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Choline Deficiency Causes Reversible Hepatic Abnormalities in Patients Receiving Parenteral Nutrition: Proof of a Human Choline Requirement: A Placebo-Controlled TrialDivision of Gastroenterology, Hepatology and Nutrition, Northwestern University Medical School, Chicago, a-buchman{at}northwestern.edu
Division of Pediatric Gastroenterology, UCLA School of Medicine, Los Angeles
Division of Gastroenterology, Hepatology and Nutrition, University of Texas Houston Health Science Center, Houston
Department of Radiology, UCLA School of Medicine, Los Angeles
Department of Pharmacology, UCLA School of Medicine, Los Angeles
Department of Pharmacology, UCLA School of Medicine, Los Angeles
Department of Medicine, Baylor College of Medicine, Houston
Department of Medicine, Baylor College of Medicine, Houston
Division of Gastroenterology, Hepatology and Nutrition
Department of Medicine, Northwestern University Medical School, Chicago Background: Previous studies have shown that plasma free choline concentrations are significantly decreased in many long-term home total parenteral nutrition (TPN) patients. Furthermore, low choline status has been associated with both hepatic morphologic and hepatic aminotransferase abnormalities. A preliminary pilot study suggested choline-supplemented TPN may be useful in reversal of these hepatic abnormalities. Methods: Fifteen patients (10 M, 5 F) who had required TPN for >80% of their nutritional needs were randomized to receive their usual TPN (n = 8), or TPN to which 2 g choline chloride had been added (n = 7) for 24 weeks. Baseline demographic data were similar between groups. Patients had CT scans of the liver and spleen, and blood for plasma free and phospholipid-bound choline, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, gamma glutamyl transferase (GGT), bilirubin, serum lipids, complete blood count (CBC), and chemistry profile obtained at baseline, and weeks 2, 4, 6, 12, 16, 20, 24, and 34. CT scans were analyzed for Hounsfield unit (HU) densities. Results: There were no significant differences in any measured parameters after 2 weeks. However, at 4 weeks, a significant difference in liver HU between groups was observed (13.3 ± 5.0 HU [choline] vs 5.8 ± 5.2 HU [placebo], p = .04). This significant trend continued through week 24. Recurrent hepatic steatosis and decreased HU were observed at week 34, 10 weeks after choline supplementation had been discontinued. A significant increase in the liver-spleen differential HU was also observed in the choline group (10.6 ± 6.2 HU [choline] vs 1.3 ± 3.3 HU [placebo], p = .01). Serum ALT decreased significantly (p = .01 to .05) in the choline group vs placebo at weeks 6,12, 20, and 24. Serum AST was significantly decreased in the choline group by week 24 (p = .02). The serum alkaline phosphatase was significantly reduced in the choline group at weeks 2, 12, 20, 24, and 34 (p = .02 to 0.07). Total bilirubin was normal in these patients and remained unchanged during the study. Serum GGT tended to decrease more in the choline group, but the greater decrease was not statistically significant. Conclusions: Choline deficiency is a significant contributor to the development of TPN-associated liver disease. The data suggest choline is a required nutrient for long-term home TPN patients. (Journal of Parenteral and Enteral Nutrition 25:260-268, 2001)
Journal of Parenteral and Enteral Nutrition, Vol. 25, No. 5,
260-268 (2001) This article has been cited by other articles:
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