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Cholesterol metabolism in pediatric short bowel syndrome after weaning off parenteral nutrition
Institution:1. Section of Pediatric Surgery, Hospital for Children and Adolescents, University of Helsinki, Helsinki, Finland;2. Department of Clinical Nutrition, University of Kuopio, Kuopio, Finland;3. Department of Medicine, Kuopio University Hospital, Kuopio, Finland;4. Department of Medicine, Division of Internal Medicine, University of Helsinki, Helsinki, Finland;5. Department of Dermatology, Skin and Allergy Hospital, Helsinki University Hospital, Helsinki, Finland;6. Hospital for Children and Adolescents, University of Helsinki, Helsinki, Finland;7. Department of Medicine, Division of Gastroenterology, University of Helsinki, Helsinki, Finland
Abstract:BackgroundSmall intestine essentially regulates cholesterol homeostasis.AimsTo evaluate cholesterol metabolism in short bowel syndrome (SBS).MethodsCholesterol precursors (e.g., cholestenol, desmosterol and lathosterol) and plant sterols (campesterol and sitosterol), respective markers of cholesterol synthesis and absorption, were determined in SBS patients (n = 12) an average of 31 months after weaning off parenteral nutrition and in age-matched controls (n = 80).ResultsAmong patients, serum cholesterol precursor sterol to cholesterol ratios were 2–10 times higher (P < 0.0001 for each). Those without any remaining ileum had 1.2–2.8 times higher precursor sterol to cholesterol ratios than those with an ileal remnant (P < 0.05 for each). Serum cholesterol concentration, campesterol/cholesterol and campesterol/sitosterol were 34–39% lower (P < 0.05 for each) in relation to controls. Bile acid absorption was markedly impaired (2.4 (0.2–3.2)%). Plant sterol ratios reflected the absolute length of remaining jejunum (r = 0.625–0.663), and precursor sterol ratios inversely that of ileum (r = ?0.589 to 0.750, P < 0.05 for all).ConclusionAfter weaning off parenteral nutrition, patients with pediatric onset SBS continue to have marked intestinal malabsorption of bile acids and moderate cholesterol malabsorption resulting in decreased serum cholesterol despite a marked compensatory increase in cholesterol synthesis.
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