title: Association of promoter polymorphism of the CD14 C (-159) T endotoxin receptor gene with chronic hepatitis B.
abstract: OBJECTIVE
  To investigate whether single-nucleotide polymorphisms in the promoter regions of endotoxin-responsive genes CD14 C (-159) T is associated with chronic hepatitis B.
  
  
  METHODS
  We obtained genomic DNA from 80 patients with established diagnosis of chronic hepatitis B and 126 healthy subjects served as a control population. The CD 14 C (-159) T polymorphism was investigated using an allele specific PCR method.
  
  
  RESULTS
  Twenty seven percent of chronic hepatitis B patients and 75% of controls were heterozygous for CT genotype. The difference between the chronic hepatitis B and control groups was statistically significant [P < 0.0001; Odds ratio (OR) = 2.887; 95% CI: 1.609-5.178]. Twenty four point six percent of chronic hepatitis B and patients 12.3% of the control group were heterozygous for TT genotype. The difference between groups was not statistically significant (P = 0.256; OR = 0.658; 95% CI: 0.319-1.358). Forty eight point four percent of chronic hepatitis B patients and 12.7% of control were homozygote for CC genotype (P < 0.004; OR = 0.416; 95% CI: 0.229-0.755). The frequency of allele C was 61.9% and allele T was 38.1% in hepatitis B patients group. The frequency of allele C was 55.2% and allele T was 44.8% for the control group (P = 0.179; OR = 1.319; 95% CI: 0.881-1.977).
  
  
  CONCLUSIONS
  The TT heterozygous genotype was not a risk factor for chronic hepatitis B. CC homozygote genotype is protective for hepatitis B. Lack of heterozygosis of genotype CT is a risk factor for chronic hepatitis B. Alleles C or T were not risk factors for chronic hepatitis B. These findings show the role of a single-nucleotide polymorphism at CD14/-159 on the development of chronic hepatitis B. Endotoxin susceptibility may play a role in the pathogenesis of chronic hepatitis B.
authors.affiliation: Research Center for Gastroenterology and Liver Disease, Shaheed Beheshti University of Medical Sciences, 7th floor, Taleghani Hospital, Yaman Str., Evin, Tehran 19857, Iran. article@rcgld.org
authors.forename: Amir Houshang
authors.initials: AH
authors.lastname: Mohammad Alizadeh
authors.forename: Mitra
authors.initials: M
authors.lastname: Ranjbar
authors.forename: Mehrdad
authors.initials: M
authors.lastname: Hajilooi
authors.forename: Farahnaz
authors.initials: F
authors.lastname: Fallahian
mesh_terms: D000328:Adult; D000483:Alleles; D016022:Case-Control Studies; D004247:DNA / Q000235:genetics; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D019694:Hepatitis B, Chronic / Q000209:etiology / Q000235:genetics*; D006579:Heterozygote; D006720:Homozygote; D006801:Humans; D018950:Lipopolysaccharide Receptors / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D011401:Promoter Regions, Genetic / Q000235:genetics*; D011971:Receptors, Immunologic / Q000235:genetics*
chemical_list: D018950:Lipopolysaccharide Receptors; D011971:Receptors, Immunologic; C048071:endotoxin receptor; D004247:DNA