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Eicosanoid synthesis in children with cholestatic disease
Author(s) -
Dupont J.,
AmédéeManesme O.,
Pepin D.,
Chambaz J.
Publication year - 1990
Publication title -
journal of inherited metabolic disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 102
eISSN - 1573-2665
pISSN - 0141-8955
DOI - 10.1007/bf01799688
Subject(s) - medicine , endocrinology , eicosanoid , arachidonic acid , eicosanoid metabolism , thromboxane , chemistry , essential fatty acid , cholestasis , platelet , fatty acid , linoleic acid , biochemistry , enzyme
Summary 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) E 1 , PGE 2 , PGI 2 , PGF 2 , and thromboxane (TXB 2 ) by whole blood incubated at 37°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 PGI 2 . Those with PILBD had low platelet arachidonate and were severely deficient in TXB 2 synthesis (<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.