Activation of the kynurenine pathway predicts mortality and neurological outcome in cardiac arrest patients: A validation study
Activation of the kynurenine pathway (KP) has been shown to predict outcome in cardiac arrest (CA) patients. We validated these findings in a Swiss cohort. We measured admission tryptophan and kynurenine levels in 270 consecutive CA patients (38 in-hospital CA) and investigated associations with in-...
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| Veröffentlicht in: | Journal of critical care 2022-02, Vol.67, p.57-65 |
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| creator | Loretz, Nina Becker, Christoph Hochstrasser, Seraina Metzger, Kerstin Beck, Katharina Mueller, Jonas Gross, Sebastian Vincent, Alessia Amacher, Simon A. Sutter, Raoul Tisljar, Kai Schuetz, Philipp Bernasconi, Luca Neyer, Peter Pargger, Hans Marsch, Stephan Hunziker, Sabina |
| description | Activation of the kynurenine pathway (KP) has been shown to predict outcome in cardiac arrest (CA) patients. We validated these findings in a Swiss cohort.
We measured admission tryptophan and kynurenine levels in 270 consecutive CA patients (38 in-hospital CA) and investigated associations with in-hospital mortality and neurological outcome at hospital discharge.
120 of 270 (44%) patients died in the hospital. Compared to survivors, non-survivors showed higher median initial kynurenine levels (5.28 μmol/l [IQR 2.91 to 7.40] vs 3.58 μmol/l [IQR 2.47 to 5.46]; p |
| doi_str_mv | 10.1016/j.jcrc.2021.09.025 |
| format | Article |
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We measured admission tryptophan and kynurenine levels in 270 consecutive CA patients (38 in-hospital CA) and investigated associations with in-hospital mortality and neurological outcome at hospital discharge.
120 of 270 (44%) patients died in the hospital. Compared to survivors, non-survivors showed higher median initial kynurenine levels (5.28 μmol/l [IQR 2.91 to 7.40] vs 3.58 μmol/l [IQR 2.47 to 5.46]; p < 0.001) and a higher median kynurenine/tryptophan ratio (0.10 μmol/l [IQR 0.07 to 0.17] vs 0.07 μmol/l [IQR 0.05 to 0.1]; p < 0.001). In a model adjusted for age, gender and comorbidities, kynurenine (OR 1.16, 95% CI 1.05 to 1.27; p = 0.001) and kynurenine/tryptophan ratio (OR 1.19, 95% CI 1.08 to 1.31; p = 0.003) were significantly associated with mortality. Results were similar for neurological outcome.
Our findings validate a previous study and show associations of the activation of the KP with unfavorable outcomes after CA. Future studies should evaluate whether therapeutic modulation of the KP may impact clinical outcomes after CA.
•Inflammation upregulates the kynurenine pathway of tryptophan degradation.•Post-cardiac arrest syndrome is an inflammatory state.•Increased kynurenine/tryptophan ratio is linked to adverse outcomes after cardiac arrest.•We validated the findings of a previous study in a Swiss cohort.</description><identifier>ISSN: 0883-9441</identifier><identifier>EISSN: 1557-8615</identifier><identifier>DOI: 10.1016/j.jcrc.2021.09.025</identifier><identifier>PMID: 34673332</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Age ; Biomarkers ; Cardiac arrest ; Cardiovascular disease ; Cohort Studies ; Coma ; Creatinine ; Critical care ; Delirium ; Heart Arrest - therapy ; Heart attacks ; Hospital Mortality ; Humans ; Intensive care medicine ; Kynurenine ; Kynurenine - metabolism ; Medical prognosis ; Metabolism ; Metabolites ; Mortality ; Patients ; Post-cardiac arrest syndrome ; Prognostication ; Regression analysis ; Tryptophan</subject><ispartof>Journal of critical care, 2022-02, Vol.67, p.57-65</ispartof><rights>2021 The Authors</rights><rights>Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.</rights><rights>2021. The Authors</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c428t-99691b1efe82b53f34c6242c9a48408c0eeff35a9a2a2e658b736ee35f94b2da3</citedby><cites>FETCH-LOGICAL-c428t-99691b1efe82b53f34c6242c9a48408c0eeff35a9a2a2e658b736ee35f94b2da3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/2608446977?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976,64364,64366,64368,72218</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34673332$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Loretz, Nina</creatorcontrib><creatorcontrib>Becker, Christoph</creatorcontrib><creatorcontrib>Hochstrasser, Seraina</creatorcontrib><creatorcontrib>Metzger, Kerstin</creatorcontrib><creatorcontrib>Beck, Katharina</creatorcontrib><creatorcontrib>Mueller, Jonas</creatorcontrib><creatorcontrib>Gross, Sebastian</creatorcontrib><creatorcontrib>Vincent, Alessia</creatorcontrib><creatorcontrib>Amacher, Simon A.</creatorcontrib><creatorcontrib>Sutter, Raoul</creatorcontrib><creatorcontrib>Tisljar, Kai</creatorcontrib><creatorcontrib>Schuetz, Philipp</creatorcontrib><creatorcontrib>Bernasconi, Luca</creatorcontrib><creatorcontrib>Neyer, Peter</creatorcontrib><creatorcontrib>Pargger, Hans</creatorcontrib><creatorcontrib>Marsch, Stephan</creatorcontrib><creatorcontrib>Hunziker, Sabina</creatorcontrib><title>Activation of the kynurenine pathway predicts mortality and neurological outcome in cardiac arrest patients: A validation study</title><title>Journal of critical care</title><addtitle>J Crit Care</addtitle><description>Activation of the kynurenine pathway (KP) has been shown to predict outcome in cardiac arrest (CA) patients. We validated these findings in a Swiss cohort.
We measured admission tryptophan and kynurenine levels in 270 consecutive CA patients (38 in-hospital CA) and investigated associations with in-hospital mortality and neurological outcome at hospital discharge.
120 of 270 (44%) patients died in the hospital. Compared to survivors, non-survivors showed higher median initial kynurenine levels (5.28 μmol/l [IQR 2.91 to 7.40] vs 3.58 μmol/l [IQR 2.47 to 5.46]; p < 0.001) and a higher median kynurenine/tryptophan ratio (0.10 μmol/l [IQR 0.07 to 0.17] vs 0.07 μmol/l [IQR 0.05 to 0.1]; p < 0.001). In a model adjusted for age, gender and comorbidities, kynurenine (OR 1.16, 95% CI 1.05 to 1.27; p = 0.001) and kynurenine/tryptophan ratio (OR 1.19, 95% CI 1.08 to 1.31; p = 0.003) were significantly associated with mortality. Results were similar for neurological outcome.
Our findings validate a previous study and show associations of the activation of the KP with unfavorable outcomes after CA. Future studies should evaluate whether therapeutic modulation of the KP may impact clinical outcomes after CA.
•Inflammation upregulates the kynurenine pathway of tryptophan degradation.•Post-cardiac arrest syndrome is an inflammatory state.•Increased kynurenine/tryptophan ratio is linked to adverse outcomes after cardiac arrest.•We validated the findings of a previous study in a Swiss cohort.</description><subject>Age</subject><subject>Biomarkers</subject><subject>Cardiac arrest</subject><subject>Cardiovascular disease</subject><subject>Cohort Studies</subject><subject>Coma</subject><subject>Creatinine</subject><subject>Critical care</subject><subject>Delirium</subject><subject>Heart Arrest - therapy</subject><subject>Heart attacks</subject><subject>Hospital Mortality</subject><subject>Humans</subject><subject>Intensive care medicine</subject><subject>Kynurenine</subject><subject>Kynurenine - metabolism</subject><subject>Medical prognosis</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Mortality</subject><subject>Patients</subject><subject>Post-cardiac arrest syndrome</subject><subject>Prognostication</subject><subject>Regression analysis</subject><subject>Tryptophan</subject><issn>0883-9441</issn><issn>1557-8615</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kTuP1DAUhS0EYoeFP0CBLNHQJPiZxIhmtOIlrbTNUluOc8M6JPZgO4NS7V9fj2ahoKC6t_jOuVfnIPSakpoS2ryf6slGWzPCaE1UTZh8gnZUyrbqGiqfoh3pOl4pIegFepHSRAhtOZfP0QUXTdk426H7vc3uaLILHocR5zvAPze_RvDOAz6YfPfbbPgQYXA2J7yEmM3s8oaNH7CHNYY5_HDWzDis2YYFsPPYmjg4Y7GJEVI-uTjwOX3Ae3ws6uF8LuV12F6iZ6OZE7x6nJfo--dPt1dfq-ubL9-u9teVFazLlVKNoj2FETrWSz5yYRsmmFVGdIJ0lgCMI5dGGWYYNLLrW94AcDkq0bPB8Ev07ux7iOHXWr7Si0sW5tl4CGvSTHZClHCIKOjbf9AprNGX7zRrSMEa1baFYmfKxpBShFEfoltM3DQl-lSPnvSpHn2qRxOlSz1F9ObReu0XGP5K_vRRgI9nAEoWRwdRJ1uysyX-CDbrIbj_-T8Aqc-jKQ</recordid><startdate>202202</startdate><enddate>202202</enddate><creator>Loretz, Nina</creator><creator>Becker, Christoph</creator><creator>Hochstrasser, Seraina</creator><creator>Metzger, Kerstin</creator><creator>Beck, Katharina</creator><creator>Mueller, Jonas</creator><creator>Gross, Sebastian</creator><creator>Vincent, Alessia</creator><creator>Amacher, Simon A.</creator><creator>Sutter, Raoul</creator><creator>Tisljar, Kai</creator><creator>Schuetz, Philipp</creator><creator>Bernasconi, Luca</creator><creator>Neyer, Peter</creator><creator>Pargger, Hans</creator><creator>Marsch, Stephan</creator><creator>Hunziker, Sabina</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>ASE</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FPQ</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K6X</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>202202</creationdate><title>Activation of the kynurenine pathway predicts mortality and neurological outcome in cardiac arrest patients: A validation study</title><author>Loretz, Nina ; Becker, Christoph ; Hochstrasser, Seraina ; Metzger, Kerstin ; Beck, Katharina ; Mueller, Jonas ; Gross, Sebastian ; Vincent, Alessia ; Amacher, Simon A. ; Sutter, Raoul ; Tisljar, Kai ; Schuetz, Philipp ; Bernasconi, Luca ; Neyer, Peter ; Pargger, Hans ; Marsch, Stephan ; Hunziker, Sabina</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c428t-99691b1efe82b53f34c6242c9a48408c0eeff35a9a2a2e658b736ee35f94b2da3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Age</topic><topic>Biomarkers</topic><topic>Cardiac arrest</topic><topic>Cardiovascular disease</topic><topic>Cohort Studies</topic><topic>Coma</topic><topic>Creatinine</topic><topic>Critical care</topic><topic>Delirium</topic><topic>Heart Arrest - therapy</topic><topic>Heart attacks</topic><topic>Hospital Mortality</topic><topic>Humans</topic><topic>Intensive care medicine</topic><topic>Kynurenine</topic><topic>Kynurenine - metabolism</topic><topic>Medical prognosis</topic><topic>Metabolism</topic><topic>Metabolites</topic><topic>Mortality</topic><topic>Patients</topic><topic>Post-cardiac arrest syndrome</topic><topic>Prognostication</topic><topic>Regression analysis</topic><topic>Tryptophan</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Loretz, Nina</creatorcontrib><creatorcontrib>Becker, Christoph</creatorcontrib><creatorcontrib>Hochstrasser, Seraina</creatorcontrib><creatorcontrib>Metzger, Kerstin</creatorcontrib><creatorcontrib>Beck, Katharina</creatorcontrib><creatorcontrib>Mueller, Jonas</creatorcontrib><creatorcontrib>Gross, Sebastian</creatorcontrib><creatorcontrib>Vincent, Alessia</creatorcontrib><creatorcontrib>Amacher, Simon A.</creatorcontrib><creatorcontrib>Sutter, Raoul</creatorcontrib><creatorcontrib>Tisljar, Kai</creatorcontrib><creatorcontrib>Schuetz, Philipp</creatorcontrib><creatorcontrib>Bernasconi, Luca</creatorcontrib><creatorcontrib>Neyer, Peter</creatorcontrib><creatorcontrib>Pargger, Hans</creatorcontrib><creatorcontrib>Marsch, Stephan</creatorcontrib><creatorcontrib>Hunziker, Sabina</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>British Nursing Index</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>British Nursing Index (BNI) (1985 to Present)</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>British Nursing Index</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of critical care</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Loretz, Nina</au><au>Becker, Christoph</au><au>Hochstrasser, Seraina</au><au>Metzger, Kerstin</au><au>Beck, Katharina</au><au>Mueller, Jonas</au><au>Gross, Sebastian</au><au>Vincent, Alessia</au><au>Amacher, Simon A.</au><au>Sutter, Raoul</au><au>Tisljar, Kai</au><au>Schuetz, Philipp</au><au>Bernasconi, Luca</au><au>Neyer, Peter</au><au>Pargger, Hans</au><au>Marsch, Stephan</au><au>Hunziker, Sabina</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of the kynurenine pathway predicts mortality and neurological outcome in cardiac arrest patients: A validation study</atitle><jtitle>Journal of critical care</jtitle><addtitle>J Crit Care</addtitle><date>2022-02</date><risdate>2022</risdate><volume>67</volume><spage>57</spage><epage>65</epage><pages>57-65</pages><issn>0883-9441</issn><eissn>1557-8615</eissn><abstract>Activation of the kynurenine pathway (KP) has been shown to predict outcome in cardiac arrest (CA) patients. We validated these findings in a Swiss cohort.
We measured admission tryptophan and kynurenine levels in 270 consecutive CA patients (38 in-hospital CA) and investigated associations with in-hospital mortality and neurological outcome at hospital discharge.
120 of 270 (44%) patients died in the hospital. Compared to survivors, non-survivors showed higher median initial kynurenine levels (5.28 μmol/l [IQR 2.91 to 7.40] vs 3.58 μmol/l [IQR 2.47 to 5.46]; p < 0.001) and a higher median kynurenine/tryptophan ratio (0.10 μmol/l [IQR 0.07 to 0.17] vs 0.07 μmol/l [IQR 0.05 to 0.1]; p < 0.001). In a model adjusted for age, gender and comorbidities, kynurenine (OR 1.16, 95% CI 1.05 to 1.27; p = 0.001) and kynurenine/tryptophan ratio (OR 1.19, 95% CI 1.08 to 1.31; p = 0.003) were significantly associated with mortality. Results were similar for neurological outcome.
Our findings validate a previous study and show associations of the activation of the KP with unfavorable outcomes after CA. Future studies should evaluate whether therapeutic modulation of the KP may impact clinical outcomes after CA.
•Inflammation upregulates the kynurenine pathway of tryptophan degradation.•Post-cardiac arrest syndrome is an inflammatory state.•Increased kynurenine/tryptophan ratio is linked to adverse outcomes after cardiac arrest.•We validated the findings of a previous study in a Swiss cohort.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>34673332</pmid><doi>10.1016/j.jcrc.2021.09.025</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Age Biomarkers Cardiac arrest Cardiovascular disease Cohort Studies Coma Creatinine Critical care Delirium Heart Arrest - therapy Heart attacks Hospital Mortality Humans Intensive care medicine Kynurenine Kynurenine - metabolism Medical prognosis Metabolism Metabolites Mortality Patients Post-cardiac arrest syndrome Prognostication Regression analysis Tryptophan |
| title | Activation of the kynurenine pathway predicts mortality and neurological outcome in cardiac arrest patients: A validation study |
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