دورية أكاديمية
Clinical reactivation during lamivudine treatment correlates with mutations in the precore/core promoter and polymerase regions of hepatitis B virus in patients with anti-hepatitis B e-positive chronic hepatitis.
العنوان: | Clinical reactivation during lamivudine treatment correlates with mutations in the precore/core promoter and polymerase regions of hepatitis B virus in patients with anti-hepatitis B e-positive chronic hepatitis. |
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المؤلفون: | MARRONE, A.1 (AUTHOR), ZAMPINO, R.1 (AUTHOR), KARAYANNIS, P.2 (AUTHOR), CIRILLO, G.3 (AUTHOR), CESARO, G.1 (AUTHOR), GUERRERA, B.1 (AUTHOR), RICCIOTTI, R.1 (AUTHOR), MIRAGLIA DEL GIUDICE, E.3 (AUTHOR), UTILI, R.4 (AUTHOR), ADINOLFI, L. E.1 (AUTHOR), RUGGIERO, G.1 (AUTHOR) |
المصدر: | Alimentary Pharmacology & Therapeutics. Oct2005, Vol. 22 Issue 8, p707-714. 8p. 3 Charts. |
مصطلحات موضوعية: | *HEPATITIS B virus, *DRUG resistance, *VIRUS inhibitors, *ANTIVIRAL agents, *LIVER diseases, *VIRAL hepatitis, *GENETIC mutation, *THERAPEUTICS |
مستخلص: | Background : Drug-resistant mutants may emerge in patients with chronic hepatitis B receiving lamivudine therapy. Aim : To evaluate whether different viral mutational patterns may be associated with clinical reactivation during lamivudine treatment in patients with chronic B hepatitis. Methods : Eight anti-hepatitis B e-positive patients with (group A) and 14 patients without clinical exacerbation (five anti-hepatitis B e-positive, group B1; nine hepatitis B e antigen-positive, group B2) during lamivudine treatment were investigated. Results : ‘Polymerase region’: M204V/I variants were found in all group A patients, but in none of group B1 ( P = 0.0007) and in four of nine of group B2 (44%; P = 0.02) patients. The L180M substitution was detected in four of eight (50%) of group A and in none of groups B1 and B2. ‘Core promoter’: the double basic core promoter (A1762T/G1764A) variant was detected in seven of eight (87%) of group A and in one of five (20%; P = 0.03) of group B1 and one of nine (11%; P = 0.002) of group B2 patients. ‘Precore’: the G1896A stop codon mutation was present in seven of eight (87%) of group A and in zero of five ( P = 0.004) of group B1 and one of nine (11%; P = 0.002) of group B2. Conclusions : Different mutational patterns were observed in the lamivudine-treated patients with and without exacerbation. There was an association of the basic core promoter and stop codon mutations with lamivudine resistance in patients with disease exacerbation. [ABSTRACT FROM AUTHOR] |
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