P.102 Long-term adefovir dipivoxil treatment induces regression of liver fibrosis in patients with HBeAg-negative chronic hepatitis B: results after 5 years of therapy

Hadziyannis, S.; Tassopoulos, Nicholas C.; Chang, Ting‐Tsung; Heathcote, Jenny; Kitis, G.; Rizzetto, Mario; Marcellin, Patrick; Lim, S.G.; Goodman, Z.; Arterburn, Sarah; Ma, Jianmin; Borroto–Esoda, Katyna; Mondou, Elsa; Chuck, Steven L.

doi:10.1016/s1386-6532(06)80284-2

Cited by 33 publications

(46 citation statements)

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“…47 The first pattern of ETV resistance includes: rtI169T ϩ rtL180M ϩ rtM204V ϩ rtM250V and the second pattern includes: rtL180M ϩ rtT184G ϩ rtS202I ϩrtM204V (Table 3). Other patterns including triple ETV-associated mutations have also been 78 ; f Hadziyannis et al 79 ; g Fung et al 57 ; h Lee et al 80 ; i Colonno et al 62 ; j Colonno et al 81 ; k . 82 observed.…”

Section: (A) Resistance To Monotherapiesmentioning

confidence: 99%

Antiviral drug-resistant HBV: Standardization of nomenclature and assays and recommendations for management

et al. 2007

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Section: (A) Resistance To Monotherapiesmentioning

confidence: 99%

Antiviral drug-resistant HBV: Standardization of nomenclature and assays and recommendations for management

et al. 2007

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“…15,16 The cumulative percentages of patients who showed ADV resistance have been reported to be 0% in year 1, 3% in year 2, 11% in year 3, 18% in year 4, and 28% in year 5. 17,18 Although ADV has a unique profile of delayed and infrequent resistance in treatment-naïve patients, ADV resistance in patients with LAM resistance is not well understood. In this study, we compared the emergence of ADV-resistant mutations between LAM-resistant patients and treatment-naïve patients.…”

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confidence: 99%

Increased risk of adefovir resistance in patients with lamivudine-resistant chronic hepatitis B after 48 weeks of adefovir dipivoxil monotherapy

et al. 2006

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Although adefovir dipivoxil (ADV) has a unique profile of delayed and infrequent resistance in treatment-naïve chronic hepatitis B patients, the association of ADV resistance with previous lamivudine (LAM) resistance is not well understood. We compared the emergence of the ADV-resistant mutations rtA181V/T and rtN236T between LAM-resistant patients and treatment-naïve patients at 48 weeks of ADV monotherapy. Fifty-seven LAM-resistant patients and 38 treatment-naïve patients were treated with 10 mg/d ADV for more than 48 weeks. Both baseline and 48-week blood samples were analyzed for ADV-resistant mutations via restriction fragment mass polymorphism analysis. Antiviral responses were evaluated according to changes in serum HBV DNA (measured via real-time polymerase chain reaction) and alanine aminotransferase (ALT) levels and loss of hepatitis B e antigen (HBeAg). After 48 weeks, 10 (18%) of the 57 LAM-resistant patients were found to have developed ADV-resistant mutations, whereas none of the 38 treatment-naïve patients developed such mutations (P < .01). Among LAM-resistant patients, the reduction in serum HBV DNA levels was significantly lower in patients with ADV-resistant mutations than in those without such mutations (؊1.04 vs. ؊2.63 log 10 copies/mL) (P ‫؍‬ .01). However, the rates of serum ALT normalization (60% vs. 55%) and HBeAg loss (14% vs. 21%) were not significantly different between the 2 groups (P > .05). In conclusion, the emergence of the rtA181V/T and rtN236T mutations was more common in LAM-resistant patients than in treatmentnaïve patients after 48 weeks of ADV therapy and was associated with reduced antiviral efficacy to drug treatment. (HEPATOLOGY 2006;43:1385-1391

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“…At 2 and 5 years, HBV DNA suppression was 71% and 67%, with ALT normalisation of 73% and 69%, respectively [43,46]. Liver histology improved in 75-80% after 5 years of adefovir therapy [46].…”

Section: Nucleos(t)ide Analogues: Lamivudine Adefovir Telbivudine mentioning

confidence: 97%

“…Treatment of patients with HBeAg-negative CHB with adefovir induced ALT normalisation in 72% of patients and HBV DNA suppression to <1,000 copies/ml (~200 IU/ml) in 51% compared with 29% and 0% of placebo-treated controls at 1 year [45]. At 2 and 5 years, HBV DNA suppression was 71% and 67%, with ALT normalisation of 73% and 69%, respectively [43,46]. Liver histology improved in 75-80% after 5 years of adefovir therapy [46].…”

Section: Nucleos(t)ide Analogues: Lamivudine Adefovir Telbivudine mentioning

confidence: 99%

Chronic hepatitis B: a global health problem requiring coherent worldwide treatment strategies

2007

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Chronic hepatitis B virus infection, a major cause of end-stage liver disease and hepatocellular carcinoma, is a worldwide health concern. While the past two decades have brought major advances in the availability of treatments to help delay or prevent these outcomes, treatment of chronic hepatitis B remains a serious challenge, not least due to the ability of the virus to remain in hepatocyte nuclei as a source of potential reactivation-hence the term chronic hepatitis B infection. This article reviews the current treatments available and suggests a framework for a rational approach to managing the disease.

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P.102 Long-term adefovir dipivoxil treatment induces regression of liver fibrosis in patients with HBeAg-negative chronic hepatitis B: results after 5 years of therapy

Cited by 33 publications

References 0 publications

Antiviral drug-resistant HBV: Standardization of nomenclature and assays and recommendations for management

Antiviral drug-resistant HBV: Standardization of nomenclature and assays and recommendations for management

Increased risk of adefovir resistance in patients with lamivudine-resistant chronic hepatitis B after 48 weeks of adefovir dipivoxil monotherapy

Chronic hepatitis B: a global health problem requiring coherent worldwide treatment strategies

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