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PubMed ID:
25203057
Public Release Type:
Journal
Publication Year: 2015
Affiliation: Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus, Denmark.
DOI:
https://doi.org/10.1111/liv.12682
Authors:
Zaman A,
Laursen TL,
Sandahl TD,
Støy S,
Schiødt FV,
Lee WM,
Vilstrup H,
Thiel S,
Grønbaek H,
US Acute Liver Failure Study Group,
Lee WM,
Polson J,
Pezzia C,
Lalani E,
Hynan LS,
Reisch JS,
Larson AM,
Crippin JS,
Gerstle L,
Davern TJ,
Partovi K,
Emre S,
McCashland TM,
Bernard T,
Hay J,
Groettum C,
Murray N,
Coultrup S,
Shakil A,
Morton D,
Blei AT,
Gottstein J,
Schwartz J,
Ingram K,
Han S,
Peacock V,
Fontana RJ,
Welch S,
McGuire B,
Avant L,
Chung R,
Casson D,
Brown R Jr,
Schilsky M,
Senkbeil L,
Harrison M,
Rush R,
Reuben A,
Huntley N,
Munoz S,
Misra C,
Stravitz T,
Salvatori J,
Rossaro L,
Prosser C,
Satyanarayana R,
Taylor W,
Reddy R,
Campbell M,
Hassenein T,
Barakat F,
Smith A
Studies:
Acute Liver Failure Study Group: Adult Acute Liver Failure Study
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.
