title: Hepatitis C virus-associated hypobetalipoproteinemia is correlated with plasma viral load, steatosis, and liver fibrosis.
abstract: OBJECTIVE
  A relationship between chronic hepatitis C virus (HCV) infection and lipid metabolism has recently been suggested. The aim of this study was to determine the correlation between lipid profile and virology, histologic lesions, and response to alpha interferon therapy in noncirrhotic, nondiabetic patients with hepatitis C.
  
  
  METHODS
  A total of 109 consecutive untreated chronic hepatitis C patients were studied to assess the following: 1) the effects of HCV genotype, viral load, steatosis, hepatic fibrosis, and body mass index (BMI) on lipid profile; and 2) whether lipid parameters could predict response to antiviral therapy.
  
  
  RESULTS
  The control group showed a significantly higher apolipoprotein B (apoB) concentration compared with patients with chronic hepatitis C. Hypobetalipoproteinemia (apo B <0.7 g/L) was found in 27 (24.7%) chronic HCV patients and in five (5.3%) control subjects (p = 0.0002). Levels of apo B were negatively correlated with steatosis and HCV viral load (r = -0.22; p = 0.03). This last correlation was strong for non-1 genotype and genotype 3 (r = -0.48; p = 0.0005, and r = -0.47; p = 0.007, respectively) but was not found in genotype 1. In multivariate analysis, low apo B concentration was significantly associated with fibrosis grade 2 or 3 versus grade 0 or 1 (p < 0.001), steatosis >5% (p < 0.001), low body mass index (p < 0.001), and high HCV viral load (p < 0.014). No correlation was found in the 76 treated patients between apo B and response to interferon therapy.
  
  
  CONCLUSIONS
  In chronic HCV patients, hypobetalipoproteinemia occurs already in the early stages of HCV infection before the development of liver cirrhosis. The correlation between apo B levels and HCV viral load seems to confirm the interaction between hepatitis C infection and beta-lipoprotein metabolism.
authors.affiliation: Services de Diabétologie et Endocrinologie, Dijon cedex, France.
authors.forename: Jean Michel
authors.initials: JM
authors.lastname: Petit
authors.forename: Muriel
authors.initials: M
authors.lastname: Benichou
authors.forename: Laurence
authors.initials: L
authors.lastname: Duvillard
authors.forename: Valerie
authors.initials: V
authors.lastname: Jooste
authors.forename: Jean Baptiste
authors.initials: JB
authors.lastname: Bour
authors.forename: Anne
authors.initials: A
authors.lastname: Minello
authors.forename: Bruno
authors.initials: B
authors.lastname: Verges
authors.forename: Jean Marcel
authors.initials: JM
authors.lastname: Brun
authors.forename: Philippe
authors.initials: P
authors.lastname: Gambert
authors.forename: Patrick
authors.initials: P
authors.lastname: Hillon
mesh_terms: D000328:Adult; D000998:Antiviral Agents / Q000627:therapeutic use; D001055:Apolipoproteins B / Q000097:blood; D015992:Body Mass Index; D018450:Disease Progression; D005234:Fatty Liver / Q000097:blood / Q000188:drug therapy / Q000821:virology*; D005260:Female; D016679:Genome, Viral; D016174:Hepacivirus / Q000235:genetics*; D019698:Hepatitis C, Chronic / Q000097:blood / Q000188:drug therapy / Q000821:virology*; D006801:Humans; D006995:Hypobetalipoproteinemias / Q000097:blood / Q000188:drug therapy / Q000821:virology*; D016898:Interferon-alpha / Q000627:therapeutic use; D008099:Liver / Q000473:pathology / Q000821:virology; D008103:Liver Cirrhosis / Q000097:blood / Q000188:drug therapy / Q000821:virology*; D008111:Liver Function Tests; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D012367:RNA, Viral / Q000097:blood*; D012044:Regression Analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D019562:Viral Load
chemical_list: D000998:Antiviral Agents; D001055:Apolipoproteins B; D016898:Interferon-alpha; D012367:RNA, Viral