<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Laursen TL</submitter><funding>Danish Council for Independent Research - Medical Sciences</funding><funding>NOVO Nordisk Foundation</funding><funding>NIDDK NIH HHS</funding><funding>National Institutes of Health</funding><funding>Novo Nordisk Fonden</funding><pagination>756-63</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4329085</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>35(3)</volume><pubmed_abstract>&lt;h4>Background &amp; aims&lt;/h4>The complement system is activated in liver diseases including acute liver failure (ALF); however, the role of the lectin pathway of complement has scarcely been investigated in ALF. The pathway is initiated by soluble pattern recognition molecules: mannan-binding lectin (MBL), M-, L-, and H-ficolin and collectin-liver-1 (CL-L1), which are predominantly synthesized in the liver. We aimed to study lectin levels in ALF patients and associations with clinical outcome.&lt;h4>Methods&lt;/h4>Serum samples from 75 patients enrolled by the US ALF Study Group were collected on days 1 and 3. We included 75 healthy blood donors and 20 cirrhosis patients as controls. Analyses were performed using sandwich-type immunoassays (ELISA, TRIFMA).&lt;h4>Results&lt;/h4>At day 1, the MBL level in </pubmed_abstract><journal>Liver international : official journal of the International Association for the Study of the Liver</journal><pubmed_title>Circulating mannan-binding lectin, M-, L-, H-ficolin and collectin-liver-1 levels in patients with acute liver failure.</pubmed_title><pmcid>PMC4329085</pmcid><funding_grant_id>U01-DK-58369</funding_grant_id><funding_grant_id>12-132318</funding_grant_id><funding_grant_id>NNF10OC1013267</funding_grant_id><funding_grant_id>U01 DK058369</funding_grant_id><funding_grant_id>NNF13OC0007989</funding_grant_id><pubmed_authors>Prosser C</pubmed_authors><pubmed_authors>Lalani E</pubmed_authors><pubmed_authors>Larson AM</pubmed_authors><pubmed_authors>Vilstrup H</pubmed_authors><pubmed_authors>Laursen TL</pubmed_authors><pubmed_authors>Taylor W</pubmed_authors><pubmed_authors>Senkbeil L</pubmed_authors><pubmed_authors>Bernard T</pubmed_authors><pubmed_authors>Hay J</pubmed_authors><pubmed_authors>McGuire B</pubmed_authors><pubmed_authors>Thiel S</pubmed_authors><pubmed_authors>Pezzia C</pubmed_authors><pubmed_authors>Reuben A</pubmed_authors><pubmed_authors>Emre S</pubmed_authors><pubmed_authors>Ingram K</pubmed_authors><pubmed_authors>Gronbaek H</pubmed_authors><pubmed_authors>Murray N</pubmed_authors><pubmed_authors>Fontana RJ</pubmed_authors><pubmed_authors>Stoy S</pubmed_authors><pubmed_authors>Polson J</pubmed_authors><pubmed_authors>Munoz S</pubmed_authors><pubmed_authors>Welch S</pubmed_authors><pubmed_authors>Sandahl TD</pubmed_authors><pubmed_authors>Zaman A</pubmed_authors><pubmed_authors>Reddy R</pubmed_authors><pubmed_authors>Coultrup S</pubmed_authors><pubmed_authors>Satyanarayana R</pubmed_authors><pubmed_authors>Rush R</pubmed_authors><pubmed_authors>Davern TJ</pubmed_authors><pubmed_authors>Misra C</pubmed_authors><pubmed_authors>McCashland TM</pubmed_authors><pubmed_authors>Gottstein J</pubmed_authors><pubmed_authors>Avant L</pubmed_authors><pubmed_authors>Peacock V</pubmed_authors><pubmed_authors>Groettum C</pubmed_authors><pubmed_authors>Shakil A</pubmed_authors><pubmed_authors>US Acute Liver Failure Study Group</pubmed_authors><pubmed_authors>Crippin JS</pubmed_authors><pubmed_authors>Hassenein T</pubmed_authors><pubmed_authors>Han S</pubmed_authors><pubmed_authors>Schiodt FV</pubmed_authors><pubmed_authors>Gerstle L</pubmed_authors><pubmed_authors>Casson D</pubmed_authors><pubmed_authors>Schilsky M</pubmed_authors><pubmed_authors>Huntley N</pubmed_authors><pubmed_authors>Reisch JS</pubmed_authors><pubmed_authors>Harrison M</pubmed_authors><pubmed_authors>Partovi K</pubmed_authors><pubmed_authors>Barakat F</pubmed_authors><pubmed_authors>Blei AT</pubmed_authors><pubmed_authors>Lee WM</pubmed_authors><pubmed_authors>Chung R</pubmed_authors><pubmed_authors>Salvatori J</pubmed_authors><pubmed_authors>Smith A</pubmed_authors><pubmed_authors>Schwartz J</pubmed_authors><pubmed_authors>Rossaro L</pubmed_authors><pubmed_authors>Morton D</pubmed_authors><pubmed_authors>Campbell M</pubmed_authors><pubmed_authors>Stravitz T</pubmed_authors><pubmed_authors>Hynan LS</pubmed_authors><pubmed_authors>Brown R</pubmed_authors></additional><is_claimable>false</is_claimable><name>Circulating mannan-binding lectin, M-, L-, H-ficolin and collectin-liver-1 levels in patients with acute liver failure.</name><description>&lt;h4>Background &amp; aims&lt;/h4>The complement system is activated in liver diseases including acute liver failure (ALF); however, the role of the lectin pathway of complement has scarcely been investigated in ALF. The pathway is initiated by soluble pattern recognition molecules: mannan-binding lectin (MBL), M-, L-, and H-ficolin and collectin-liver-1 (CL-L1), which are predominantly synthesized in the liver. We aimed to study lectin levels in ALF patients and associations with clinical outcome.&lt;h4>Methods&lt;/h4>Serum samples from 75 patients enrolled by the US ALF Study Group were collected on days 1 and 3. We included 75 healthy blood donors and 20 cirrhosis patients as controls. Analyses were performed using sandwich-type immunoassays (ELISA, TRIFMA).&lt;h4>Results&lt;/h4>At day 1, the MBL level in </description><dates><release>2015-01-01T00:00:00Z</release><publication>2015 Mar</publication><modification>2025-04-04T14:39:41.752Z</modification><creation>2019-03-27T01:45:15Z</creation></dates><accession>S-EPMC4329085</accession><cross_references><pubmed>25203057</pubmed><doi>10.1111/liv.12682</doi></cross_references></HashMap>