Essential fatty acid deficiencies in patients with chronic liver disease are not reversed by short-term intravenous lipid supplementation
- PMID: 10489916
- DOI: 10.1023/a:1026683214681
Essential fatty acid deficiencies in patients with chronic liver disease are not reversed by short-term intravenous lipid supplementation
Abstract
The purpose of this study was to determine the plasma triglyceride and phospholipid fatty acid (FA) composition of severely malnourished patients with chronic liver disease and to examine the effects of parenteral nutrition with a total nutrient admixture (TNA) on these profiles. Nine consecutive patients with end-stage chronic liver disease were compared with 35 patients admitted for elective surgery of upper gastrointestinal malignancy. Baseline laboratory values and the FA profiles of the plasma triglyceride and phospholipids were analyzed. FA profiles were also performed after infusion of a TNA including 33+/-7 g of lipid/24 hr for 7.9+/-4 days in the patients with chronic liver disease. Compared with control patients, the plasma phospholipid fatty acid analysis results (relative mole percentage) of patients with chronic liver disease were significantly lower in the two essential FA, linoleic acid (15.4+/-3.4% vs. 20.8+/-2.9%, P<0.001) and alpha-linolenic acid (0.02+/-0.05% vs. 0.08+/-0.10%, P<0.001). Similar changes were demonstrated in the FA composition of the triglyceride fraction. Short-term infusion of intravenous lipid resulted in a significant increase in linoleic acid in the triglyceride fraction (9.9+/-2.8% before supplementation vs. 20.7+/-9.4% after supplementation, P<0.01) and a decrease in oleic acid (38.7+/-5.2% before supplementation vs. 29.3+/-7.5 after supplementation, P<0.01). In conclusion, acute and chronic deficiencies of essential FA occurs in patients with chronic liver disease. The clinical significance of these deficiencies is unknown, but they potentially may impact on eicosanoid metabolism. Short-term supplementation with modest amounts of intravenous lipid has only a minimal effect on normalization of longer-chain fatty acids.
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