title: Long-term reversal of hypocholesterolaemia in patients with chronic hepatitis C is related to sustained viral response and viral genotype.
abstract: BACKGROUND
  Genotype-3 of hepatitis C virus (HCV) has been associated with serum lipid changes (reversible with sustained viral response) and liver steatosis.
  
  
  OBJECTIVE
  To characterize the relationships among hepatic steatosis, cholesterol and sustained viral response in these patients.
  
  
  METHODS
  Patients (n = 215) with chronic hepatitis C (157 with genotype-1 of HCV) had age, body mass index, gender, alcohol intake, glycaemia, serum lipids, transaminases, grade and stage (METAVIR and Scheuer), degree of liver steatosis, sustained viral response, insulinaemia, leptinaemia, beta-hydroxybutyrate and glycerol measured, and were compared with 32 hepatitis B virus (HBV)-infected subjects.
  
  
  RESULTS
  Genotype-3 of HCV patients had age-adjusted hypocholesterolaemia and more frequent hepatic steatosis (P < 0.001). Steatosis was inversely correlated with serum cholesterol (P < 0.01) and directly with viral load (P < 0.03). In patients with genotype-3 of HCV and sustained viral response, serum cholesterol increased from 138 (95% CI: 120-151) to 180 mg/dL (95% CI: 171-199) 12 months after treatment conclusion (P < 0.0001). By contrast, cholesterol values were unchanged in genotype-3 of HCV non-responders and in patients with genotype-1 of HCV regardless of response. Rising cholesterol in sustained viral response did not parallel the changes in beta-hydroxybutyrate.
  
  
  CONCLUSIONS
  Besides causing hepatic steatosis, genotype-3 specifically decreases serum cholesterol. This interference with the metabolic lipid pathway is related to viral load, is reversed with sustained viral response, and seems unrelated to mitochondrial dysfunction.
authors.affiliation: Units of Gastroenterology and Liver Diseases, Fundación Hospital Alorcón, Madrid, Spain. cfernandez@fhalcorcon.es
authors.forename: C M
authors.initials: CM
authors.lastname: Fernández-Rodríguez
authors.forename: P
authors.initials: P
authors.lastname: López-Serrano
authors.forename: S
authors.initials: S
authors.lastname: Alonso
authors.forename: M L
authors.initials: ML
authors.lastname: Gutiérrez
authors.forename: J L
authors.initials: JL
authors.lastname: Lledó
authors.forename: J L
authors.initials: JL
authors.lastname: Pérez-Calle
authors.forename: R
authors.initials: R
authors.lastname: Temiño
authors.forename: G
authors.initials: G
authors.lastname: Cacho
authors.forename: M
authors.initials: M
authors.lastname: Nevado
authors.forename: M L
authors.initials: ML
authors.lastname: Casas
authors.forename: J M
authors.initials: JM
authors.lastname: Gasalla
authors.forename: B
authors.initials: B
authors.lastname: Bonet
mesh_terms: D002096:C-Peptide / Q000378:metabolism*; D002784:Cholesterol / Q000097:blood* / Q000172:deficiency; D050171:Dyslipidemias / Q000821:virology*; D005234:Fatty Liver / Q000209:etiology; D005260:Female; D005838:Genotype; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000235:genetics*; D006801:Humans; D020738:Leptin / Q000378:metabolism*; D008297:Male; D008875:Middle Aged
chemical_list: D002096:C-Peptide; D020738:Leptin; D002784:Cholesterol