SERUM BILE ACIDS IN PREMATURE INFANTS WITH TPN- ASSOCIATED LIVER DISEASE

Abstract

The etiology of the cholestasis and/or hepatocellular damage observed in some children on total parenteral nutrition (TPN) remains undefined. Although amino acid imbalance in the infused solution has been implicated, we have not demonstrated any consistent correlation between serum amino acids and liver disease. However, because of the unresolved question of the role of bile acids in the pathogenesis of the condition, we studied bile acids in 8 premature infants on a Freamine II-Intralipid-based solution and were able to separate them into two groups. Four developed hepatomegaly, marked elevations in serum enzymes (SGPT, LAP, GGT), and hyperbilirubinemia. Liver biopsies were obtained from 3 of the 4, and demonstrated canalicular cholestasis. The other 4 demonstrated less pronounced increases in serum enzymes and bilirubin, no clinically demonstrable hepatomegaly, and were not biopsied. Quantitative serum bile acids determined by TLC in the two groups demonstrated a 50% increase in serum levels of unconjugated, secondary bile acids (CDC, DOC, LiC) in the more severely affected group. Although this proves no cause-effect relationship between TPN-associated liver disease and serum bile acids, it documents a distinct difference in the serum bile acid concentrations of those infants with frank liver disease and others with only biochemical changes.