title: Atorvastatin improves disease activity of nonalcoholic steatohepatitis partly through its tumour necrosis factor-α-lowering property.
abstract: BACKGROUND
  We have previously found that atorvastatin decreases liver injury markers in patients with nonalcoholic steatohepatitis. However, how atorvastatin treatment ameliorates the disease activity in nonalcoholic steatohepatitis patients remains unknown.
  
  
  OBJECTIVE
  We examined here which anthropometric, metabolic and inflammatory variables were improved and related with amelioration of disease activity in atorvastatin-treated nonalcoholic steatohepatitis patients.
  
  
  METHODS
  Forty-two biopsy-proven nonalcoholic steatohepatitis patients with dyslipidemia were enrolled. Patients were treated with atorvastatin (10mg/day) for 12 months.
  
  
  RESULTS
  Atorvastatin significantly decreased liver transaminase, γ-glutamyl transpeptidase, low-density lipoprotein-cholesterol, triglycerides, type IV collagen, and tumour necrosis factor-α levels, whilst it increased adiponectin and high-density lipoprotein-cholesterol. Atorvastatin improved nonalcoholic fatty liver disease activity score and increased liver to spleen density ratio. Multiple stepwise regression analysis revealed that γ-glutamyl transpeptidase, tumour necrosis factor-α and liver to spleen density ratio (inversely) were independently associated with nonalcoholic fatty liver disease activity score. Aspartate aminotransferase, low-density lipoprotein-cholesterol and nonalcoholic fatty liver disease activity score were independent determinants of decreased liver to spleen density ratio.
  
  
  CONCLUSIONS
  The present study suggests that atorvastatin improves the disease activity of nonalcoholic steatohepatitis partly via its tumour necrosis factor-α-lowering property.
authors.affiliation: Department of Medicine and Molecular Sciences, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan.
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Hyogo
authors.forename: Sho-ichi
authors.initials: S
authors.lastname: Yamagishi
authors.forename: Sayaka
authors.initials: S
authors.lastname: Maeda
authors.forename: Yuki
authors.initials: Y
authors.lastname: Kimura
authors.forename: Tomokazu
authors.initials: T
authors.lastname: Ishitobi
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Chayama
mesh_terms: D052242:Adiponectin / Q000097:blood; D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D000924:Anticholesteremic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001219:Aspartate Aminotransferases / Q000097:blood; D000069059:Atorvastatin; D001786:Blood Glucose / Q000187:drug effects; D015992:Body Mass Index; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D024141:Collagen Type IV / Q000097:blood; D050171:Dyslipidemias / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D005234:Fatty Liver / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D005260:Female; D006538:Heptanoic Acids / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D065626:Non-alcoholic Fatty Liver Disease; D011758:Pyrroles / Q000494:pharmacology / Q000627:therapeutic use*; D012044:Regression Analysis; D012720:Severity of Illness Index; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*; D005723:gamma-Glutamyltransferase / Q000097:blood
chemical_list: D052242:Adiponectin; D000924:Anticholesteremic Agents; D001786:Blood Glucose; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D024141:Collagen Type IV; D006538:Heptanoic Acids; D011758:Pyrroles; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D000069059:Atorvastatin; D005723:gamma-Glutamyltransferase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase