title: Effect of interleukin-10 gene promoter polymorphisms -1082 G/A and -592 C/A on response to therapy in children and adolescents with chronic hepatitis C virus infection.
abstract: OBJECTIVE
  Studying predictors of response to therapy for hepatitis C virus (HCV) infection in children may help avoid the inappropriate use of currently available costly therapy associated with numerous adverse effects. We tested the hypothesis that inheritance of single nucleotide polymorphisms (SNPs) of the interleukin-10 (IL-10) promoter gene might influence response to HCV treatment.
  
  
  METHODS
  The impact of SNPs, -1082 G/A and -592 C/A, in the promoter region of IL-10 gene, on response to HCV therapy was assessed in a cohort of 40 children treated with a combination of pegylated interferon (Peg-IFN) α2b and ribavirin.
  
  
  RESULTS
  Sustained virological response was achieved in 48.7%. High viral load was associated with non-response to therapy. There was no association between histopathological degree of inflammation or fibrosis and response to therapy. There was no direct statistically significant association between polymorphisms in the IL-10 gene (-1082G/A and -592 C/A) as regards inflammation or response to therapy in children. As for the SNP -592 C/A; there was a statistically significant association with the score of fibrosis (P<0.004), concluding that the A allele was protective from moderate and severe fibrosis. Meanwhile the SNP -1082G/A did not show any association with the fibrosis score.
  
  
  CONCLUSIONS
  We could not associate response to therapy for HCV with IL-10 polymorphisms -1082 G/A and -592 C/A. For the SNP -592 C/A, the A allele protected from moderate and severe fibrosis.
authors.affiliation: Department of Pediatrics, Kasr Al Ainy School of Medicine, Cairo University, Egypt. Electronic address: hanaakaraksy@kasralainy.edu.eg.
authors.forename: Hanaa M
authors.initials: HM
authors.lastname: El-Karaksy
authors.affiliation: Department of Clinical and Chemical Pathology, Kasr Al Ainy School of Medicine, Cairo University, Egypt.
authors.forename: Sahar A
authors.initials: SA
authors.lastname: Sharaf
authors.affiliation: Department of Clinical and Chemical Pathology, Kasr Al Ainy School of Medicine, Cairo University, Egypt.
authors.forename: Iman A
authors.initials: IA
authors.lastname: Mandour
authors.affiliation: Department of Pediatrics, Kasr Al Ainy School of Medicine, Cairo University, Egypt.
authors.forename: Engy A
authors.initials: EA
authors.lastname: Mogahed
authors.affiliation: Department of Clinical and Chemical Pathology, Kasr Al Ainy School of Medicine, Cairo University, Egypt.
authors.forename: Normeen H
authors.initials: NH
authors.lastname: Rady
authors.affiliation: Department of Clinical and Chemical Pathology, Kasr Al Ainy School of Medicine, Cairo University, Egypt.
authors.forename: Fatma A
authors.initials: FA
authors.lastname: El-Mougy
mesh_terms: D000293:Adolescent; D000483:Alleles; D000998:Antiviral Agents / Q000627:therapeutic use; D002648:Child; D004359:Drug Therapy, Combination; D005260:Female; D005355:Fibrosis; D005838:Genotype; D016174:Hepacivirus / Q000502:physiology*; D019698:Hepatitis C, Chronic / Q000188:drug therapy / Q000235:genetics*; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000008:administration & dosage; D016753:Interleukin-10 / Q000235:genetics*; D008099:Liver / Q000187:drug effects / Q000473:pathology*; D008297:Male; D020641:Polymorphism, Single Nucleotide; D011401:Promoter Regions, Genetic / Q000235:genetics*; D012254:Ribavirin / Q000008:administration & dosage; D016896:Treatment Outcome; D019562:Viral Load / Q000187:drug effects
chemical_list: D000998:Antiviral Agents; C508609:IL10 protein, human; D000077190:Interferon alpha-2; D016898:Interferon-alpha; C000614170:Interferon-alpha2b; D016753:Interleukin-10; D012254:Ribavirin
keywords: HCV; Interleukin-10; Peg-IFN; SNP -1082 G/A; SNP -592 C/A