title: Effects of tumor necrosis factor antagonist treatment on hepatitis C-related immunological abnormalities.
abstract: BACKGROUND
  Chronic hepatitis C infection is frequently associated with a mixed cryoglobulinaemia and circulating auto-antibodies, especially anti-smooth muscle cells (SMA) and anti-liver/kidney/microsome type 1 (LKM-1) anti-tissue antibodies. Treatments with TNF antagonists favour the emergence of auto-antibodies, and particularly anti-dsDNA antibodies.
  
  
  OBJECTIVE
  To determine the impact of TNF antagonists on hepatitis C-related immune abnormalities.
  
  
  METHODS
  We prospectively monitored for 14 weeks, six patients with actively replicating chronic hepatitis C, initiating an anti-TNF treatment for an associated rheumatoid arthritis.
  
  
  RESULTS
  Anti-nuclear and anti-dsDNA antibodies were induced in two and three patients, respectively. Treatment had no impact on the production of antibodies against extractable nuclear antigens, and it did not induce anti-tissues antibodies in any patient. Cryoglobulinaemia appeared in 2/6 patients, and it persisted in 2 others. No patient developed any news signs of autoimmunity. HCV viraemia remained unchanged.
  
  
  CONCLUSIONS
  Induction of auto-antibodies by TNF antagonist treatments does not involve anti-tissues antibodies, even in patients with actively replicating chronic hepatitis C prone to produce anti-SMA and anti-LKM-1 antibodies. In contrast, TNF antagonists may favour emergence of cryoglobulinaemia in such patients.
authors.affiliation: Service de Microbiologie-Immunologie Biologique, hôpital A. Béclère, Assistance Publique-Hôpitaux de Paris.
authors.forename: Christelle
authors.initials: C
authors.lastname: Vauloup
authors.forename: Roman
authors.initials: R
authors.lastname: Krzysiek
authors.forename: Liliane
authors.initials: L
authors.lastname: Greangeot-Keros
authors.forename: Daniel
authors.initials: D
authors.lastname: Wendling
authors.forename: Phillippe
authors.initials: P
authors.lastname: Goupille
authors.forename: Rachel
authors.initials: R
authors.lastname: Brault
authors.forename: Christine
authors.initials: C
authors.lastname: Brousse
authors.forename: Xavier
authors.initials: X
authors.lastname: Mariette
authors.forename: Dominique
authors.initials: D
authors.lastname: Emilie
mesh_terms: D000328:Adult; D000974:Antibodies, Antinuclear / Q000097:blood; D000911:Antibodies, Monoclonal / Q000009:adverse effects / Q000627:therapeutic use*; D018501:Antirheumatic Agents / Q000009:adverse effects / Q000627:therapeutic use; D001323:Autoantibodies / Q000097:blood*; D003449:Cryoglobulinemia / Q000209:etiology; D000068800:Etanercept; D005260:Female; D016174:Hepacivirus / Q000235:genetics; D019698:Hepatitis C, Chronic / Q000097:blood / Q000188:drug therapy* / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000009:adverse effects / Q000627:therapeutic use; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D011446:Prospective Studies; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D013997:Time Factors; D016896:Treatment Outcome; D000079424:Tumor Necrosis Factor Inhibitors; D048069:Tumor Necrosis Factors / Q000276:immunology*; D019562:Viral Load; D014766:Viremia / Q000188:drug therapy
chemical_list: D000974:Antibodies, Antinuclear; D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D001323:Autoantibodies; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D000079424:Tumor Necrosis Factor Inhibitors; D048069:Tumor Necrosis Factors; D000069285:Infliximab; D000068800:Etanercept