title: Dietary cholesterol intake is associated with progression of liver disease in patients with chronic hepatitis C: analysis of the Hepatitis C Antiviral Long-term Treatment Against Cirrhosis trial.
abstract: OBJECTIVE
  Little is known about whether dietary cholesterol affects disease progression in patients with chronic hepatitis C virus infection.
  
  
  METHODS
  We analyzed data from the Hepatitis C Antiviral Long-term Treatment Against Cirrhosis trial, which included patients with advanced fibrosis and compensated cirrhosis. Cholesterol intake was determined for 608 participants on the basis of responses to food frequency questionnaires, administered at baseline and 1.8 years later. We investigated whether cholesterol intake was associated with clinical progression (death, variceal bleeding, encephalopathy, ascites, peritonitis, Child-Turcotte-Pugh score ≥ 7, or hepatocellular carcinoma) or histologic progression of disease (an increase in Ishak fibrosis score of 2 or more points in a second liver biopsy compared with the first).
  
  
  RESULTS
  After adjustments for age, sex, race, presence of cirrhosis, body mass index, treatment with peginterferon, lifetime alcohol consumption, smoking, health status, and coffee and macronutrient intake, each higher quartile of cholesterol intake was associated with a 46% increase in the risk of clinical or histologic progression (adjusted hazard ratio [AHR], 1.46; 95% confidence interval [CI], 1.13-1.87; P for the trend = .004). Compared with patients in the lowest quartile of cholesterol intake (32-152 mg/day), those in the 3rd (224-310 mg/day; AHR, 2.83; 95% CI, 1.45-5.51) and 4th quartiles (>310 mg/day; AHR, 2.74; 95% CI, 1.22-6.16) had significantly increased risk of disease progression.
  
  
  CONCLUSIONS
  On the basis of analysis of data from the Hepatitis C Antiviral Long-term Treatment Against Cirrhosis trial, higher dietary cholesterol intake is associated with higher risk of disease progression in HCV-infected patients with advanced fibrosis or compensated cirrhosis.
authors.affiliation: Division of Gastroenterology, University of Washington, Seattle, Washington. Electronic address: leiy@medicine.washington.edu.
authors.forename: Lei
authors.initials: L
authors.lastname: Yu
authors.forename: Chihiro
authors.initials: C
authors.lastname: Morishima
authors.forename: George N
authors.initials: GN
authors.lastname: Ioannou
mesh_terms: D000328:Adult; D001201:Ascites / Q000453:epidemiology; D006528:Carcinoma, Hepatocellular / Q000453:epidemiology; D002791:Cholesterol, Dietary / Q000378:metabolism*; D015331:Cohort Studies; D018450:Disease Progression; D005247:Feeding Behavior; D005260:Female; D019698:Hepatitis C, Chronic / Q000473:pathology*; D006801:Humans; D008113:Liver Neoplasms / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D010538:Peritonitis / Q000453:epidemiology; D012307:Risk Factors; D012720:Severity of Illness Index; D011795:Surveys and Questionnaires; D016019:Survival Analysis
chemical_list: D002791:Cholesterol, Dietary
keywords: AHR; BMI; CI; CTP; Child–Turcotte–Pugh; Cholesterol; Cirrhosis; Diet; FFQ; HALT-C; HCC; HCV; Hepatitis C; Hepatitis C Antiviral Long-term Treatment Against Cirrhosis; MTP; TLR; Toll-like receptor; adjusted hazard ratio; body mass index; confidence interval; food frequency questionnaire; hepatitis C virus; hepatocellular carcinoma; microsomal triglyceride transfer protein