between 1% and 10% of patients who use this drug) can cause abdominal pain, nausea, flatulence, intestinal discomfort/gas), diarrhea, poor digestion, headache.16 Entecavir ETV is a nucleoside analogue (guanosine) that inhibits three steps of HBV replication: the initiation of HBV DNA polymerase17. Reverse transcription of HBV-DNA negative strand from pregenomic messenger RNA; and HBV-DNA positive strand synthesis. It is the most potent antiviral among the current nucleoside/nucleotide analogues approved for use in patients with chronic hepatitis B, in addition to having a high genetic barrier, requiring three mutations for the patient to develop drug resistance.7,12 After four years of ETV therapy, in patients who had not previously used nucleoside/nucleotide analogues, less than 1% of patients did not show resistance to therapy.9,10 ETV was active not only in HBeAg positive patients, but also in HBeAg negative patients and in LMV resistant patients.10,18 The most common adverse events of any severity (≥3%) were: Headache, fatigue, dizziness and nausea. 1% of patients treated with Entecavir, discontinued due to adverse events or abnormal laboratory test results.2 Drug treatment of chronic hepatitis b in Brazil: a review 184 Copyright: ©2021 Lobato et al. Citation: Lobato GDS, Farias AA, Belo AMB, et al. Drug treatment of chronic hepatitis b in Brazil: a review. Gastroenterol Hepatol Open Access. 2021;12(6):182‒185. DOI: 10.15406/ghoa.2021.12.00483 Clinical adverse effects in nucleoside-naive patients were evaluated. Where, 679 use ETV 0.5mg once a day for an average time of 54weeks. Adverse reactions of moderate or severe potency and leading to treatment with ETV are insomnia; nervous system disorders, 30 such as headache, uncommon, dizziness, drowsiness; gastrointestinal disorders such as nausea, diarrhea, dyspepsia, vomiting and; and general disorders such as fatigue.16 Tenofovir TDF was initially approved for the treatment of HIV infection. It is phosphorylated in its active form, and binds directly with HBV DNA polymerase thus suppressing viral replication.10 TDF is structurally similar to ADV, but it is less nephrotoxic, which proves that it is applied in higher doses, increasing its effectiveness. Many studies show a good efficacy of TDF in patients with resistance to LMV, yet it has less potency in patients with resistance to ADV.8 Thus, like ETV, TDF has a high potency and good genetic barrier to resistance.7 Tenofovir disoproxil fumarate in the body is transformed into tenofovir, which prevents viral polymerases from attaching directly to them. TDF has minimal intervention in the synthesis of human DNA, which leads to greater safety in its use. When patients receive Tenofovir Desoproxil Fumarate concomitantly with lopinavir/ritonavir, atazanavir boosted with ritonavir or darunavir should be monitored for adverse reactions associated with Tenofovir Desoproxil Fumarate. In patients who develop adverse reactions to Tenofovir Desoproxil Fumarate associated with it, it should be discontinued.2 Treatment-emergent adverse reactions reported in >5% of patients treated with Tenofovir Desoproxil Fumarate included: abdominal pain, diarrhea, headache, dizziness, fatigue, nasopharyngitis, back pain and rash.2 Interferons Interferon’s are a group of immunoregulatory proteins synthesized by T lymphocytes, macrophages, fibroblasts and other types of cells, after being stimulated with viruses, antigens, mitogens, double-stranded DNA or lectins. Synthesized for therapeutic purposes, they were the first medications approved for the treatment of HBV infection. Interferon increases the ability of macrophages to destroy tumor cells, viruses and bacteria. They block viral replication, potentiate NK, natural killer, cell lytic activity, increase MHC, major histocompatibility complex, class I expression in virus-infected cells, and induce Th1, type 1 T helper, cell development. They are capable of preventing viral replication, are anti-proliferative and fever-inducing. Have an immunomodulatory effect.8 Furthermore, they increase seroconversion from HBeAg to anti-HBe, however, their benefit is achieved in only one third of treated patients, and no advantages in