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Protein-energy malnutrition is associated with cardiac atrophy and adaptive reduction in cardiac output.Refeeding increases cardiac output and oxygen consumption. Rapid refeeding of severely malnourished patients can precipitate heart failure. Micronutrient deficiencies also contribute to cardiac dysfunction. Cardiac failure can cause weight loss and malnutrition. The most extreme degrees of cardiac malnutrition occur in patients with right heart failure and tricuspid incompetence. These patients have increased mortality but feeding protein and energy does not improve cardiac function. The hearts in patients with cardiac failure have mitochondrial dysfunction and these mitochondria are depleted of carnitine, coenzyme Q10 and taurine. The severity of depletion is related to the severity of heart failure. In controlled trials, repletion of carnitine and coenzyme Q10 improves outcome. Furthermore, in heart failure oxidative stress is increased and there may be thiamin deficiency. It is proposed that the nutritional therapy of heart failure should be directed to the replacement of carnitine, coenzyme Q10 and taurine as well as antioxidants and thiamin rather than protein-energy.

Thrombosis is a common sequela of total parenteral nutrition. We have recently demonstrated in vitro that hypertonic total parenteral nutrition solutions are potent inducers of a tissue factor monocyte procoagulant activity, the initiating cofactor of the extrinsic clotting cascade. We have further studied, in vitro, the effects of the component solutions of total parenteral nutrition on the induction and modulation of endothelial cell procoagulant activity. Cultured porcine aortic endothelial cells were incubated with (a) 200 μl of dextrose solution (5%, 10%, 20%, 25%, and 50%), (b) 200 μl of amino acid solution [full strength (N), one-fourth strength, and one-half strength], and (c) 200 μl of 10% lipid emulsion. Cocultures of lipid emulsion and 20% dextrose, lipid emulsion and full-strength 10% amino acid solution (N-amino acid), and lipid emulsion and bacterial lipopolysaccharide also were studied. Cells were incubated for intervals of 3–108 h, washed and frozen, harvested, and assayed for endothelial cell procoagulant activity. Units of endothelial cell procoagulant activity were derived from a standard thromboplastin curve. Our results show that amino acid and hypertonic dextrose total parenteral nutrition solutions are able to strongly induce endothelial cell procoagulant activity expression in vitro. In contrast, lipid emulsion significantly inhibited the induction of endothelial cell procoagulant activity by 20% dextrose, N-amino acid, and lipopolysaccharide. These results provide further evidence for the role of the cellular pathways of coagulation in total parenteral nutritioninduced thrombosis. Furthermore, the inhibitory properties of lipid emulsion may be of practical advantage in reducing total parenteral nutritioninduced thrombosis.

Although thrombosis is a frequent complication of total parenteral nutrition (TPN), its pathogenesis has received little scientific attention. We have studied, in vitro, the effects of the component solutions of TPN on the induction and modulation of human monocyte procoagulant activity, an initiator of coagulation. Human peripheral blood mononuclear cells were cultured with (a) 200 μl of dextrose solution (10%, 15%, 20%, 25%, and 50%), (b) 200 μl of amino acid solution (full, one-half, and onequarter strength), and (c) 200 μl of isosmolar 10% lipid emulsion (LE). Cocultures of LE and 20% dextrose, LE and full-strength amino acid solution, and LE and bacterial lipopolysaccharide were also studied. Cells cultured with lipopolysaccharide or medium alone constituted positive and negative controls, respectively. In addition, cocultures of LE and 20% dextrose, LE and full-strength amino acid solution, and LE and lipopolysaccharide were also studied. Cells were incubated for intervals of 12–72 h, washed, frozen, and assayed for monocyte procoagulant activity (MPCA). Milliunits of MPCA were derived from a standard thromboplastin curve. In addition, spontaneous MPCA levels were measured in healthy volunteers (n = 4) and “home” total parenteral nutrition patients (n = 4) before and after a 2-h infusion of 500 ml of LE. Our results show that, in vitro, hypertonic dextrose and fullstrength amino acid solutions induce significant levels of MPCA. Induction of MPCA by dextrose was lymphocyte-independent. Although a significant increase in MPCA by full-strength amino acid solution was seen in cultures of isolated monocytes, a lymphocyte requirement was demonstrated for full MPCA. In contrast, LE significantly inhibited the induction of MPCA by 20% dextrose and fullstrength amino acid solution. This inhibitory activity was at the monocyte level. Subfractionation of the LE into triglyceride and phospholipid phases showed the inhibitory capacity to reside in the former. In vivo, patients on home total parenteral nutrition expressed higher spontaneous MPCA levels than normal controls. Ten percent lipid emulsion infusion abolished MPCA expression in both groups. These corroborative in vitro and in vivo data suggest a mechanism for the thrombogenicity of total parenteral nutrition solutions and that the inhibitory properties of LE may be of practical advantage in preventing thrombosis.

Patients with chronic diarrhea not due to pathogens, anatomical lesions of the small bowel, or lesions of the colon were studied