title: Circulating mannan-binding lectin, M-, L-, H-ficolin and collectin-liver-1 levels in patients with acute liver failure.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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).
  
  
  RESULTS
  At day 1, the MBL level in ALF patients was 40% lower compared with healthy controls {[median (interquartile range) 0.72 μg/ml(0.91) vs. 1.15 (1.92)(P = 0.02]}, and increased significantly by day 3 [0.83 μg/ml(0.94)(P = 0.01)]. The M-ficolin level was 60% lower [0.54 μg/ml(0.50) vs. 1.48(1.01)(P < 0.0001)]. The CL-L1 level at day 1 was slightly higher compared with healthy controls [3.20 μg/ml(2.37) vs. 2.64(0.72)(P = 0.11)]; this was significant at day 3 [3.35(1.84)(P = 0.006)]. H- and L-ficolin levels were similar to healthy controls. Spontaneous ALF survivors had higher levels of MBL at day 1 [0.96 μg/ml(1.15) vs. 0.60(0.60)(P = 0.02)] and lower levels of L-ficolin by day 3 compared with patients who died or were transplanted [1.61 μg/ml(1.19) vs. 2.17(2.19)(P = 0.02)].
  
  
  CONCLUSIONS
  We observed significant dynamics in lectin levels in ALF patients, which may suggest they play a role in ALF pathogenesis. High MBL and low L-ficolin levels are associated with survival.
authors.affiliation: Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus, Denmark.
authors.forename: Tea L
authors.initials: TL
authors.lastname: Laursen
authors.forename: Thomas D
authors.initials: TD
authors.lastname: Sandahl
authors.forename: Sidsel
authors.initials: S
authors.lastname: Støy
authors.forename: Frank V
authors.initials: FV
authors.lastname: Schiødt
authors.forename: William M
authors.initials: WM
authors.lastname: Lee
authors.forename: Hendrik
authors.initials: H
authors.lastname: Vilstrup
authors.forename: Steffen
authors.initials: S
authors.lastname: Thiel
authors.forename: Henning
authors.initials: H
authors.lastname: Grønbaek
mesh_terms: D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D037222:Collectins / Q000097:blood*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006023:Glycoproteins / Q000097:blood*; D006801:Humans; D037102:Lectins / Q000097:blood*; D008099:Liver / Q000378:metabolism / Q000503:physiopathology; D017114:Liver Failure, Acute / Q000097:blood* / Q000150:complications; D008297:Male; D037601:Mannose-Binding Lectin / Q000097:blood*; D008875:Middle Aged; D018746:Systemic Inflammatory Response Syndrome / Q000150:complications; D055815:Young Adult; D000097604:Ficolins
chemical_list: D037222:Collectins; D006023:Glycoproteins; D037102:Lectins; D037601:Mannose-Binding Lectin; D000097604:Ficolins; C445459:COLEC10 protein, human; C109662:FCN3 protein, human
keywords: acute liver failure; collectin-liver-1; complement system; ficolins; mannan-binding lectin; the lectin pathway