title: Anti-Golgi complex antibodies during pegylated-interferon therapy for hepatitis C.
abstract: OBJECTIVE
  Pegylated interferon (Peg-IFN) plus ribavirin is the standard therapy for hepatitis C. Peg-IFN has several antiviral mechanisms, but its role in hepatitis C treatment seems to be related to its immunomodulatory effect. Ribavirin, an antiviral agent, potentiates IFN activity when added to it. Both drugs are associated with adverse reactions of different magnitudes. Autoimmune phenomena have been reported with this treatment. In this paper, we describe cases of ALT/GGT flares during Peg-IFN plus ribavirin treatment, which related to the appearance of anti-Golgi antibody and disease progress.
  
  
  METHODS
  We investigated three patients with hepatitis C and severe ALT/GGT flares during Peg-IFN and ribavirin treatment coinciding with anti-Golgi complex antibody as the only marker of autoimmunity. We then reviewed the medical files and tested anti-Golgi antibody in stored sera from 25 patients treated with conventional IFN and in 14 patients treated with Peg-IFN.
  
  
  RESULTS
  The three patients were male, over 45 years of age; all were relapsers and non-responders. Anti-Golgi antibody was positive during treatment coinciding with ALT/GGT flares but with hepatitis C virus (HCV)-RNA negativity, disappearing after stopping treatment, with normalization of ALT/AST levels. One patient had progression of fibrosis from F2 to F3 despite negativity of HCV-RNA. In the last group, only two patients treated with Peg-IFN experienced ALT/GGT flares but without anti-Golgi antibody
  
  
  CONCLUSIONS
  The presence of anti-Golgi complex antibody could be a marker of a temporary autoimmune phenomenon and progressive disease.
authors.affiliation: Gastro-Hepatology Unit, Faculty of Medicine, University Hospital of Bahia, Bahia, Brazil. unif@svn.com.br
authors.forename: Raymundo
authors.initials: R
authors.lastname: Paraná
authors.forename: Maria Isabel
authors.initials: MI
authors.lastname: Schinoni
authors.forename: Luiz A R
authors.initials: LA
authors.lastname: de Freitas
authors.forename: Liana
authors.initials: L
authors.lastname: Codes
authors.forename: Marla
authors.initials: M
authors.lastname: Cruz
authors.forename: Zilton
authors.initials: Z
authors.lastname: Andrade
authors.forename: Christian
authors.initials: C
authors.lastname: Trepo
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000998:Antiviral Agents / Q000009:adverse effects* / Q000627:therapeutic use; D001323:Autoantibodies / Q000097:blood*; D018450:Disease Progression; D004359:Drug Therapy, Combination; D006056:Golgi Apparatus / Q000276:immunology*; D016174:Hepacivirus / Q000235:genetics; D006526:Hepatitis C / Q000097:blood* / Q000150:complications / Q000188:drug therapy* / Q000821:virology; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000009:adverse effects* / Q000627:therapeutic use; D008099:Liver / Q000473:pathology; D008103:Liver Cirrhosis / Q000473:pathology / Q000821:virology; D008297:Male; D008875:Middle Aged; D011092:Polyethylene Glycols / Q000009:adverse effects* / Q000627:therapeutic use; D012367:RNA, Viral / Q000097:blood; D011994:Recombinant Proteins; D012254:Ribavirin / Q000009:adverse effects* / Q000627:therapeutic use; D005723:gamma-Glutamyltransferase / Q000097:blood
chemical_list: D000998:Antiviral Agents; D001323:Autoantibodies; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D012367:RNA, Viral; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; D012254:Ribavirin; D005723:gamma-Glutamyltransferase; D000410:Alanine Transaminase; C100416:peginterferon alfa-2a