oral availability and high patient acceptability, early control of hepatitis (fall of ALT) and considerable improvement in liver histology; the latter including interruption or partial reversal of fibrosis if viral suppression can be maintained. Disadvantages are relatively low rates of sustained post-treatment response (hence prolonged therapy is required in most cases) and a high rate of drug resistance. This resistance is often followed by a resumption of hepatitis activity.11 Lamivudina LMV was approved by the US, United States, FDA, Food and Drugs Administration in 1998 as the first nucleoside analogue for the treatment of chronic hepatitis B. LMV is incorporated into the growing strand of DNA during reverse transcription of the first strand of DNA and synthesis of the second, resulting in inhibition of HBVDNA synthesis.10 LMV is effective in suppressing viral replication in both HBeAg positive and HBeAg negative patients and is associated with histological improvement, HBeAg seroconversion and ALT normalization.7 The biggest problem with long-term therapy with this drug is drug resistance. There is a low genetic barrier to LMV resistance (the lowest among current drugs), amplifying resistance with a mutation. As a result, the use of LMV monotherapy is not recommended as the first choice for the treatment of chronic hepatitis B, both in HBeAg positive and negative patients.12 Its use is applied in short-term therapy, as protection against reactivation during chemotherapy, last trimester of pregnancy in pregnant women with high viral load (usually greater than 100million copies/ mL) or fulminant hepatitis by HBV, despite effectiveness in the latter situation has not yet been proven.7 LMV is a drug considered safe from a pharmacological point of view, with few reports of adverse reactions, and therefore, it is one of the most used NRTIs in antiretroviral therapy regimens.2 Diarrhea may occasionally arise while using the medication. Dose reduction has been shown to be necessary in patients with renal failure.13 Adefovir It is a nucleotide analogue (adenosine) that acts by inhibiting HBV reverse transcriptase. It is potentially nephrotoxic. It is an acyclic that acts as a DNA chain terminator and induces the production of endogenous INF.14 HBeAg positive patients, after one year of treatment with this drug, showed histological improvement, reduced serum levels of HBV-DNA and high rates of HBeAg seroconversion. When the treatment is prolonged for over a year, the benefits of therapy with this drug are even greater.15 ADV has a low potency and a genetic barrier to median resistance. Its use in monotherapy should be continued only in patients who reach HBV-DNA negative after 48weeks of treatment.12 When the patient is resistant to this drug, can be used in conjunction with LMV.10 ADV manifests persistence that can result in viral load rebound, which in turn can cause exacerbation of hepatitis B and, in a scenario of decreased liver function, lead to liver decompensation, with possible fatal consequences.5 To mitigate the risk of resistance in patients who do not respond to lamivudine, adefovir dipivoxil should be used in combination with lamivudine rather than as monotherapy. In order to reduce the risk of resistance in patients receiving adefovir dipivoxil as monotherapy, treatment modification should be considered if serum HBV DNA levels remain above 1,000 copies/ml.16 According to ANVISA’s, Agência Nacional de Vigilância Sanitária, CPTG, Clinical Protocol and Therapeutic Guidelines, for Hepatitis B and Co-infections, after oral administration, adefovir dipivoxil is rapidly biotransforming to adefovir. At concentrations substantially higher (>4,000-fold) than those observed in vivo, adefovir did not prevent any of the following CYP450, Cytochrome P450, isoforms: CYP1A2, CYP2D6, CYP2C9, CYP2C19, CYP3A4. Based on the responses of this in vitro knowledge and the known extinction pathway of adefovir, the potential for CYP450-mediated interactions involving these drugs with other medicinal products is low.2 Very common reactions (occur in 10% of patients who use this drug) can cause the absence or loss of muscle strength. On the other hand, common reactions (occur