title: Changes in adipocytokines and insulin sensitivity during and after antiviral therapy for hepatitis C genotype 4.
abstract: BACKGROUND
  Hepatitis C virus (HCV) infection, especially genotypes 1 and 4, is associated with wide metabolic disarrangements.
  
  
  OBJECTIVE
  To assess whether host metabolic factors influence sustained virological response (SVR) in patients with chronic hepatitis C genotype 4 (HCV-4) treated with peginterferon / ribavirin and to evaluate the impact of antiviral therapy on insulin resistance (IR) and serum levels of adipocytokines.
  
  
  METHODS
  Changes in levels of adiponectin, leptin, TNF-α and the homeostasis model assessment for insulin resistance (HOMA-IR) on antiviral combination in patients with HCV-4 were analyzed and effect on response was studied.
  
  
  RESULTS
  107 patients were included (M/F 86/21; mean age 41.4±5.6 years). Neither serum adipocytokines nor HOMA-IR was correlated with viral load. SVR was achieved by 57% of patients and was associated with fibrosis score (odds ratio: 6.5; P = 0.001) and adiponectin level (odds ratio: 1.3; P = 0.01). At the end of follow-up, HOMA-IR, adiponectin, leptin and TNF-α were reduced, all these changes unrelated to predicting the outcome of treatment. At follow-up, HOMA-IR and adiponectin continued to decrease in patients with SVR, but remained unchanged significantly in patients who did not response or relapse.
  
  
  CONCLUSIONS
  Serum adiponectin at baseline appears to be an independent predictor for the achievement of SVR and can be utilized as an additional predictive marker. Changes of IR and adipocytokines occur under treatment which is more evident with the resolution of HCV infection, suggesting that HCV could have a direct role in these metabolic changes.
authors.affiliation: Department of Internal Medicine, Minia University, Minia, Egypt. mkhattabmed@hotmail.com
authors.forename: Mahmoud Aboelneen
authors.initials: MA
authors.lastname: Khattab
authors.forename: Mohammed
authors.initials: M
authors.lastname: Eslam
authors.forename: Mohammed
authors.initials: M
authors.lastname: Shatat
authors.forename: Hesham
authors.initials: H
authors.lastname: Abd-Aalhalim
authors.forename: Yousef I
authors.initials: YI
authors.lastname: Mousa
authors.forename: Fatma
authors.initials: F
authors.lastname: Samir
authors.forename: Hanan
authors.initials: H
authors.lastname: Aly
authors.forename: Olfat
authors.initials: O
authors.lastname: Shaker
authors.forename: Yehia
authors.initials: Y
authors.lastname: Shaker
mesh_terms: D054392:Adipokines / Q000097:blood*; D000328:Adult; D000998:Antiviral Agents / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D004334:Drug Administration Schedule; D004359:Drug Therapy, Combination; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D016174:Hepacivirus / Q000235:genetics* / Q000378:metabolism; D019698:Hepatitis C, Chronic / Q000097:blood / Q000188:drug therapy* / Q000821:virology; D006801:Humans; D007333:Insulin Resistance; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D011092:Polyethylene Glycols / Q000627:therapeutic use; D011994:Recombinant Proteins / Q000627:therapeutic use; D012254:Ribavirin / Q000627:therapeutic use; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D019562:Viral Load
chemical_list: D054392:Adipokines; D000998:Antiviral Agents; D015415:Biomarkers; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D011092:Polyethylene Glycols; D012254:Ribavirin; C417083:peginterferon alfa-2b; C100416:peginterferon alfa-2a