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Treatment of hepatitis B: Is there still a role for interferon?
Author(s) -
Viganò Mauro,
Grossi Glenda,
Loglio Alessandro,
Lampertico Pietro
Publication year - 2018
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1111/liv.13635
Subject(s) - hbsag , medicine , entecavir , pegylated interferon , hepatitis b virus , hepatitis b , tenofovir alafenamide , immunology , gastroenterology , virology , viral load , virus , chronic hepatitis , ribavirin , antiretroviral therapy , lamivudine
The treatment of chronic hepatitis B ( CHB ) patients is based on monotherapy with pegylated‐interferon (Peg‐ IFN ) or with one of the three most potent nucleot(s)ide analogues ( NUC s) with the best resistance profiles, i.e. entecavir ( ETV ), tenofovir disoproxil fumarate ( TDF ) and tenofovir alafenamide ( TAF ). Long‐term NUC s treatment can achieve virological suppression in almost all patients. However, this requires lifelong therapy, is costly and the rate of hepatitis B surface antigen ( HB sAg) seroclearance is low. A one‐year course of Peg‐ IFN has the advantage of providing immune‐mediated control of the hepatitis B virus ( HBV ) infection, the possibility of achieving a sustained off‐treatment response in nearly 30% of the patients and ultimately, HB sAg loss in approximately 30%‐50% of the latter patients during long‐term off treatment follow‐up. However, the major limitations to the extensive use of this treatment are the need for parenteral therapy and clinical and laboratory monitoring, the side‐effects profile and contraindications in certain patients and the limited effectiveness in a large proportion of patients. Nevertheless, the cost‐effectiveness of Peg‐ IFN can be significantly increased by careful patient selection based upon baseline alanine aminotransferase ( ALT ), HBV DNA levels, viral genotype, host genetic variants and especially by applying early on‐treatment stopping rules based upon HB sAg kinetics. Recently, because of the different mechanisms of action of Peg‐ IFN and NUC s, the strategy of “adding‐on” or “switching to” Peg‐ IFN in patients being treated with NUC s to accelerate the decline in HB sAg and enhance HB sAg seroclearance rates, has provided interesting results.