Persistence of hepatocellular carcinoma risk in hepatitis C patients with a response to IFN and cirrhosis regression

Roberta D'Ambrosio, Alessio Aghemo, Maria Grazia Rumi, Elisabetta Degasperi, Angelo Sangiovanni, Marco Maggioni, Mirella Fraquelli, Riccardo Perbellini, William Rosenberg, Pierre Bedossa, Massimo Colombo, Pietro Lampertico

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Background and Aim: In patients with HCV-related cirrhosis, a sustained virological response may lead to cirrhosis regression. Whether histological changes translate into prevention of long-term complications, particularly hepatocellular carcinoma is still unknown. This was investigated in a cohort of histological cirrhotics who had been prospectively followed-up for 10 years after the achievement of a sustained virological response to IFN. Methods: In all, 38 sustained virological response cirrhotics who underwent a liver biopsy 5 years post-SVR were prospectively followed to assess the impact of cirrhosis regression on clinical endpoints. Results: During a follow-up of 86 (30-96) months from liver biopsy, no patients developed clinical decompensation, whilst 5 (13%) developed hepatocellular carcinoma after 79 (7-88) months. The 8-year cumulative probability of hepatocellular carcinoma was 17%, without differences between patients with or without cirrhosis regression (19% [95% CI 6%-50%] vs 14% [95% CI 4%-44%], P = .88). Patients who developed or did not an hepatocellular carcinoma had similar rates of residual cirrhosis (P = 1.0), collagen content (P = .48), METAVIR activity (P = .34), portal inflammation (P = .06) and steatosis (P = .17). At baseline, patients who developed an hepatocellular carcinoma had higher γGT (HR 1.03, 95% CI 1.00-1.06; P = .014) and glucose (HR 1.02, 95% CI 1.00-1.02; P = .012) values; moreover, they had increased Forns Score (HR 12.8, 95% CI 1.14-143.9; P = .039), Lok Index (HR 6.24, 95% CI 1.03-37.6; P = .046) and PLF (HR 19.3, 95% CI 1.72-217.6; P = .016) values. One regressor died of lung cancer. The 8-year cumulative survival probability was 97%, independently on cirrhosis regression (96% vs 100%, P = 1.0) or hepatocellular carcinoma (100% vs 97%, P = 1.0). Conclusions: Post-SVR cirrhosis regression does not prevent hepatocellular carcinoma occurrence.

Original languageEnglish
Pages (from-to)1459-1467
JournalLiver International
Volume38
Issue number8
DOIs
Publication statusPublished - 2018

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Hepatitis C
Hepatocellular Carcinoma
Fibrosis
Biopsy
Liver
Lung Neoplasms
Collagen
Inflammation
Glucose
Survival

Keywords

  • Cirrhosis regression
  • Hepatocellular carcinoma
  • Liver biopsy
  • Non-invasive tests
  • Sustained virological response
  • Transient elastography

ASJC Scopus subject areas

  • Hepatology

Cite this

Persistence of hepatocellular carcinoma risk in hepatitis C patients with a response to IFN and cirrhosis regression. / D'Ambrosio, Roberta; Aghemo, Alessio; Rumi, Maria Grazia; Degasperi, Elisabetta; Sangiovanni, Angelo; Maggioni, Marco; Fraquelli, Mirella; Perbellini, Riccardo; Rosenberg, William; Bedossa, Pierre; Colombo, Massimo; Lampertico, Pietro.

In: Liver International, Vol. 38, No. 8, 2018, p. 1459-1467.

Research output: Contribution to journalArticle

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abstract = "Background and Aim: In patients with HCV-related cirrhosis, a sustained virological response may lead to cirrhosis regression. Whether histological changes translate into prevention of long-term complications, particularly hepatocellular carcinoma is still unknown. This was investigated in a cohort of histological cirrhotics who had been prospectively followed-up for 10 years after the achievement of a sustained virological response to IFN. Methods: In all, 38 sustained virological response cirrhotics who underwent a liver biopsy 5 years post-SVR were prospectively followed to assess the impact of cirrhosis regression on clinical endpoints. Results: During a follow-up of 86 (30-96) months from liver biopsy, no patients developed clinical decompensation, whilst 5 (13{\%}) developed hepatocellular carcinoma after 79 (7-88) months. The 8-year cumulative probability of hepatocellular carcinoma was 17{\%}, without differences between patients with or without cirrhosis regression (19{\%} [95{\%} CI 6{\%}-50{\%}] vs 14{\%} [95{\%} CI 4{\%}-44{\%}], P = .88). Patients who developed or did not an hepatocellular carcinoma had similar rates of residual cirrhosis (P = 1.0), collagen content (P = .48), METAVIR activity (P = .34), portal inflammation (P = .06) and steatosis (P = .17). At baseline, patients who developed an hepatocellular carcinoma had higher γGT (HR 1.03, 95{\%} CI 1.00-1.06; P = .014) and glucose (HR 1.02, 95{\%} CI 1.00-1.02; P = .012) values; moreover, they had increased Forns Score (HR 12.8, 95{\%} CI 1.14-143.9; P = .039), Lok Index (HR 6.24, 95{\%} CI 1.03-37.6; P = .046) and PLF (HR 19.3, 95{\%} CI 1.72-217.6; P = .016) values. One regressor died of lung cancer. The 8-year cumulative survival probability was 97{\%}, independently on cirrhosis regression (96{\%} vs 100{\%}, P = 1.0) or hepatocellular carcinoma (100{\%} vs 97{\%}, P = 1.0). Conclusions: Post-SVR cirrhosis regression does not prevent hepatocellular carcinoma occurrence.",
keywords = "Cirrhosis regression, Hepatocellular carcinoma, Liver biopsy, Non-invasive tests, Sustained virological response, Transient elastography",
author = "Roberta D'Ambrosio and Alessio Aghemo and Rumi, {Maria Grazia} and Elisabetta Degasperi and Angelo Sangiovanni and Marco Maggioni and Mirella Fraquelli and Riccardo Perbellini and William Rosenberg and Pierre Bedossa and Massimo Colombo and Pietro Lampertico",
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T1 - Persistence of hepatocellular carcinoma risk in hepatitis C patients with a response to IFN and cirrhosis regression

AU - D'Ambrosio, Roberta

AU - Aghemo, Alessio

AU - Rumi, Maria Grazia

AU - Degasperi, Elisabetta

AU - Sangiovanni, Angelo

AU - Maggioni, Marco

AU - Fraquelli, Mirella

AU - Perbellini, Riccardo

AU - Rosenberg, William

AU - Bedossa, Pierre

AU - Colombo, Massimo

AU - Lampertico, Pietro

PY - 2018

Y1 - 2018

N2 - Background and Aim: In patients with HCV-related cirrhosis, a sustained virological response may lead to cirrhosis regression. Whether histological changes translate into prevention of long-term complications, particularly hepatocellular carcinoma is still unknown. This was investigated in a cohort of histological cirrhotics who had been prospectively followed-up for 10 years after the achievement of a sustained virological response to IFN. Methods: In all, 38 sustained virological response cirrhotics who underwent a liver biopsy 5 years post-SVR were prospectively followed to assess the impact of cirrhosis regression on clinical endpoints. Results: During a follow-up of 86 (30-96) months from liver biopsy, no patients developed clinical decompensation, whilst 5 (13%) developed hepatocellular carcinoma after 79 (7-88) months. The 8-year cumulative probability of hepatocellular carcinoma was 17%, without differences between patients with or without cirrhosis regression (19% [95% CI 6%-50%] vs 14% [95% CI 4%-44%], P = .88). Patients who developed or did not an hepatocellular carcinoma had similar rates of residual cirrhosis (P = 1.0), collagen content (P = .48), METAVIR activity (P = .34), portal inflammation (P = .06) and steatosis (P = .17). At baseline, patients who developed an hepatocellular carcinoma had higher γGT (HR 1.03, 95% CI 1.00-1.06; P = .014) and glucose (HR 1.02, 95% CI 1.00-1.02; P = .012) values; moreover, they had increased Forns Score (HR 12.8, 95% CI 1.14-143.9; P = .039), Lok Index (HR 6.24, 95% CI 1.03-37.6; P = .046) and PLF (HR 19.3, 95% CI 1.72-217.6; P = .016) values. One regressor died of lung cancer. The 8-year cumulative survival probability was 97%, independently on cirrhosis regression (96% vs 100%, P = 1.0) or hepatocellular carcinoma (100% vs 97%, P = 1.0). Conclusions: Post-SVR cirrhosis regression does not prevent hepatocellular carcinoma occurrence.

AB - Background and Aim: In patients with HCV-related cirrhosis, a sustained virological response may lead to cirrhosis regression. Whether histological changes translate into prevention of long-term complications, particularly hepatocellular carcinoma is still unknown. This was investigated in a cohort of histological cirrhotics who had been prospectively followed-up for 10 years after the achievement of a sustained virological response to IFN. Methods: In all, 38 sustained virological response cirrhotics who underwent a liver biopsy 5 years post-SVR were prospectively followed to assess the impact of cirrhosis regression on clinical endpoints. Results: During a follow-up of 86 (30-96) months from liver biopsy, no patients developed clinical decompensation, whilst 5 (13%) developed hepatocellular carcinoma after 79 (7-88) months. The 8-year cumulative probability of hepatocellular carcinoma was 17%, without differences between patients with or without cirrhosis regression (19% [95% CI 6%-50%] vs 14% [95% CI 4%-44%], P = .88). Patients who developed or did not an hepatocellular carcinoma had similar rates of residual cirrhosis (P = 1.0), collagen content (P = .48), METAVIR activity (P = .34), portal inflammation (P = .06) and steatosis (P = .17). At baseline, patients who developed an hepatocellular carcinoma had higher γGT (HR 1.03, 95% CI 1.00-1.06; P = .014) and glucose (HR 1.02, 95% CI 1.00-1.02; P = .012) values; moreover, they had increased Forns Score (HR 12.8, 95% CI 1.14-143.9; P = .039), Lok Index (HR 6.24, 95% CI 1.03-37.6; P = .046) and PLF (HR 19.3, 95% CI 1.72-217.6; P = .016) values. One regressor died of lung cancer. The 8-year cumulative survival probability was 97%, independently on cirrhosis regression (96% vs 100%, P = 1.0) or hepatocellular carcinoma (100% vs 97%, P = 1.0). Conclusions: Post-SVR cirrhosis regression does not prevent hepatocellular carcinoma occurrence.

KW - Cirrhosis regression

KW - Hepatocellular carcinoma

KW - Liver biopsy

KW - Non-invasive tests

KW - Sustained virological response

KW - Transient elastography

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