title: Hepatic steatosis in chronic hepatitis B develops due to host metabolic factors: a comparative approach with genotype 1 chronic hepatitis C.
abstract: OBJECTIVE
  Hepatic steatosis has not been adequately studied in chronic hepatitis B, while it is considered to be a cardinal feature in chronic hepatitis C and to be mainly metabolically induced in patients infected with genotype 1. We investigated the prevalence of and the parameters associated with steatosis in HBeAg-negative chronic hepatitis B.
  
  
  METHODS
  We studied 213 patients with HBeAg-negative chronic hepatitis B and compared them with 163 patients with genotype-1 chronic hepatitis C. Steatosis was semi-quantitatively graded.
  
  
  RESULTS
  Steatosis was significantly less frequent in chronic hepatitis B than chronic hepatitis C (60% versus 72%, P=0.016), but there was no difference in the prevalence of moderate/severe steatosis. In chronic hepatitis B, steatosis was associated only with higher body mass index (P=0.002), while moderate/severe steatosis was associated only with higher body mass index (P=0.043) and diabetes (P=0.031). Steatosis was relatively less frequent in chronic hepatitis B than chronic hepatitis C non-diabetic, normal-weight patients (45.6% versus 62.5%, P=0.063), but it did not differ in diabetic and/or overweight/obese patients with chronic hepatitis B or chronic hepatitis C.
  
  
  CONCLUSIONS
  Hepatic steatosis in HBeAg-negative chronic hepatitis B (a) is less frequent than in genotype-1 chronic hepatitis C, (b) is mainly associated with presence of host metabolic factors, such as high body mass index and diabetes and (c) does not seem to be associated with the severity of liver histological lesions.
authors.affiliation: 2nd Department of Internal Medicine, Athens University Medical School, Hippokration General Hospital, 114 Vas. Sophias Ave., 11527 Athens, Greece.
authors.forename: E
authors.initials: E
authors.lastname: Tsochatzis
authors.forename: G V
authors.initials: GV
authors.lastname: Papatheodoridis
authors.forename: E K
authors.initials: EK
authors.lastname: Manesis
authors.forename: N
authors.initials: N
authors.lastname: Chrysanthos
authors.forename: G
authors.initials: G
authors.lastname: Kafiri
authors.forename: A J
authors.initials: AJ
authors.lastname: Archimandritis
mesh_terms: D001706:Biopsy; D015992:Body Mass Index; D004279:DNA, Viral / Q000235:genetics*; D048909:Diabetes Complications / Q000150:complications* / Q000378:metabolism; D005234:Fatty Liver / Q000453:epidemiology / Q000209:etiology* / Q000378:metabolism; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000235:genetics*; D006514:Hepatitis B Surface Antigens / Q000276:immunology; D006513:Hepatitis B e Antigens / Q000276:immunology; D006515:Hepatitis B virus / Q000235:genetics / Q000276:immunology; D019694:Hepatitis B, Chronic / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D019698:Hepatitis C, Chronic / Q000150:complications / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D007124:Immunoenzyme Techniques; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D015995:Prevalence; D011379:Prognosis; D012189:Retrospective Studies
chemical_list: D004279:DNA, Viral; D006514:Hepatitis B Surface Antigens; D006513:Hepatitis B e Antigens