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Lamivudine resistance

Shi M, Wang RS, Zhang H, Zhu YF, Han B, Zhang Y, Jin LJ, Yang ZJ, Xu YP (2006) Sequential treatment with lamivudine and interferon-alpha monotherapies in hepatitis B e antigennegative Chinese patients and its suppression of lamivudine-resistant mutations, J Antimicrob Chemother 58 1031-1035... [Pg.240]

This decrease in viral replication can be partially restored by mutations elsewhere in the HBV polymerase. For instance, the rtL180M change not only increases the level of lamivudine resistance, but also partially restores the decreased RC of the rtM204V variant. Other mutations that have been described to act as compensatory... [Pg.307]

Warner N, Locamini S, Kuiper M, Bartholomeusz A, Ayres A, Yuen L, Shaw T (2007) The L80I substitution in the reverse transcriptase domain of the hepatitis B virus polymerase is associated with lamivudine resistance and enhanced viral replication in vitro, Antimicrob Agents Chemother 51 2285-2292... [Pg.320]

Lamivudine resistance Adefovir resistance Entecavir resistance Telbivudine resistance... [Pg.327]

Patients who develop resistance to lamivudine have significant improvement in histology while receiving entecavir, but higher doses (1 mg daily) are required. Additionally, 19% of lamivudine-resistant patients had undetectable HBV DNA levels compared to 1% of those who continued treatment with lamivudine.36 At present, no resistance has been associated with entecavir in patients treated for 1 year, but the data beyond 1 year of therapy are unknown. Entecavir resistance has only been seen in patients who already had lamivudine resistance.37... [Pg.355]

Coadministration with lamivudine or lamivudine-resistant patientsiThe recommended dosage in adults and adolescents 16 years of age and older is 1 mg once daily. Renal function impairment ... [Pg.1797]

Adefovir dipivoxil, more recently introduced, is an option in those who have unsuccessful therapy with relapse after use of interferon alpha, and/or have become lamivudine resistant. [Pg.633]

Lamivudine is the best-tolerated NRTI. Its most common adverse effects include headache, malaise, fatigue, and insomnia. Pancreatitis is rare. Gastrointestinal complaints are common with lamivudine-zidovudine therapy but are probably mainly due to the zidovudine component. Lamivudine resistance sometimes occurs early in treatment. Cross-resistance to zal-citabine, didanosine, and abacavir can occur simultaneously. Withdrawal of lamivudine in patients infected with both hepatitis B virus and HIV can cause a flare-up of hepatitis symptoms. [Pg.588]

Although lamivudine results in rapid and potent virus suppression, chronic therapy may ultimately be limited by the emergence of lamivudine-resistant HBV isolates (eg, L180M or M204I/V), estimated at 15-30% at 1 year and 70% at 5 years of therapy. Resistance has been associated with flares of hepatitis and progressive liver disease. Cross-resistance between lamivudine and emtricitabine or entecavir may occur however, adefovir maintains activity against lamivudine-resistant strains of HBV. [Pg.1085]

Chronic therapy with lamivudine in patients with hepatitis may ultimately be limited by the emergence of lamivudine-resistant HBV isolates with YMDD mutation. Emergence of this mutation, which typically occurs within 8-9 months of therapy, is associated with reappearance of detectable levels of HBV DNA. The estimated rate of YMDD mutation is about 20% per year. [Pg.1147]

Adefovir maintains activity against lamivudine-resistant strains of HBV, and no resistance to adefovir was detected in patients who had received continuous treatment for up to 1 year. [Pg.1148]

Viral mutants As the duration of lamivudine therapy increases, the number of mutants rises, especially those resulting from YMDD-polymerase mutation. Viral mutants are found in about 20% of cases after 1 year, in 35-40% after 2 years and in 60-70% after 4 years. (159) Clinically, lamivudine resistance is recognizable due to an increase of transaminases and a recurrence of vir-aemia. Risk factors include high GPT (ALT) values, an elevated HBV-DNA level and a pathological body mass index. In the case of resistance, the use of adefovir is recommended, since this nucleoside is also efficacious against HBV mutants. [Pg.704]

Entecavir is a guanosine nucleoside with strong antiviral activity. It is also effective in lamivudine-resistant patients. After 48 weeks of treatment comprising a daily dose of 0.5 or 1.0 mg, there was elimination of HBV DNA in 25 — 30% and normalization of the transaminases in 60—70% of lamivudine-resistant patients. Tolerance is good. Entecavir-induced mutants were not detected. (173)... [Pg.705]

Benhamou Y, Bochet M, Thibault V, Calvez V, Fievet MH, Vig P, Gibbs CS, Brosgart C, Fry J, Namini H, Katlama C, Poynard T. Safety and efficacy of adefovir dipivoxil in patients co-infected with HIV-1 and lamivudine-resistant hepatitis B virus an open-label pilot study. Lancet 2001 358(9283) 718-23. [Pg.35]

Hertogs K, Bloor S, De Vroey V, van Den Eynde C, Dehertogh P, van Cauwenberge A, et al. A novel human immunodeficiency virus type 1 reverse transcriptase mutational pattern confers phenotypic lamivudine resistance in the absence of mutation 184V. Antimicrob Agents Chemother 2000 44 568-73. [Pg.1582]

Long-term therapy with lamivudine is associated with the development of hepatitis B virus strains that are resistant to this agent. Although the impact of developing lamivudine-resistant hepatitis B virus is not known, adefovir may be used to treat these resistant strains. [Pg.737]

Adefovir dipivoxil (Hepsera) was approved for use in chronic HBV, including lamivudine-resistant HBV, in 2002. End points of therapy for HBV include disappearance of HBV DNA and elimination of HBeAg (virologic response), resolution of elevated aminotransferases (biochemical response), and improvement of liver histology. HBeAg seroconversion, an even stricter marker of viral response, denotes the loss of both HBeAg and HBV DNA and the appearance of anti-HBe. Loss of HBsAg can occur even years after completion of therapy. [Pg.744]

Adefovir is a nucleotide analog of deoxyadenosine monophosphate that is active against retroviruses (like HIV), herpes viruses, and hepadnaviruses. Adefovir dipivoxil 10 mg by mouth once daily for 48 weeks has been approved for use in adult patients with chronic HBV who are either treatment naive or have lamivudine-resistant... [Pg.748]

It is inhibitory in vitro against a range of DNA and RNA viruses, but its clinical use is limited to HBV infections. Inhibitory concentrations for HBV range from 0.2 to 1.2 xM in cell culture, and it is active against lamivudine-resistant HBV strains. Oral adefovir dipivoxil shows dose-dependent inhibition of hepad navirus replication in animal models. In vitro combinations of adefovir and lamivudine or other anti-HBV nucleosides show enhanced antihepad-navirus activity in vitro. [Pg.46]

Famciclovir is associated with dose-related reductions in HBV DNA and transaminase levels in patients with chronic HBV hepatitis, but is less effective than lamivudine. Famciclovir is also ineffective in treating lamivudine-resistant HBV infections owing to emergence of multiply-resistant variants. [Pg.554]

Chnical use is limited to HBV infections, including lamivudine-resistant HBV strains. Oral adefovir dipivoxil shows dose-dependent inhibition of hepadnavirus replication. In vitro combinations of adefovir and lamivudine or other anti-HBV nucleosides show enhanced antihepadnavirus activity. [Pg.829]


See other pages where Lamivudine resistance is mentioned: [Pg.20]    [Pg.75]    [Pg.82]    [Pg.224]    [Pg.224]    [Pg.236]    [Pg.307]    [Pg.307]    [Pg.307]    [Pg.308]    [Pg.308]    [Pg.325]    [Pg.325]    [Pg.326]    [Pg.326]    [Pg.327]    [Pg.355]    [Pg.355]    [Pg.355]    [Pg.181]    [Pg.1085]    [Pg.87]    [Pg.1811]    [Pg.746]    [Pg.747]    [Pg.748]    [Pg.748]    [Pg.378]    [Pg.379]   
See also in sourсe #XX -- [ Pg.355 ]

See also in sourсe #XX -- [ Pg.747 ]

See also in sourсe #XX -- [ Pg.834 , Pg.845 ]




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