Choline deficiency causes reversible hepatic abnormalities in patients receiving parenteral nutrition: Proof of a human choline requirement: A placebo-controlled trial

A. L. Buchman, M. E. Ament, M. Sohel, M. Dubin, D. J. Jenden, M. Roch, H. Pownall, W. Farley, M. Awal, C. Ahn

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Abstract

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 liverspleen 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.

Original languageEnglish (US)
Pages (from-to)260-268
Number of pages9
JournalJournal of Parenteral and Enteral Nutrition
Volume25
Issue number5
StatePublished - 2001

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Choline Deficiency
Parenteral Nutrition
parenteral feeding
choline
Choline
placebos
Placebos
liver
Liver
total parenteral nutrition
Total Parenteral Nutrition
blood serum
Home Total Parenteral Nutrition
Serum
gamma-glutamyltransferase
Transferases
Aspartate Aminotransferases
bilirubin
Alanine Transaminase
Bilirubin

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Food Science

Cite this

Choline deficiency causes reversible hepatic abnormalities in patients receiving parenteral nutrition : Proof of a human choline requirement: A placebo-controlled trial. / Buchman, A. L.; Ament, M. E.; Sohel, M.; Dubin, M.; Jenden, D. J.; Roch, M.; Pownall, H.; Farley, W.; Awal, M.; Ahn, C.

In: Journal of Parenteral and Enteral Nutrition, Vol. 25, No. 5, 2001, p. 260-268.

Research output: Contribution to journalArticle

Buchman, A. L. ; Ament, M. E. ; Sohel, M. ; Dubin, M. ; Jenden, D. J. ; Roch, M. ; Pownall, H. ; Farley, W. ; Awal, M. ; Ahn, C. / Choline deficiency causes reversible hepatic abnormalities in patients receiving parenteral nutrition : Proof of a human choline requirement: A placebo-controlled trial. In: Journal of Parenteral and Enteral Nutrition. 2001 ; Vol. 25, No. 5. pp. 260-268.
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title = "Choline deficiency causes reversible hepatic abnormalities in patients receiving parenteral nutrition: Proof of a human choline requirement: A placebo-controlled trial",
abstract = "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 liverspleen 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.",
author = "Buchman, {A. L.} and Ament, {M. E.} and M. Sohel and M. Dubin and Jenden, {D. J.} and M. Roch and H. Pownall and W. Farley and M. Awal and C. Ahn",
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TY - JOUR

T1 - Choline deficiency causes reversible hepatic abnormalities in patients receiving parenteral nutrition

T2 - Proof of a human choline requirement: A placebo-controlled trial

AU - Buchman, A. L.

AU - Ament, M. E.

AU - Sohel, M.

AU - Dubin, M.

AU - Jenden, D. J.

AU - Roch, M.

AU - Pownall, H.

AU - Farley, W.

AU - Awal, M.

AU - Ahn, C.

PY - 2001

Y1 - 2001

N2 - 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 liverspleen 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.

AB - 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 liverspleen 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.

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