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Role of immunohistochemistry for hepatitis D and hepatitis B virus in hepatitis delta
Gökhan Kabaçam1, Heiner Wedemeyer, Berna Savaş
1Department of Gastroenterology, University of Ankara Medical School, Ankara, Turkey.
Insights
Hepatitis D antigen (HDAg) liver staining correlates with liver injury in chronic delta hepatitis (CDH). Hepatitis B core antigen (HBcAg) does not appear to contribute to liver injury in CDH.
Area of Science:
- Hepatology
- Virology
- Immunohistochemistry
Background:
- Chronic delta hepatitis (CDH) is a significant liver disease.
- Immunohistochemical assessment of liver tissue in CDH requires further investigation.
Purpose of the Study:
- To evaluate variables associated with hepatitis D antigen (HDAg), hepatitis B surface antigen (HBsAg), and hepatitis B core antigen (HBcAg) liver staining in CDH.
- To understand the role of these antigens in liver injury and disease progression.
Main Methods:
- Utilized demographic, biochemical, and virologic data from the HIDIT 1 study.
- Performed semiquantitative immunohistochemical (IHC) assessment of HBsAg, HBcAg, and HDAg staining in liver tissue.
Main Results:
- HDAg staining correlated positively with age and ALT, and negatively with serum HBsAg.
- HBsAg staining showed varied correlations with HBV DNA, serum HBsAg, and HBeAg serology.
- HBcAg staining was primarily nuclear and negatively correlated with serum HBsAg and histologic activity.
Conclusions:
- HDAg expression is associated with liver injury in CDH.
- HBcAg expression does not appear to contribute to liver injury in CDH.
- HBsAg staining profiles differ in various stages of CDH, highlighting its importance in disease progression.
Background & Aims:
Immunohistochemical assessment of liver tissue in chronic delta hepatitis (CDH) is underinvestigated. Aim of the study was (i) to assess variables associated with hepatitis D antigen (HDAg), hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg) staining in the liver.
Methods:
Demographic, biochemical and virologic data collected from the HIDIT 1 study were used. HBsAg, HBcAg and HDAg immunohistochemical (IHC) staining was semiquantitatively assessed.
Results:
Hepatitis D antigen immunohistochemical staining displayed positive correlations with age and alanine aminotransferase (ALT) and negative correlations with serum HBsAg (P = 0.01 for all). HBsAg IHC displayed a negative correlation with gamma glutamyl transferase and positive correlations with serum HBV DNA, serum HBsAg levels and HBeAg serology (P < 0.001, P = 0.02 and P = 0.007 respectively). HBcAg staining was mainly nuclear and displayed negative correlations with serum HBsAg and histologic activity (P = 0.002 and P = 0.02 respectively). Pegylated IFN based treatment led to a decline of all IHC markers, however, these markers had no impact on treatment outcome.
Conclusions:
These data suggest an association of liver injury with HDAg expression in CDH whereas the negative correlation between HBcAg expression and liver injury and the overall nuclear localization of HBcAg suggest that HBcAg does not contribute to liver injury in CDH. HDV cases with high level of HBV replication, high serum HBsAg levels, HBeAg positivity, that are probably in the earlier stages of disease (low gamma-glutamyl transferase), had a more intense HBsAg staining profile. Overall, the data enforce the importance of HDAg and HBsAg in different phases of CDH infection.
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