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Eicosanoid synthesis in children with cholestatic disease
J Dupont1, O Amédée-Manesme, D Pepin
1Department of Food and Nutrition, Iowa State University, Ames 50011.
Insights
Children with cholestasis show essential fatty acid deficiency, impacting eicosanoid metabolism. Supplementation trials did not significantly improve linoleate absorption or eicosanoid synthesis in these patients.
Area of Science:
- Biochemistry
- Pediatric Gastroenterology
- Nutrition Science
Background:
- Cholestasis in children can lead to malabsorption of dietary triglycerides, potentially causing essential fatty acid deficiencies.
- Essential fatty acids are crucial precursors for eicosanoids, which play vital roles in various physiological processes.
Purpose of the Study:
- To investigate the impact of cholestasis on essential fatty acid composition and eicosanoid synthesis in children.
- To evaluate the efficacy of linoleate supplementation in addressing these deficiencies.
Main Methods:
- Analysis of plasma and platelet fatty acid composition in children with biliary atresia (BA) and paucity of interlobular bile ducts (PILBD).
- Measurement of prostaglandin (PG) and thromboxane (TXB2) synthesis in whole blood samples.
- Assessment of linoleate absorption following structured triglyceride supplementation in a subset of PILBD patients.
Main Results:
- Both BA and PILBD groups exhibited linoleate deficiency (low 18:2 fatty acids).
- PILBD patients showed significantly reduced thromboxane B2 (TXB2) synthesis (<10% of controls).
- Linoleate supplementation in three PILBD cases did not improve plasma linoleate levels or alter eicosanoid synthesis.
Conclusions:
- Essential fatty acid deficiency and altered eicosanoid metabolism are evident in pediatric cholestasis.
- Current linoleate supplementation strategies may be insufficient to correct these metabolic derangements in affected children.
Abstract:
The possibility of malabsorption of triglycerides contained in the diets of children with cholestasis suggests a deficiency of essential fatty acids and, therefore, probable effects on eicosanoid metabolism. Children with either biliary atresia (BA) or syndromatic paucity of interlobular bile ducts (PILBD) were evaluated as to plasma and platelet total lipid fatty acid composition and synthesis of prostaglandins (PG) E1, PGE2, PGI2, PGF2, and thromboxane (TXB2) by whole blood incubated at 37 degrees C for 10 min. In both diseases linoleate deficiency was present as shown by low 18:2 fatty acids in plasma lipids. The children with BA had lower plasma arachidonate than controls but normal eicosanoid synthesis except for excess PGI2. Those with PILBD had low platelet arachidonate and were severely deficient in TXB2 synthesis (less than 10% of controls). Three children with PILBD were fed a supplement of structured triglyceride (Captex 810) intended to provide as much as 10% of energy as linoleate for 2-3 months. Results for these three cases suggested that insufficient linoleate was absorbed to increase plasma linoleate and differences in eicosanoids could not be attributed to linoleate supplementation.