Plasma concentrations of transsulfuration pathway products during nasoenteral and intravenous hyperalimentation of malnourished patients

Abstract

We have monitored the plasma concentrations of products of the transsulfuration pathway in 11 undernourished noncirrhotic patients, and in 10 cachectic cirrhotic subjects, before and during nasoenteral nutrition with Vivonex (Norwich-Eaton Pharmaceuticals, Norwich, NY) or total parenteral nutrition (TPN) with FreAmine III (American McGaw, Irvine, CA). In the cirrhotic cases eating a mixed diet, levels of taurine, cysteine, plasma glutathione, and free choline were subnormal. During nasoenteral hyperalimentation, methionine was elevated while cysteine, glutathione, and free choline levels remained depressed. During TPN, levels of taurine, cysteine, protein-bound cysteine, glutathione, free choline, and phosphatidyl choline were depressed and methionine was elevated. In the noncirrhotic cases eating a mixed diet, only the free choline concentration was low. During nasoenteral hyperalimentation, the plasma levels of both free choline and total carnitine were depressed. During TPN, plasma levels of cystine, protein-bound cysteine, total carnitine, free choline, and phosphatidyl choline were subnormal. These data suggest that biosynthesis of several products of the transsulfuration pathway may be inadequate in both cirrhotic and noncirrhotic patients during TPN with FreAmine III.

Appropriate Protein and Specific Amino Acid Delivery Can Improve Patient Outcome: Fact or Fantasy?

“…There is some evidence to support that this choline deficiency plays a role in the hepatic impairment seen in patients on longterm PN. Enteral repletion of choline to prevent or treat PN-induced hepatic failure is currently under research and shows a lot of promise [53].…”

Choline Deficiency During Parenteral Nutrition in Humans

“…Lipid emulsion supplied a very minimal amount of choline (24 Ϯ 6 nmol/mL) and therefore is an inadequate source of choline for patients requiring long-term home TPN. 25 Chawla et al 40 …”

“…39 It was also assumed that this nutrient could be synthesized from methionine (contained in the TPN solution) through the hepatic transsulfuration pathway. However, several studies have suggested that the transsulfuration pathway is impaired or nonfunctional in patients receiving TPN; 24,40 choline deficiency may result. The Food and Nutrition Board of the National Academy of Sciences designated an adequate intake for choline in 1998 for the first time.…”

The Depression of Hepatic Drug Conjugation Reactions in Rats After Lipid‐Free Total Parenteral Nutrition Administered via the Portal Vein

“…methionine has been shown to be inhibited during TPN. 36 Additionally, sulfoester excretion products have been shown to decrease in infants receiving a TPN diet that was deficient in inorganic sulfate but not sulfur-containing amino acids.37 Therefore, it is possible that decreased PAPS availability could be responsible for the observed decrease in sulfation during TPN. Plasma sulfate concentrations measured before acetaminophen administration, however, were higher in the group receiving TPN, suggesting that initial sulfate availability was not a factor in the decrease in acetaminophen sulfation seen in vivo in the TPN animals.…”