Background: Although annular fibrosis is the hallmark of cirrhosis, other microscopic changes impacting on liver function such as sinusoid capillarization or loss of metabolic zonation are common. A sustained virological response (SVR) may halt fibrosis deposition in hepatitis C virus (HCV) infected patients, but its impact on the other cirrhosis-associated lesions is unknown.AIMS:To assess the impact of an SVR on cirrhosis-related histopathological features.MATERIAL AND METHODS:Paired pre- and post-treatment liver biopsies from 38 HCV cirrhotics with an SVR were analysed. Fibrosis was staged by METAVIR and the area of fibrosis by morphometry. Ductular proliferation, metabolic zonation, sinusoid capillarization and hepatic stellate cells activation were assessed by anti-cytokeratin7 (CK7), -glutamine synthetase (GS), -cytochrome P4502E1 (CYP2E1), -CD34 and alpha-smooth muscle actine (αSMA).RESULTS:After 61 months from an SVR, cirrhosis regression was observed in 61%, and the collagen content decreased in 89%. Although periportal and lobular necroinflammation vanished, portal inflammation persisted in 66%. Ductular proliferation decreased in 92%. Before treatment, metabolic zonation was lost, as shown by GS and CYP2E1, in 71% and 88%, respectively, with normalization in 79% and 73%, after an SVR. Conversely, no changes in sinusoidal capillarization were observed after treatment, as assessed by CD34 (p=0.41) and αSMA (p=0.95). Finally, no differences in all the immunohistochemical scores emerged whether or not cirrhosis persisted.CONCLUSION:Cirrhosis regression and fibrosis amount decrease are frequently observed among HCV cirrhotic patients with an SVR. Despite ductular proliferation vanishing and lobular zonation restoration, portal inflammation and sinusoidal capillarization may not regress after viral eradication (HEPATOLOGY 2012.)

A morphometric and immunohistochemical study to assess the benefit of a sustained virological response in hepatitis C virus patients with cirrhosis

Aghemo A;
2012-01-01

Abstract

Background: Although annular fibrosis is the hallmark of cirrhosis, other microscopic changes impacting on liver function such as sinusoid capillarization or loss of metabolic zonation are common. A sustained virological response (SVR) may halt fibrosis deposition in hepatitis C virus (HCV) infected patients, but its impact on the other cirrhosis-associated lesions is unknown.AIMS:To assess the impact of an SVR on cirrhosis-related histopathological features.MATERIAL AND METHODS:Paired pre- and post-treatment liver biopsies from 38 HCV cirrhotics with an SVR were analysed. Fibrosis was staged by METAVIR and the area of fibrosis by morphometry. Ductular proliferation, metabolic zonation, sinusoid capillarization and hepatic stellate cells activation were assessed by anti-cytokeratin7 (CK7), -glutamine synthetase (GS), -cytochrome P4502E1 (CYP2E1), -CD34 and alpha-smooth muscle actine (αSMA).RESULTS:After 61 months from an SVR, cirrhosis regression was observed in 61%, and the collagen content decreased in 89%. Although periportal and lobular necroinflammation vanished, portal inflammation persisted in 66%. Ductular proliferation decreased in 92%. Before treatment, metabolic zonation was lost, as shown by GS and CYP2E1, in 71% and 88%, respectively, with normalization in 79% and 73%, after an SVR. Conversely, no changes in sinusoidal capillarization were observed after treatment, as assessed by CD34 (p=0.41) and αSMA (p=0.95). Finally, no differences in all the immunohistochemical scores emerged whether or not cirrhosis persisted.CONCLUSION:Cirrhosis regression and fibrosis amount decrease are frequently observed among HCV cirrhotic patients with an SVR. Despite ductular proliferation vanishing and lobular zonation restoration, portal inflammation and sinusoidal capillarization may not regress after viral eradication (HEPATOLOGY 2012.)
2012
Fibrosis; Regression; Hepatic Progenitor Cells (HPCs); Metabolic Zonation; Sinusoidal Capillarization
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11699/3128
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