Gaël Piton1,2,3, Amélie Le Gouge4,5,6, Noelle Brulé7, Benoit Cypriani8, Jean-Claude Lacherade9, Saad Nseir10,11, Jean-Paul Mira12, Emmanuelle Mercier13, Michel Sirodot14, Jean-Philippe Rigaud15, Stéphanie Malaquin16, Edouard Soum17, Michel Djibre18, Stéphane Gaudry19,20, Didier Thévenin21, Jean Reignier7,22. 1. Medical Intensive Care Unit, CHRU Besançon, Besançon, France. gpiton@chu-besancon.fr. 2. EA3920, Université de Franche Comté, Besançon, France. gpiton@chu-besancon.fr. 3. Service de Réanimation Médicale, CHRU de Besançon, Boulevard Fleming, 25030, Besançon, France. gpiton@chu-besancon.fr. 4. Inserm CIC 1415, Tours, France. 5. Université de Tours, Tours, France. 6. CHU Tours, Tours, France. 7. Médecine Intensive Réanimation, CHU de Nantes, Nantes, France. 8. Biochemistry Unit, Besançon University Hospital, Besançon, France. 9. Médecine Intensive Réanimation, Centre Hospitalier Départemental de la Vendée, La Roche sur Yon, France. 10. Medical Intensive Care Unit, CHU Lille, Lille, France. 11. Medicine School, Université Lille, Lille, France. 12. Medical Intensive Care Unit, Cochin University Hospital, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France. 13. Médecine Intensive Réanimation, Hôpital Bretonneau, CHU Tours, Tours, France. 14. Medical-Surgical Intensive Care Unit, Centre Hospitalier Annecy-Genevois, Metz-Tessy, Pringy, France. 15. Medical-Surgical Intensive Care Unit, Hôpital de Dieppe, Dieppe, France. 16. Surgical Intensive Care Unit, CHU Amiens Picardie, Amiens, France. 17. Medical Intensive Care Unit, Hôpital Gabriel Montpied, CHU de Clermont-Ferrand, Clermont-Ferrand, France. 18. Medical-Surgical Intensive Care Unit, Tenon University Hospital, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France. 19. Medical-Surgical Intensive Care Unit, Hôpital Louis Mourier, Assistance Publique-Hôpitaux de Paris (AP-HP), Colombes, France. 20. Université Paris Diderot, ECEVE, UMR 1123, Sorbonne Paris Cité, Paris, France. 21. Medical-Surgical Intensive Care Unit, Centre Hospitalier Docteur Schaffner, Lens, France. 22. Université de Nantes, Nantes, France.
Abstract
PURPOSE: The effects of the route of nutrition on the gut mucosa of patients with shock are unclear. Plasma citrulline concentration is a marker of enterocyte mass, and plasma intestinal fatty acid binding protein (I-FABP) concentration is a marker of enterocyte damage. We aimed to study the effect of the route of nutrition on plasma citrulline concentration measured at day 3 of nutrition. MATERIALS AND METHODS: Ancillary study of the NUTRIREA-2 trial. Ventilated adults with shock were randomly assigned to receive enteral or parenteral nutrition. Enterocyte biomarkers were measured at baseline, day 3, and day 8 of nutrition. RESULT: A total of 165 patients from 13 French ICUs were included in the study: 85 patients in the enteral group and 80 patients in the parenteral group. At baseline, plasma citrulline was low without difference between groups (12.2 µmol L-1 vs 13.3 µmol L-1). At day 3, plasma citrulline concentration was higher in the enteral group than in the parenteral group (18.7 µmol L-1 vs 15.3 µmol L-1, p = 0.01). Plasma I-FABP concentration was increased at baseline, without difference between groups (245 pg mL-1 vs 244 pg mL-1). Plasma I-FABP concentration was higher in the enteral group than in the parenteral group at day 3 and day 8 (158 pg mL-1 vs 50 pg mL-1, p = 0.005 and 225 pg mL-1 vs 50 pg mL-1, p = 0.03). CONCLUSION:Plasma citrulline concentration was higher after 3 days of enteral nutrition than after 3 days of parenteral nutrition. This result raises the question of the possibility that enteral nutrition is associated with a more rapid restoration of enterocyte mass than parenteral nutrition.
RCT Entities:
PURPOSE: The effects of the route of nutrition on the gut mucosa of patients with shock are unclear. Plasma citrulline concentration is a marker of enterocyte mass, and plasma intestinal fatty acid binding protein (I-FABP) concentration is a marker of enterocyte damage. We aimed to study the effect of the route of nutrition on plasma citrulline concentration measured at day 3 of nutrition. MATERIALS AND METHODS: Ancillary study of the NUTRIREA-2 trial. Ventilated adults with shock were randomly assigned to receive enteral or parenteral nutrition. Enterocyte biomarkers were measured at baseline, day 3, and day 8 of nutrition. RESULT: A total of 165 patients from 13 French ICUs were included in the study: 85 patients in the enteral group and 80 patients in the parenteral group. At baseline, plasma citrulline was low without difference between groups (12.2 µmol L-1 vs 13.3 µmol L-1). At day 3, plasma citrulline concentration was higher in the enteral group than in the parenteral group (18.7 µmol L-1 vs 15.3 µmol L-1, p = 0.01). Plasma I-FABP concentration was increased at baseline, without difference between groups (245 pg mL-1 vs 244 pg mL-1). Plasma I-FABP concentration was higher in the enteral group than in the parenteral group at day 3 and day 8 (158 pg mL-1 vs 50 pg mL-1, p = 0.005 and 225 pg mL-1 vs 50 pg mL-1, p = 0.03). CONCLUSION: Plasma citrulline concentration was higher after 3 days of enteral nutrition than after 3 days of parenteral nutrition. This result raises the question of the possibility that enteral nutrition is associated with a more rapid restoration of enterocyte mass than parenteral nutrition.
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