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Fibrosis in Chronic Hepatitis C: Correlation between Immunohistochemically-Assessed Virus Load with Steatosis and Cellular Iron Content

2016-12-15 19:14:54

Semantics Scholar; December 15, 2016: /DOI:10.3889/oamjms.2016.122



Maha Akl1, Ali EL Hindawi2, Maha Mosaad2, Ahmed Montasser1*, Ahmed El Ray3, Heba Khalil1, Amgad Anas3, Raffat Atta3, Valerie Paradis4, Ahmed Abdel Hadi1, Olfat Hammam1



Abstract


AIM: 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.


MATERIAL AND 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).


CONCLUSION: 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.



Introduction


Hepatitis C virus (HCV) is a global epidemic affecting approximately 3% of the world's population. Egypt has the highest prevalence of hepatitis C virus (HCV) in the world, estimated nationally at 14.7%. Our study's objective was to delineate the evidence on the epidemiology of HCV infection among the different population groups in Egypt and to draw analytical inferences about the nature of HCV transmission in this country. In the 15–59 year age groups, the prevalence of HCV antibody was found to be 10.0% (95% CI = 9.5 –10.5) and that of HCV RNA to be 7.0% (95% CI = 6.6–7.4). In children, 1–14 years old, the prevalence of HCV antibody and HCV RNA were 0.4% (95% CI = 0.3–0.5) and 0.2% (95% CI = 0.1– 0.3) respectively. Approximately, 3.7 million persons have chronic HCV infection in the age group 15–59 in 2015. An estimated 29% reduction in HCV RNA prevalence has been seen since 2008, which is largely attributable to the ageing of the group infected 40–50 years ago during the mass schistosomiasis treatment campaigns. Prevention efforts may have also contributed to this decline, with an estimated 75% (95% CI = 6–45) decrease in HCV incidence in the 0– 19 year age groups over the past 20 years.



Steatosis is a complication of HCV infection and the mechanisms of its development are complex, involving viral and host factors. Steatosis that is
Akl et al. Fibrosis in Chronic Hepatitis C prevalently viral is associated with HCV genotype 3, and steatosis that is prevalently metabolic is associated with non-3 genotypes. Viral steatosis is correlated with the level of HCV replication, whereas metabolic steatosis is related to insulin resistance. The two types of steatosis have a different impact on HCV disease and may have an additive effect.



It has been generally accepted that either steatosis by itself aggravates fibrosis or the factors that are causing steatosis may be aggravating fibrosis. Overall, steatosis, whether metabolic or HCV induced, worsens the sequence of events leading to advanced fibrosis in patients with HCV and needs to be addressed when managing patients with HCV.




Empire Genomic's VEGFR2 FISH probe was used in this publication.



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