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Published on: February 10, 2015
Racial differences in liver inflammation and fibrosis related to chronic hepatitis C
Kester Crosse1, Onuora G Umeadi, Frank A Anania
1Department of Medicine, The University of Maryland Baltimore School of Medicine, USA.
Insights
Black Americans with Hepatitis C virus (HCV) infection show milder liver disease progression compared to white Americans. This study found less liver inflammation and fibrosis in Black patients, irrespective of iron levels.
Area of Science:
- Hepatology
- Infectious Diseases
- Clinical Research
Background:
- Hepatitis C virus (HCV) infection is more common in Black Americans than White Americans.
- The natural history of HCV in Black patients remains underexplored.
- Understanding racial differences in HCV progression is crucial for tailored treatment strategies.
Purpose of the Study:
- To define the natural course of HCV infection in Black Americans.
- To compare liver histology and clinical parameters between Black and White HCV patients.
- To investigate potential factors influencing disease severity across racial groups.
Main Methods:
- Retrospective comparison of 87 Black and 136 White American patients with chronic HCV.
- Analysis of initial liver tests, HCV genotype, viral load, and liver biopsy findings.
- Liver biopsies assessed using the Knodell Histologic Activity Index (HAI).
Main Results:
- Black HCV patients were older and more likely to have HCV genotype 1.
- Despite similar transmission modes and duration, Black patients exhibited lower mean HAI scores, indicating less necroinflammation and fibrosis.
- Lower mean serum alanine transaminase (ALT) and iron levels were observed in Black patients.
Conclusions:
- Black chronic HCV patients demonstrate less severe liver necroinflammation and fibrosis compared to White patients.
- These histological differences are not attributable to variations in hepatic iron loading.
- Findings suggest distinct disease trajectories for HCV in different racial groups.
Background & Aims:
Hepatitis C virus (HCV) infection is more prevalent in black compared with white Americans. However, the natural course of HCV in black patients has not been defined.
Methods:
We performed a retrospective comparison of initial liver tests, HCV genotype and viral load, and liver histology findings in 87 black and 136 white American chronic hepatitis C patients who were evaluated at the University of Maryland between 1995 and 1998. The liver biopsy examinations were interpreted by using the Knodell Histologic Activity Index (HAI) criteria.
Results:
Black HCV patients were older (46.3 vs. 43.3 yr; P = 0.004) and were more likely to be infected with HCV genotype 1 (95% vs. 75%). The modes of HCV transmission, estimated duration of HCV infection, and prevalence of alcohol abuse were similar in the 2 groups. Yet, black patients had lower mean total HAI scores (7.6 vs. 8.7; P = 0.021), periportal hepatocyte necrosis scores (P = 0.021), and liver fibrosis scores (P = 0.049). In keeping with less hepatic necroinflammatory activity, black patients had a lower mean serum alanine transaminase (ALT) level (85.5 vs. 122.7; P = 0.002). Black patients also had lower serum iron levels (P = 0.009). There were no racial differences in the prevalence of increased iron studies and hepatic iron loading.
Conclusions:
Black chronic HCV patients have milder liver necroinflammation and fibrosis than white patients with similar HCV duration. These differences in liver histology were not explained by a variance in hepatic iron loading.
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