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Minerva Gastroenterologica e Dietologica 2020 Nov 19

DOI: 10.23736/S1121-421X.20.02791-9

Copyright © 2020 EDIZIONI MINERVA MEDICA

language: English

Hepatocellular carcinoma risk in patients with HBV-related liver disease receiving anti-viral therapy

Sara BATTISTELLA, Erica N. LYNCH, Martina GAMBATO, Alberto ZANETTO, Monica PELLONE, Sara SHALABY, Salvatore SCIARRONE, Alberto FERRARESE, Giacomo GERMANI, Marco SENZOLO, Patrizia BURRA, Francesco P. RUSSO

Gastroenterology and Multivisceral Transplant Unit, Department of Surgery, Oncology and Gastroenterology, Padua University Hospital, Padua, Italy


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Hepatitis B virus is a major health problem worldwide, with approximatively 240 million people living with a chronic HBV infection. HBV chronic infection remains the major cause of hepatocellular carcinoma worldwide, with more than half of HCC patients being chronic HBV carriers, even if underlying mechanisms of tumourigenesis are not totally understood. HBV-related HCC can be prevented by reducing the exposure to HBV by vaccination or by treatment of CHB infection. Current treatment of CHB are Peg-IFN alpha and oral NUCs. Treating HBV infection, either with IFN or NUCs, substantially reduces the risk of HCC development, even if anti-viral therapy fails to completely eliminate HCC risk. Among treated patients, cirrhosis, HBeAg negative at baseline, and failure to remain in virological remission were associated with an increased risk of HCC. The reduction of the risk of developing HCC during anti-viral therapy is largely dependent upon the maintenance of virological remission, since viral load is found to be the most important factor leading to cirrhosis and its complications, including liver cancer development. The question whether Peg-IFN-alpha is superior to NUCs and whether there is a superior agent among NUCs is still controversial. Several studies demonstrated that anti-viral therapy with NUCs could reduce the risk of HCC recurrence after curative treatment of HBV-related HCC.


KEY WORDS: Hepatocellular Carcinoma; Anti-viral therapy; Cirrhosis; Hepatitis B virus; Nucleos(t)ide analogues; Pegylated interferon

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