title: Lectin pathway of complement activation and relation with clinical complications in critically ill children.
abstract: BACKGROUND
  Critically ill children are susceptible to nosocomial infections, which contribute to adverse outcomes. Deficiencies in the innate immunity lectin pathway of complement activation are implicated in a child's vulnerability to infections in conditions such as cancer, but the role during critical illness remains unclear. We hypothesized that low on-admission levels of the pathway proteins are, in part, genetically determined and associated with susceptibility to infectious complications and adverse outcomes.
  
  
  METHODS
  We studied protein levels of mannose-binding lectin (MBL), H-ficolin and M-ficolin, three MBL-associated-serine proteases (MASPs) and MBL-associated protein (MAp44), and relation with functional genetic polymorphisms, in 130 healthy children and upon intensive care unit (ICU) admission in 700 critically ill children of a randomized study on glycemic control.
  
  
  RESULTS
  Levels of MASP-1, MASP-2, MASP-3, and MAp-44 were lower and the levels of M-ficolin were higher in ICU patients on admission than those in matched healthy controls. Only a low on-admission MASP-3 level was independently associated with risk of new ICU infections and prolonged ICU stay, after correcting for other risk factors. On-admission MASP-3 varied with age, illness severity, and genetic variation.
  
  
  CONCLUSIONS
  Low on-admission MASP-3 levels in critically ill children were independently associated with subsequent acquisition of infection and prolonged ICU stay. The biological explanation needs further investigation.
authors.affiliation: Clinical Department and Laboratory of Intensive Care Medicine, Division of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium.
authors.forename: Catherine
authors.initials: C
authors.lastname: Ingels
authors.affiliation: Clinical Department and Laboratory of Intensive Care Medicine, Division of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium.
authors.forename: Ilse
authors.initials: I
authors.lastname: Vanhorebeek
authors.affiliation: Regional Centre for Blood Transfusion and Clinical Immunology, Aalborg University Hospital, Aalborg, Denmark.
authors.forename: Rudi
authors.initials: R
authors.lastname: Steffensen
authors.affiliation: Clinical Department and Laboratory of Intensive Care Medicine, Division of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium.
authors.forename: Inge
authors.initials: I
authors.lastname: Derese
authors.affiliation: Department of Biomedicine, Medical Microbiology and Immunology, Aarhus University, Aarhus, Denmark.
authors.forename: Lisbeth
authors.initials: L
authors.lastname: Jensen
authors.affiliation: Clinical Department and Laboratory of Intensive Care Medicine, Division of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium.
authors.forename: Pieter J
authors.initials: PJ
authors.lastname: Wouters
authors.affiliation: Clinical Department and Laboratory of Intensive Care Medicine, Division of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium.
authors.forename: Greet
authors.initials: G
authors.lastname: Hermans
authors.affiliation: Department of Biomedicine, Medical Microbiology and Immunology, Aarhus University, Aarhus, Denmark.
authors.forename: Steffen
authors.initials: S
authors.lastname: Thiel
authors.affiliation: Clinical Department and Laboratory of Intensive Care Medicine, Division of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium.
authors.forename: Greet
authors.initials: G
authors.lastname: Van den Berghe
mesh_terms: D002648:Child; D003167:Complement Activation / Q000502:physiology*; D016638:Critical Illness; D006801:Humans; D015278:Intensive Care Units, Pediatric; D037102:Lectins / Q000378:metabolism / Q000502:physiology*; D010343:Patient Admission; D057057:Serine Proteases / Q000378:metabolism
chemical_list: D037102:Lectins; D057057:Serine Proteases