Evaluation of patients treated with direct-acting anti-viral therapy for chronic hepatitis C and their risk of hepatocellular carcinoma in Hong Kong
Abstract Background & aim To evaluate the risk of early hepatocellular carcinoma (HCC) in chronic hepatitis C patients treated with direct-acting antivirals (DAAs) in Hong Kong, as it has not been studied before in this locality. Methods Three hundred thirty-three consecutive chronic hepatitis C...
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BMC
2024-01-01
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Series: | BMC Gastroenterology |
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Online Access: | https://doi.org/10.1186/s12876-023-03099-2 |
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author | Victor Yung Sin Chow Wing I Cheung |
author_facet | Victor Yung Sin Chow Wing I Cheung |
author_sort | Victor Yung Sin Chow |
collection | DOAJ |
description | Abstract Background & aim To evaluate the risk of early hepatocellular carcinoma (HCC) in chronic hepatitis C patients treated with direct-acting antivirals (DAAs) in Hong Kong, as it has not been studied before in this locality. Methods Three hundred thirty-three consecutive chronic hepatitis C patients treated with DAAs from two hospitals over the past 6 years were identified. Kaplan-Meier method was used to calculate cumulative HCC incidence. Cox regression was used to identify factors associated with HCC development. Results During a median follow-up of 23.4 months after DAA started, 15 (5.4%, 95% CI 3.3–8.7%) out of 279 total included patients developed HCC. The overall sustained virological response (SVR) rate was 98.9%. The 1-year cumulative incidence for de-novo HCC and HCC recurrence were 0.8 and 30.9%, respectively (log-rank test p < 0.001). The 1-year cumulative HCC incidence for patients without and with cirrhosis were 0.7 and 5.1%, respectively (log-rank test p = 0.036). Univariate analysis showed that significant factors associated with HCC after DAA were: history of treated HCC, cirrhosis, evidence of portal hypertension, higher AFP at the start or end of DAA therapy, higher bilirubin, lower platelets, lower albumin, and older age. From receiver operating characteristic curve analysis, the optimal cut-off level of AFP for predicting HCC was 10.5 ng/mL at the start and 5.6 ng/mL at the end of DAA therapy. Conclusions The risk of early HCC recurrence remains high despite achieving SVR following DAA therapy, whereas the risk of early de-novo HCC occurence is low. AFP levels, both at the start and end of DAA therapy, can be useful in stratifying risks of HCC development. |
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issn | 1471-230X |
language | English |
last_indexed | 2024-03-07T15:29:28Z |
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spelling | doaj.art-2c1a7e99ada14654ab9790a5af04a4de2024-03-05T16:31:34ZengBMCBMC Gastroenterology1471-230X2024-01-0124111610.1186/s12876-023-03099-2Evaluation of patients treated with direct-acting anti-viral therapy for chronic hepatitis C and their risk of hepatocellular carcinoma in Hong KongVictor Yung Sin Chow0Wing I Cheung1Our Lady of Maryknoll HospitalOur Lady of Maryknoll HospitalAbstract Background & aim To evaluate the risk of early hepatocellular carcinoma (HCC) in chronic hepatitis C patients treated with direct-acting antivirals (DAAs) in Hong Kong, as it has not been studied before in this locality. Methods Three hundred thirty-three consecutive chronic hepatitis C patients treated with DAAs from two hospitals over the past 6 years were identified. Kaplan-Meier method was used to calculate cumulative HCC incidence. Cox regression was used to identify factors associated with HCC development. Results During a median follow-up of 23.4 months after DAA started, 15 (5.4%, 95% CI 3.3–8.7%) out of 279 total included patients developed HCC. The overall sustained virological response (SVR) rate was 98.9%. The 1-year cumulative incidence for de-novo HCC and HCC recurrence were 0.8 and 30.9%, respectively (log-rank test p < 0.001). The 1-year cumulative HCC incidence for patients without and with cirrhosis were 0.7 and 5.1%, respectively (log-rank test p = 0.036). Univariate analysis showed that significant factors associated with HCC after DAA were: history of treated HCC, cirrhosis, evidence of portal hypertension, higher AFP at the start or end of DAA therapy, higher bilirubin, lower platelets, lower albumin, and older age. From receiver operating characteristic curve analysis, the optimal cut-off level of AFP for predicting HCC was 10.5 ng/mL at the start and 5.6 ng/mL at the end of DAA therapy. Conclusions The risk of early HCC recurrence remains high despite achieving SVR following DAA therapy, whereas the risk of early de-novo HCC occurence is low. AFP levels, both at the start and end of DAA therapy, can be useful in stratifying risks of HCC development.https://doi.org/10.1186/s12876-023-03099-2Hepatitis CDirect-acting anti-viral therapyHepatocellular carcinoma |
spellingShingle | Victor Yung Sin Chow Wing I Cheung Evaluation of patients treated with direct-acting anti-viral therapy for chronic hepatitis C and their risk of hepatocellular carcinoma in Hong Kong BMC Gastroenterology Hepatitis C Direct-acting anti-viral therapy Hepatocellular carcinoma |
title | Evaluation of patients treated with direct-acting anti-viral therapy for chronic hepatitis C and their risk of hepatocellular carcinoma in Hong Kong |
title_full | Evaluation of patients treated with direct-acting anti-viral therapy for chronic hepatitis C and their risk of hepatocellular carcinoma in Hong Kong |
title_fullStr | Evaluation of patients treated with direct-acting anti-viral therapy for chronic hepatitis C and their risk of hepatocellular carcinoma in Hong Kong |
title_full_unstemmed | Evaluation of patients treated with direct-acting anti-viral therapy for chronic hepatitis C and their risk of hepatocellular carcinoma in Hong Kong |
title_short | Evaluation of patients treated with direct-acting anti-viral therapy for chronic hepatitis C and their risk of hepatocellular carcinoma in Hong Kong |
title_sort | evaluation of patients treated with direct acting anti viral therapy for chronic hepatitis c and their risk of hepatocellular carcinoma in hong kong |
topic | Hepatitis C Direct-acting anti-viral therapy Hepatocellular carcinoma |
url | https://doi.org/10.1186/s12876-023-03099-2 |
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