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Chronic liver disease in children on long-term parenteral nutrition
S Misra1, M E Ament, J H Vargas
1Division of Pediatric Gastroenterology and Nutrition, UCLA Medical Center 90095-1752, USA.
Insights
Long-term total parenteral nutrition (TPN) is generally thought to cause liver problems. However, this study found that severe liver dysfunction is uncommon in patients receiving TPN for over 2.5 years.
Area of Science:
- Hepatology
- Gastroenterology
- Pediatric Nutrition
Background:
- Long-term total parenteral nutrition (TPN) is frequently associated with hepatic dysfunction.
- The actual incidence and severity of liver issues in patients on extended TPN remain a concern.
Purpose of the Study:
- To investigate the prevalence and characteristics of liver dysfunction in patients receiving TPN for over 2.5 years.
- To assess the relationship between TPN duration and severity of liver disease in pediatric and adult patients.
Main Methods:
- Retrospective chart review of patients on TPN for >2.5 years.
- Analysis of liver function tests, clinical signs of hepatomegaly/splenomegaly, and liver biopsy results.
- Evaluation of hepatic synthetic function markers (albumin, pre-albumin, prothrombin time).
Main Results:
- Most patients (21/26) had normal transaminases; some had past enzyme elevations.
- While some had abnormal bilirubin levels, only one patient experienced hepatic decompensation.
- Liver biopsies revealed varying degrees of pathology, including cirrhosis and fibrosis, but TPN was not solely implicated.
Conclusions:
- Clinical hepatic failure is rare in patients on long-term TPN (>2.5 years).
- Pathological findings like cirrhosis and fibrosis may not be solely attributable to TPN.
- Further research is needed to elucidate the multifactorial causes of liver disease in TPN-dependent patients.
Abstract:
Use of long-term total parenteral nutrition (TPN) is often presumed to be associated with serious hepatic dysfunction. In this retrospective study, we reviewed the complete charts of patients who had received TPN for more than 2.5 years, starting in infancy or childhood, for evidence of liver dysfunction. There were 16 male and 10 female patients with a total of 254.5 patient years on TPN. Seventeen patients have been on TPN since birth or early infancy. Thirteen of 26 patients derive > or = 90% of their calorie intake from TPN. Six patients had hepatomegaly; two of them also had splenomegaly. Twenty-one patients had normal transaminases, nine have had past episodes of raised enzymes ranging from 2.5 to 7.5 times normal. Seventeen patients always had normal bilirubin levels, five had past episodes of hyperbilirubinaemia, while four patients had persistently raised bilirubin levels (range 1.5-20.7 g/dl). Alkaline phosphatase was normal for age in all patients except two. Hepatic synthetic function, as measured by albumin, pre-albumin levels and prothrombin time, was within the normal range in all patients except one. Liver biopsies were performed in eight patients. Two biopsies showed cirrhosis, one showed chronic active hepatitis (CAH) with cholestasis, two patients had fibrosis, one showed cholestasis and two biopsies were normal. One patient with cirrhosis and one with CAH were positive for hepatitis C antibody. Another asymptomatic patient was positive for hepatitis B. Only the patient with CAH had hepatic decompensation. We conclude that clinical hepatic failure is uncommon in our group of patients on long-term TPN for 2.5 years or more. Cirrhosis and fibrosis, when found, could not be solely attributed to TPN.