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:
Fontana RJ,
Lee WM,
Lee WM,
Avant L,
Barakat F,
Bernard T,
Blei AT,
Brown R Jr,
Campbell M,
Casson D,
Chung R,
Coultrup S,
Crippin JS,
Davern TJ,
Emre S,
Gerstle L,
Gottstein J,
Groettum C,
Grønbaek H,
Han S,
Harrison M,
Hassenein T,
Hay J,
Huntley N,
Hynan LS,
Ingram K,
Lalani E,
Larson AM,
Laursen TL,
McCashland TM,
McGuire B,
Misra C,
Morton D,
Munoz S,
Murray N,
Partovi K,
Peacock V,
Pezzia C,
Polson J,
Prosser C,
Reddy R,
Reisch JS,
Reuben A,
Rossaro L,
Rush R,
Salvatori J,
Sandahl TD,
Satyanarayana R,
Schilsky M,
Schiødt FV,
Schwartz J,
Senkbeil L,
Shakil A,
Smith A,
Støy S,
Stravitz T,
Taylor W,
Thiel S,
US Acute Liver Failure Study Group,
Vilstrup H,
Welch S,
Zaman 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.