bile acids in serum and bile of infants with cholestatic syndromes
Insights
Bile acid ratios in infants with cholestasis can indicate liver injury. Cholestyramine may help diagnose bile duct patency in cholestasis, differentiating conditions like neonatal hepatitis syndrome and biliary atresia.
Area of Science:
- Pediatric Gastroenterology
- Hepatology
- Biochemistry
Background:
- Cholestasis in neonates and infants presents diagnostic challenges.
- Bile acid profiles in serum can reflect liver function and biliary status.
Purpose of the Study:
- To analyze serum bile acid concentrations and ratios in infants with various cholestatic conditions.
- To evaluate the diagnostic utility of cholestyramine in assessing bile duct patency.
Main Methods:
- Serum bile acid concentrations (individual and total) were measured.
- The cholate/chenodeoxycholate ratio was analyzed in relation to clinical conditions.
- Cholestyramine was administered to assess its effect on bile acid levels and ratios.
Main Results:
- The cholate/chenodeoxycholate ratio was <1 in neonatal hepatitis syndrome and extrahepatic biliary atresia, indicating liver cell injury.
- The ratio was >1 in chronic intrahepatic cholestasis.
- Cholestyramine administration decreased total bile acids and increased the cholate/chenodeoxycholate ratio in patients with patent bile ducts.
- 3beta-hydroxy-5-cholenoic acid was detected in serum but not bile, suggesting impaired biliary excretion.
Conclusions:
- Serum bile acid patterns, particularly the cholate/chenodeoxycholate ratio, can differentiate cholestatic conditions in infants.
- Cholestyramine may serve as a diagnostic tool for evaluating bile duct patency.
- Elevated 3beta-hydroxy-5-cholenoic acid in serum points to impaired biliary excretion as a cause of cholestasis.
Abstract:
The concentration of individual bile acids in serum was measured in 18 neonates and infants with various cholestatic conditions (extrahepatic biliary atresia, neonatal hepatitis syndrome, chronic intrahepatic cholestasis and posthemolytic cholestasis). The cholate/chenodeoxycholate ratio in serum was smaller than one in all patients with neonatal hepatitis syndrome or extrahepatic biliary atresia, cholestatic conditions which were accompanied by signs of liver cell injury. It was greater than one in the patients with chronic intrahepatic cholestasis. Administration of cholestyramine to patients with patent extrahepatic bile ducts decreased the total concentration bile acids in serum and elevated the cholate/chenodeoxycholate ratio. Thus, cholestyramine administration may be of diagnostic value for evaluation of bile duct patency in cholestasis of infancy. Differences between the bile acid pattern in serum and bile were observed. Thus, the cholate/chenodeoxycholate ratio was always higher in bile than in serum. 3beta-hydroxy-5-cholenoic acid found in serum was not detectable in bile. This finding suggests that impairment of biliary excretion rather than increased hepatic synthesis is responsible for elevation of this monohydroxy bile acid in serum.