title: Fibrosis in Chronic Hepatitis C: Correlation between Immunohistochemically-Assessed Virus Load with Steatosis and Cellular Iron Content.
abstract: OBJECTIVE
  We aimed study impact of hepatocytic viral load, steatosis, and iron load on fibrosis in chronic hepatitis C and role of VEGF and VEGFR overexpression in cirrhotic cases in evolving HCC.
  
  
  METHODS
  Total of 120 cases were included from TBRI and Beaujon Hospital as chronic hepatitis C (CHC), post-hepatitis C cirrhosis, and HCC. Cases of CHC were stained for Sirius red, Prussian blue and immunohistochemically (IHC) for HCV-NS3/NS4. HCC were stained IHC for VEGF and by FISH.
  
  
  RESULTS
  Stage of fibrosis was significantly correlated with inflammation in CHC (P < 0.01). Noticed iron load did not correlate with fibrosis. Steatosis was associated with higher inflammation and fibrosis. The cellular viral load did not correlate with inflammation, steatosis or fibrosis. VEGF by IHC was significantly higher in cases of HCC when compared to cirrhotic group (P < 0.001). Amplification of VEGFR2 was confirmed in 40% of cases of HCC. Scoring of VEGF by IHC was the good indicator of VEGFR2 amplification by FISH (P < 0.005).
  
  
  CONCLUSIONS
  Grade of inflammation is the factor affecting fibrosis in CHC. The degree of liver damage is not related to cellular viral load or iron load. Steatosis is associated with higher inflammation and fibrosis. VEGF by IHC is correlated with overexpression of VEGFR2 by FISH.
authors.affiliation: Department of Pathology, Theodor Bilharz Research Institute, Imbaba, Giza, Egypt.
authors.forename: Maha
authors.initials: M
authors.lastname: Akl
authors.affiliation: Department of Pathology, Faculty of Medicine Cairo University, Cairo, Egypt.
authors.forename: Ali El
authors.initials: AE
authors.lastname: Hindawi
authors.affiliation: Department of Pathology, Faculty of Medicine Cairo University, Cairo, Egypt.
authors.forename: Maha
authors.initials: M
authors.lastname: Mosaad
authors.affiliation: Department of Pathology, Theodor Bilharz Research Institute, Imbaba, Giza, Egypt.
authors.forename: Ahmed
authors.initials: A
authors.lastname: Montasser
authors.affiliation: Department of Gastroenterology, Theodor Bilharz Research Institute, Imbaba, Giza, Egypt.
authors.forename: Ahmed El
authors.initials: AE
authors.lastname: Ray
authors.affiliation: Department of Pathology, Theodor Bilharz Research Institute, Imbaba, Giza, Egypt.
authors.forename: Heba
authors.initials: H
authors.lastname: Khalil
authors.affiliation: Department of Gastroenterology, Theodor Bilharz Research Institute, Imbaba, Giza, Egypt.
authors.forename: Amgad
authors.initials: A
authors.lastname: Anas
authors.affiliation: Department of Gastroenterology, Theodor Bilharz Research Institute, Imbaba, Giza, Egypt.
authors.forename: Raffat
authors.initials: R
authors.lastname: Atta
authors.affiliation: Deparment of Pathology, Beaujon Hospital, Clichy, France.
authors.forename: Valerie
authors.initials: V
authors.lastname: Paradis
authors.affiliation: Department of Pathology, Theodor Bilharz Research Institute, Imbaba, Giza, Egypt.
authors.forename: Ahmed Abdel
authors.initials: AA
authors.lastname: Hadi
authors.affiliation: Department of Pathology, Theodor Bilharz Research Institute, Imbaba, Giza, Egypt.
authors.forename: Olfat
authors.initials: O
authors.lastname: Hammam
keywords: FISH; Fibrosis; HCC; HCV; NS3/NS4; VEGF; VEGFR2