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Liver Test Alterations With Total Parenteral Nutrition and Nutritional Status

Department of Dietetics and Nutrition, The University of Kansas Medical Center, Kansas City

Norma J. Winn, MS, RD

Department of Dietetics and Nutrition, The University of Kansas Medical Center, Kansas City

Paul R. Schloerb, MD

Department of Surgery, The University of Kansas Medical Center, Kansas City

Liver test abnormalities are a well-recognized complication in the parenterally fed population. Numerous etiologies for the development of elevated liver tests have been suggested. However, the etiology and clinical significance remain unclear. The aim of this retrospective study was to determine the extent of liver-associated test (LAT) abnormalities in patients receiving total parenteral nutrition (TPN) and to investigate whether the composition of TPN solutions and the magnitude of malnutrition could be used to predict subsequent LAT abnormalities. Medical records of 78 adult patients who received TPN for at least 2 weeks were reviewed. All subjects had normal LAT results before TPN, were not receiving hepatotoxic drugs, and had no underlying liver disease. Aspartate aminotransferase peaked transiently during week 2 and returned to normal during week 4. Alkaline phosphatase and total bilirubin peaked during weeks 4 and 3, respectively. The average nonprotein kilocalorie distribution was approximately 80% dextrose and 20% lipid. Caloric intake ranged from 7% to 23% above estimated needs. The mean nutritional status score was 22 ± 15, with a possible range of 0 to 75 (0 indicates no malnutrition). The composition of TPN solutions was not significantly associated with the changes in the three LATs during any week of the 4-week study. The nutritional status score was significantly associated (p < .05) with the change in alkaline phosphatase during week 1. This study confirms that LAT abnormalities occur during TPN, but the composition of the solution has no significant ability to predict subsequent LAT abnormalities. Factors associated with cholestasis may have contributed to the LAT abnormalities in this group of subjects because the pattern of LAT elevations suggested cholestasis more than hepatocellular damage. The magnitude of malnutrition before TPN may identify patients likely to develop early alkaline phosphatase abnormalities. (Journal of Parenteral and Enteral Nutrition 16:348-352, 1992)

Journal of Parenteral and Enteral Nutrition, Vol. 16, No. 4, 348-352 (1992)
DOI: 10.1177/0148607192016004348


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