title: MCP-1 and MIP3-alpha serum levels in acute liver failure and molecular adsorbent recirculating system (MARS) treatment: a pilot study.
abstract: OBJECTIVE
  The CC chemokines monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-3 alpha (MIP3-alpha) may be involved in the pathogenesis of acute liver failure (ALF) and acute-on-chronic liver failure (ACLF). In ALF and ACLF, the molecular adsorbent recirculating system (MARS) has been used to support liver function. Enhancement of MCP-1, as seen in other extracorporeal support systems such as haemodialysis, might thus have mitigated the beneficial effects of the MARS system in acute hepatic failure.
  
  
  METHODS
  Serum concentrations of MCP-1 and MIP3-alpha were measured in 10 patients with ALF or ACLF treated with MARS. Thirteen patients suffering from chronic hepatic failure (CHF) and 15 healthy individuals served as controls.
  
  
  RESULTS
  Baseline MCP-1 serum concentrations were significantly increased in ALF and ACLF patients as compared to patients with CHF (p=0.0027 and p=0.0046, respectively) and controls (p=0.0006 and p=0.0012, respectively). MIP3-alpha serum concentrations were also significantly enhanced in the ALF and ACLF groups as compared with those in CHF patients (p=0.0002 and p=0.0003, respectively) and controls (p<0.0001 and p<0.0001, respectively). Moreover, MIP3-alpha levels were significantly increased in CHF patients as compared to controls (p=0.0002). MCP-1 and MIP3-alpha concentrations did not change significantly during MARS treatment in ALF and ACLF patients.
  
  
  CONCLUSIONS
  The CC chemokines MCP-1 and MIP3-alpha are increased in ALF and ACLF patients. MARS had no effect on MCP-1 and MIP3-alpha serum concentrations in patients with ALF and ACLF, and yielded no evidence of any harmful effects of the increase of these potentially hepatocidal chemokines.
authors.affiliation: Department of Anaesthesiology, General Intensive Care and Pain Medicine, Center for Physiology, Pathophysiology and Immunology, Medical University of Vienna, Vienna, Austria. georg.roth@meduniwien.ac.at
authors.forename: Georg A
authors.initials: GA
authors.lastname: Roth
authors.forename: Peter
authors.initials: P
authors.lastname: Faybik
authors.forename: Hubert
authors.initials: H
authors.lastname: Hetz
authors.forename: Hendrik J
authors.initials: HJ
authors.lastname: Ankersmit
authors.forename: Konrad
authors.initials: K
authors.lastname: Hoetzenecker
authors.forename: Andreas
authors.initials: A
authors.lastname: Bacher
authors.forename: Theresia
authors.initials: T
authors.lastname: Thalhammer
authors.forename: Claus G
authors.initials: CG
authors.lastname: Krenn
mesh_terms: D000293:Adolescent; D000328:Adult; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000097:blood*; D054418:Chemokine CCL20 / Q000097:blood*; D005260:Female; D006801:Humans; D017114:Liver Failure, Acute / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010865:Pilot Projects
chemical_list: C111835:CCL2 protein, human; C108355:CCL20 protein, human; D018932:Chemokine CCL2; D054418:Chemokine CCL20