Enterocyte damage: a piece in the puzzle of post-cardiac arrest syndrome

Gael Piton, Nicolas Belin, Loic Barrot, Francois Belon, Benoit Cypriani, Jean-Christophe Navellou, Gilles Capellier

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Abstract

Cardiac arrest is considered to be a cause of small bowel ischemia, but the consequences of cardiac arrest on the human small bowel have been rarely studied. Plasma citrulline concentration is a marker of functional enterocyte mass, and plasma intestinal fatty acid-binding protein (I-FABP) concentration is a marker of enterocyte damage. We aimed to measure enterocyte biomarkers after cardiac arrest and to study the prognostic value of biomarker abnormalities. This is a prospective, observational, single-center study of patients admitted to the intensive care unit (ICU) for cardiac arrest, evaluating plasma citrulline and I-FABP concentrations at admission and after 24 h and variables according to the Utstein criteria. Variables according to 28-day Cerebral Performance Category score of 1 to 2 (good neurological outcome) versus 3 to 5 (poor neurological outcome) were compared. Sixty-nine patients with cardiac arrest of both cardiac and hypoxic origin were included. At ICU admission, plasma citrulline concentration was low in 65 and plasma I-FABP was elevated in 82 of the patients. After 24 h, plasma citrulline was low in 82 and I-FABP was normal in 60 of the patients. Patients with a poor neurological outcome had a lower plasma citrulline concentration and a higher I-FABP concentration at ICU admission. By multivariate analysis, plasma citrulline levels of 13.1 mmol L1 or less and I-FABP more than 260 pg mL1 were independently associated with a poor neurological outcome (odds ratio, 21.9 [2.2-215], and odds ratio, 13.6 [1.4-129], respectively). Cardiac arrest resuscitation is associated with evidence of small bowel mucosal damage in most patients, with a short and intense I-FABPelevation at admission and a decrease in citrulline concentration during the first day. In this study, low plasma citrulline and high I-FABP concentrations at ICU admission were predictive of a poor neurological outcome. This study confirms that cardiac arrest is a model of small bowel mucosal ischemia and suggests that enterocyte damage is a piece in the puzzle of post-cardiac arrest syndrome.
Original languageEnglish
Pages (from-to)438 - 444
Number of pages7
JournalShock
Volume44
Issue number5
DOIs
Publication statusPublished - 2015

Cite this

Piton, G., Belin, N., Barrot, L., Belon, F., Cypriani, B., Navellou, J-C., & Capellier, G. (2015). Enterocyte damage: a piece in the puzzle of post-cardiac arrest syndrome. Shock, 44(5), 438 - 444. https://doi.org/10.1097/SHK.0000000000000440