title: Post-load insulin resistance does not predict virological response to treatment of chronic hepatitis C patients without the metabolic syndrome.
abstract: OBJECTIVE
  The role of insulin resistance in predicting virological response to therapy of chronic hepatitis C is debated. We assessed the association between basal (defined as homeostasis model assessment of insulin resistance (HOMA-IR)>2) and post-load insulin resistance (as oral glucose insulin sensitivity index<9.8 mg/kg/min) with the rapid and sustained virological responses in chronic hepatitis C.
  
  
  METHODS
  Observational prospective study of 124 treatment-naïve patients with chronic hepatitis C not fulfilling the metabolic syndrome criteria, adherent to a standard treatment with pegylated interferon alpha plus ribavirin.
  
  
  RESULTS
  Insulin resistance was detected in 50% (by HOMA-IR) and 29% (by oral glucose insulin sensitivity index) of patients. Independent predictors of rapid virologic response were hepatitis C virus (HCV) genotype 2 (odds ratio 5.66; 95% confidence interval 1.88-17.01), HCV genotype 3 (odds ratio 5.23; 95% confidence interval 1.84-14.84) and lower basal ferritin levels (odds ratio 0.99; 95% confidence interval 0.993-0.998). Independent predictors of sustained virologic response were HCV genotype 2 (odds ratio 19.54; 95% confidence interval 2.29-166.41) and HCV genotype 3 (odds ratio 3.24; 95% confidence interval 1.10-9.58). Rapid virologic response was by itself predictive of sustained virologic response (odds ratio 40.90; 95% confidence interval 5.37-311.53).
  
  
  CONCLUSIONS
  Insulin resistance, measured by both static and dynamic methods, does not predict rapid or sustained virologic response in chronic hepatitis C patients without the metabolic syndrome.
authors.affiliation: Department of Medicine, University of Verona, Verona, Italy. giovanna.fattovich@univr.it
authors.forename: Giovanna
authors.initials: G
authors.lastname: Fattovich
authors.forename: Gianluca Svegliati
authors.initials: GS
authors.lastname: Baroni
authors.forename: Michela
authors.initials: M
authors.lastname: Pasino
authors.forename: Irene
authors.initials: I
authors.lastname: Pierantonelli
authors.forename: Loredana
authors.initials: L
authors.lastname: Covolo
authors.forename: Donatella
authors.initials: D
authors.lastname: Ieluzzi
authors.forename: Nicola
authors.initials: N
authors.lastname: Passigato
authors.forename: Angelo
authors.initials: A
authors.lastname: Tonon
authors.forename: Maria Grazia
authors.initials: MG
authors.lastname: Faraci
authors.forename: Maria
authors.initials: M
authors.lastname: Guido
authors.forename: Francesco
authors.initials: F
authors.lastname: Negro
mesh_terms: D000998:Antiviral Agents / Q000627:therapeutic use*; D001786:Blood Glucose / Q000032:analysis; D005260:Female; D005293:Ferritins / Q000097:blood; D005838:Genotype; D016174:Hepacivirus / Q000235:genetics; D019698:Hepatitis C, Chronic / Q000188:drug therapy* / Q000821:virology*; D006801:Humans; D007333:Insulin Resistance; D016898:Interferon-alpha / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D011092:Polyethylene Glycols / Q000627:therapeutic use*; D011446:Prospective Studies; D012313:RNA / Q000378:metabolism; D011994:Recombinant Proteins / Q000627:therapeutic use; D012254:Ribavirin / Q000627:therapeutic use*
chemical_list: D000998:Antiviral Agents; D001786:Blood Glucose; D016898:Interferon-alpha; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; D012254:Ribavirin; D012313:RNA; D005293:Ferritins; C100416:peginterferon alfa-2a