title: Serum apolipoprotein C-III is independently associated with chronic hepatitis C infection and advanced fibrosis.
abstract: BACKGROUND
  The hepatitis C virus (HCV) is known to disrupt lipid metabolism, making serum lipoprotein levels good candidates to explore as markers of HCV disease progression. Assessment of the major apolipoproteins (Apo) and their relationship to hepatic fibrosis remain largely unexplored.
  
  
  METHODS
  We compared the levels of total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C), and Apo A-I, -B, -C-III, and -E between patients with cleared versus active infection (n = 83), and between those chronically infected patients (n = 216) with advanced versus mild-moderate hepatic fibrosis (METAVIR stage F3-4 vs. F0-2) using multiple logistic regression.
  
  
  RESULTS
  Apo C-III levels were 25% higher in subjects with cleared infection versus those with active infection (p = 0.009). Low levels of Apo C-III (p = 1.3 × 10(-5)), Apo A-I (p = 2.9 × 10(-5)), total cholesterol (p = 5.0 × 10(-4)), LDL-C (p = 0.005), and HDL-C (p = 2.0 × 10(-4)) were associated with advanced fibrosis in univariate analyses. Multivariable analysis revealed Apo C-III as the most significant factor associated with advanced fibrosis (p = 0.0004), followed by age (p = 0.013) and Apo A-I (p = 0.022). Inclusion of both Apo C-III and Apo A-I in a model to predict advanced fibrosis improved the area under the receiver operator curve only modestly.
  
  
  CONCLUSIONS
  Relative to other lipoproteins, low serum Apo C-III levels are the most strongly associated with chronic versus cleared infection and decline with increasing severity of hepatic fibrosis. Apo C-III deserves further attention as a possible marker of HCV disease progression.
authors: Division of Endocrinology, Department of Medicine, Metabolism and Nutrition, Duke University, Durham, NC, USA.
authors: J
authors: J
authors: Rowell
authors: Department of GI/Hepatology Research Program, Duke Clinical Research Institute, Duke University, PO Box 17969, Durham, NC, 27715, USA.
authors: A J
authors: AJ
authors: Thompson
authors: Division of Endocrinology, Department of Medicine, Metabolism and Nutrition, Duke University, Durham, NC, USA.
authors: J R
authors: JR
authors: Guyton
authors: Institute for Genome Sciences and Policy, Duke University, Durham, NC, USA.
authors: X Q
authors: XQ
authors: Lao
authors: Department of GI/Hepatology Research Program, Duke Clinical Research Institute, Duke University, PO Box 17969, Durham, NC, 27715, USA.
authors: J G
authors: JG
authors: McHutchison
authors: Institute for Genome Sciences and Policy, Duke University, Durham, NC, USA.
authors: J J
authors: JJ
authors: McCarthy
authors: Department of GI/Hepatology Research Program, Duke Clinical Research Institute, Duke University, PO Box 17969, Durham, NC, 27715, USA. keyur.patel@duke.edu.
authors: K
authors: K
authors: Patel