Biomarkers of gut barrier failure in the ICU.
Identifieur interne : 002257 ( PubMed/Checkpoint ); précédent : 002256; suivant : 002258Biomarkers of gut barrier failure in the ICU.
Auteurs : Gaël Piton [Australie] ; Gilles CapellierSource :
- Current opinion in critical care [ 1531-7072 ] ; 2016.
Descripteurs français
- KwdFr :
- Défaillance multiviscérale (immunologie), Défaillance multiviscérale (métabolisme), Défaillance multiviscérale (physiopathologie), Entérocytes (métabolisme), Humains, Inflammation (immunologie), Inflammation (métabolisme), Inflammation (physiopathologie), Maladie grave, Maladies intestinales (immunologie), Maladies intestinales (métabolisme), Maladies intestinales (physiopathologie), Marqueurs biologiques (métabolisme), Nutrition entérale (effets indésirables), Pronostic, Protéines de liaison aux acides gras (métabolisme), Sepsie (immunologie), Sepsie (métabolisme), Sepsie (physiopathologie), Soins de réanimation, Unités de soins intensifs.
- MESH :
- effets indésirables : Nutrition entérale.
- immunologie : Défaillance multiviscérale, Inflammation, Maladies intestinales, Sepsie.
- métabolisme : Défaillance multiviscérale, Entérocytes, Inflammation, Maladies intestinales, Marqueurs biologiques, Protéines de liaison aux acides gras, Sepsie.
- physiopathologie : Défaillance multiviscérale, Inflammation, Maladies intestinales, Sepsie.
- Humains, Maladie grave, Pronostic, Soins de réanimation, Unités de soins intensifs.
English descriptors
- KwdEn :
- Biomarkers (metabolism), Critical Care, Critical Illness, Enteral Nutrition (adverse effects), Enterocytes (metabolism), Fatty Acid-Binding Proteins (metabolism), Humans, Inflammation (immunology), Inflammation (metabolism), Inflammation (physiopathology), Intensive Care Units, Intestinal Diseases (immunology), Intestinal Diseases (metabolism), Intestinal Diseases (physiopathology), Multiple Organ Failure (immunology), Multiple Organ Failure (metabolism), Multiple Organ Failure (physiopathology), Prognosis, Sepsis (immunology), Sepsis (metabolism), Sepsis (physiopathology).
- MESH :
- chemical , metabolism : Biomarkers, Fatty Acid-Binding Proteins.
- adverse effects : Enteral Nutrition.
- immunology : Inflammation, Intestinal Diseases, Multiple Organ Failure, Sepsis.
- metabolism : Enterocytes, Inflammation, Intestinal Diseases, Multiple Organ Failure, Sepsis.
- physiopathology : Inflammation, Intestinal Diseases, Multiple Organ Failure, Sepsis.
- Critical Care, Critical Illness, Humans, Intensive Care Units, Prognosis.
Abstract
Gut barrier failure is associated with bacterial translocation, systemic inflammation, and is presumed to be associated with the development of multiple organ dysfunction syndrome. As the gut barrier function is carried out by a monolayer of enterocytes, a minimum requirement is the integrity of the enterocytes, and controlled paracellular permeability between adjacent enterocytes. Many factors can cause critically ill patients to lose gut barrier function by a mechanism of enterocyte damage; for example, small bowel ischemia or hypoxia, sepsis, systemic inflammatory response syndrome, or absence of enteral feeding.
DOI: 10.1097/MCC.0000000000000283
PubMed: 26808138
Affiliations:
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barrier failure in the ICU.</title><author><name sortKey="Piton, Gael" sort="Piton, Gael" uniqKey="Piton G" first="Gaël" last="Piton">Gaël Piton</name><affiliation wicri:level="1"><nlm:affiliation>aIntensive Care Unit, Besançon University Hospital bResearch Unit EA3920 and SFR FED 4234, University of Franche Comté, Besançon, France cDepartment of Epidemiology and Preventive Medicine, Australian and New Zealand Intensive Care Research Centre, Monash University, Clayton, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>aIntensive Care Unit, Besançon University Hospital bResearch Unit EA3920 and SFR FED 4234, University of Franche Comté, Besançon, France cDepartment of Epidemiology and Preventive Medicine, Australian and New Zealand Intensive Care Research Centre, Monash University, Clayton</wicri:regionArea><wicri:noRegion>Clayton</wicri:noRegion></affiliation></author><author><name sortKey="Capellier, Gilles" sort="Capellier, Gilles" 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(metabolism)</term><term>Multiple Organ Failure (physiopathology)</term><term>Prognosis</term><term>Sepsis (immunology)</term><term>Sepsis (metabolism)</term><term>Sepsis (physiopathology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Défaillance multiviscérale (immunologie)</term><term>Défaillance multiviscérale (métabolisme)</term><term>Défaillance multiviscérale (physiopathologie)</term><term>Entérocytes (métabolisme)</term><term>Humains</term><term>Inflammation (immunologie)</term><term>Inflammation (métabolisme)</term><term>Inflammation (physiopathologie)</term><term>Maladie grave</term><term>Maladies intestinales (immunologie)</term><term>Maladies intestinales (métabolisme)</term><term>Maladies intestinales (physiopathologie)</term><term>Marqueurs biologiques (métabolisme)</term><term>Nutrition entérale (effets indésirables)</term><term>Pronostic</term><term>Protéines de liaison aux acides gras (métabolisme)</term><term>Sepsie (immunologie)</term><term>Sepsie (métabolisme)</term><term>Sepsie (physiopathologie)</term><term>Soins de réanimation</term><term>Unités de soins intensifs</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Biomarkers</term><term>Fatty Acid-Binding Proteins</term></keywords><keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Enteral Nutrition</term></keywords><keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Nutrition entérale</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Défaillance multiviscérale</term><term>Inflammation</term><term>Maladies intestinales</term><term>Sepsie</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Inflammation</term><term>Intestinal Diseases</term><term>Multiple Organ Failure</term><term>Sepsis</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Enterocytes</term><term>Inflammation</term><term>Intestinal Diseases</term><term>Multiple Organ Failure</term><term>Sepsis</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Défaillance multiviscérale</term><term>Entérocytes</term><term>Inflammation</term><term>Maladies intestinales</term><term>Marqueurs biologiques</term><term>Protéines de liaison aux acides gras</term><term>Sepsie</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Défaillance multiviscérale</term><term>Inflammation</term><term>Maladies intestinales</term><term>Sepsie</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Inflammation</term><term>Intestinal Diseases</term><term>Multiple Organ Failure</term><term>Sepsis</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Critical Care</term><term>Critical Illness</term><term>Humans</term><term>Intensive Care Units</term><term>Prognosis</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Humains</term><term>Maladie grave</term><term>Pronostic</term><term>Soins de réanimation</term><term>Unités de soins intensifs</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Gut barrier failure is associated with bacterial translocation, systemic inflammation, and is presumed to be associated with the development of multiple organ dysfunction syndrome. As the gut barrier function is carried out by a monolayer of enterocytes, a minimum requirement is the integrity of the enterocytes, and controlled paracellular permeability between adjacent enterocytes. Many factors can cause critically ill patients to lose gut barrier function by a mechanism of enterocyte damage; for example, small bowel ischemia or hypoxia, sepsis, systemic inflammatory response syndrome, or absence of enteral feeding.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26808138</PMID><DateCreated><Year>2016</Year><Month>03</Month><Day>04</Day></DateCreated><DateCompleted><Year>2016</Year><Month>12</Month><Day>28</Day></DateCompleted><DateRevised><Year>2016</Year><Month>12</Month><Day>30</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-7072</ISSN><JournalIssue CitedMedium="Internet"><Volume>22</Volume><Issue>2</Issue><PubDate><Year>2016</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Current opinion in critical care</Title><ISOAbbreviation>Curr Opin Crit Care</ISOAbbreviation></Journal><ArticleTitle>Biomarkers of gut barrier failure in the ICU.</ArticleTitle><Pagination><MedlinePgn>152-60</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1097/MCC.0000000000000283</ELocationID><Abstract><AbstractText Label="PURPOSE OF REVIEW" NlmCategory="OBJECTIVE">Gut barrier failure is associated with bacterial translocation, systemic inflammation, and is presumed to be associated with the development of multiple organ dysfunction syndrome. As the gut barrier function is carried out by a monolayer of enterocytes, a minimum requirement is the integrity of the enterocytes, and controlled paracellular permeability between adjacent enterocytes. Many factors can cause critically ill patients to lose gut barrier function by a mechanism of enterocyte damage; for example, small bowel ischemia or hypoxia, sepsis, systemic inflammatory response syndrome, or absence of enteral feeding.</AbstractText><AbstractText Label="RECENT FINDINGS" NlmCategory="RESULTS">Two enterocyte biomarkers may help the intensivist to identify enterocyte damage and dysfunction, namely plasma citrulline, a biomarker of functional enterocyte mass, and plasma or urinary intestinal fatty acid-binding protein, a marker of enterocyte damage. This review focuses on results obtained with these biomarkers in the context of critical care, in particular: prevalence of enterocyte biomarker abnormalities; mechanisms associated with enterocyte damage and dysfunction; link with systemic inflammation, bacterial translocation, and clinical intestinal dysfunction; prognostic value of enterocyte biomarkers. Lastly, we also review the limits of these biomarkers.</AbstractText><AbstractText Label="SUMMARY" NlmCategory="CONCLUSIONS">Enterocyte biomarkers may help the intensivist to identify patients presenting with intestinal damage, and who are at risk of bacterial translocation and systemic inflammatory response syndrome, as well as those with decreased enterocyte function, at risk of malabsorption. Enterocyte biomarkers should be interpreted with caution in the critically ill and should be interpreted within the overall clinical context of the patient.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Piton</LastName><ForeName>Gaël</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>aIntensive Care Unit, Besançon University Hospital bResearch Unit EA3920 and SFR FED 4234, University of Franche Comté, Besançon, France cDepartment of Epidemiology and Preventive Medicine, Australian and New Zealand Intensive Care Research Centre, Monash University, Clayton, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Capellier</LastName><ForeName>Gilles</ForeName><Initials>G</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Curr Opin Crit Care</MedlineTA><NlmUniqueID>9504454</NlmUniqueID><ISSNLinking>1070-5295</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C493404">FABP2 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050556">Fatty Acid-Binding Proteins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="N">Biomarkers</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003422" MajorTopicYN="Y">Critical Care</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016638" MajorTopicYN="N">Critical Illness</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004750" MajorTopicYN="N">Enteral Nutrition</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020895" MajorTopicYN="N">Enterocytes</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050556" MajorTopicYN="N">Fatty Acid-Binding Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007362" MajorTopicYN="N">Intensive Care Units</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007410" MajorTopicYN="N">Intestinal Diseases</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009102" MajorTopicYN="N">Multiple Organ Failure</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011379" MajorTopicYN="N">Prognosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018805" MajorTopicYN="N">Sepsis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>1</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>1</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>12</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26808138</ArticleId><ArticleId IdType="doi">10.1097/MCC.0000000000000283</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Australie</li></country></list><tree><noCountry><name sortKey="Capellier, Gilles" sort="Capellier, Gilles" uniqKey="Capellier G" first="Gilles" last="Capellier">Gilles Capellier</name></noCountry><country name="Australie"><noRegion><name sortKey="Piton, Gael" sort="Piton, Gael" uniqKey="Piton G" first="Gaël" last="Piton">Gaël Piton</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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