GRP-129 Parenteral Nutrition-Associated Cholestasis
Background Parenteral nutrition-associated cholestasis (PNAC) results in significant morbidity and mortality. Progression to end-stage liver disease and subsequent hepatic failure is the most feared complication. A number of approaches have been proposed for the prevention and treatment of PNAC with mixed results.
Purpose To investigate the alteration of liver blood tests and the parenteral nutrition (PN) characteristics that trigger PNAC.
Materials and Methods Clinical blood tests and PN data of adults on artificial nutrition from January to August 2012 were collected.
Survival studies were conducted for each liver parameter studied. Primary endpoint was to fall above the upper limit of normal, considering them for women and men respectively: aspartate transaminase (ASP): 32, 40 IU/L; Alanine transaminase (ALT): 78, 78 IU/L; gamma-glutamyl transferase (GGT): 55, 85 IU/L; alkaline phosphatase (ALP): 136, 129 IU/L; bilirubin: <1, <1 mg/dl.
PASW Statistics 19.0 and Microsoft Office 2007 were used.
Results One thousand eight hundred and ten PN bags for 124 patients (55% men) with mean 61 years old (18–95) were analysed.
Percentage of patients with values within limits after follow-up: bilirubin 92%; ALT 76%; ASP 59%; ALP 54%; GGT 27%.
Time until values went out of normal limits (days): ALT (13); ALP (13); ASP (12); bilirubin (12); GGT (6).
Age, gender, liver enzymes value before PN, and PN characteristics (volume, timing of infusions, calories, nitrogen and carbohydrates) were not significant PNAC trigger factors when considered individually.
Risk factor: initial value of bilirubin (each 0.1 mg/dL before PN, multiplies the risk of hyperbilirubinaemia by 14.5 times).
Protective factor: PN fat content (each gramme reduces the risk of high serum GGT concentration by 3.6%).
Conclusions The results show that PN poses a risk factor for PNAC, GGT being the test most affected.
However, none of the factors surrounding the PN and the patient, individually, account for the majority of the liver damage. On the contrary it is a conglomerate of different factors contributing to the final impairment. The lack of enteral nutrition also predisposes to PNAC.
This makes it difficult to find the right approach when prescribing PN. The indications for PN should be considered responsibly as should a return to enteral feeding whenever possible.
No conflict of interest.