title: Liver dysfunction and fibrosis as predictors of biochemical response to autoimmune hepatitis treatment.
abstract: BACKGROUND
  Autoimmune hepatitis (AIH) is a disease that presents itself in various forms, ranging from aminotransferase asymptomatic alteration, acute hepatitis to decompensated cirrhosis. Few studies have evaluated the predictive criteria as a response to treatment.
  
  
  METHODS
  A cross-sectional analytical study examined patients with AIH who were visited in the hepatology clinic of a university hospital between January 2013 and July 2015.
  
  
  RESULTS
  A total of 36 patients were included (44.7 ± 14.3 years, 22.2% male, and 19.2% of patients presented with liver failure). Patients with significant fibrosis had lower mean aminotransferases and bilirubins and higher mean prothrombin activity (PA) than those with insignificant fibrosis. Most patients (94.5%) underwent treatment with azathioprine and prednisone. In a comparison between individuals who exhibited biochemical response (ALT and AST < 55 U/L in the sixth month of treatment) and those without biochemical response, it was observed that those with biochemical response presented minor proportion of patients with significant fibrosis, and these patients had a higher proportion of liver failure in initial presentation and lower mean PA. Furthermore, it was observed that the lower the PT on admission was, the lower ALT levels (r = 0.682, P = 0.020) and AST (r = 0.431, P = 0.040) in the sixth month of treatment were.
  
  
  CONCLUSIONS
  Individuals with liver dysfunction and elevated aminotransferases show insignificant fibrosis histologically. AIH patients who initially present liver failure and insignificant fibrosis are more likely to develop biochemical response to treatment.
authors.affiliation: Division of Gastroenterology, Internal Medicine, Federal University of Santa Catarina, Florianópolis, Brazil - janaina.narciso@uol.com.br.
authors.forename: Júlia C
authors.initials: JC
authors.lastname: Soares
authors.forename: Ariane
authors.initials: A
authors.lastname: Borgonovo
authors.forename: Dariana C
authors.initials: DC
authors.lastname: Maggi
authors.forename: Ana P B F
authors.initials: AP
authors.lastname: Pasinato
authors.forename: Fernanda G
authors.initials: FG
authors.lastname: Ramos
authors.forename: Esther B
authors.initials: EB
authors.lastname: Dantas-Corrêa
authors.forename: Leonardo L
authors.initials: LL
authors.lastname: Schiavon
authors.forename: Janaína L
authors.initials: JL
authors.lastname: Narciso-Schiavon
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D001219:Aspartate Aminotransferases / Q000097:blood; D001379:Azathioprine / Q000627:therapeutic use; D001663:Bilirubin / Q000097:blood; D015415:Biomarkers / Q000097:blood; D003430:Cross-Sectional Studies; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use*; D019693:Hepatitis, Autoimmune / Q000150:complications / Q000188:drug therapy*; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D008103:Liver Cirrhosis / Q000209:etiology*; D017093:Liver Failure / Q000209:etiology*; D008297:Male; D011241:Prednisone / Q000627:therapeutic use
chemical_list: D015415:Biomarkers; D005938:Glucocorticoids; D007166:Immunosuppressive Agents; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D001379:Azathioprine; D001663:Bilirubin; D011241:Prednisone