Factors associated with viral breakthrough in lamivudine monoprophylaxis of hepatitis B virus recurrence after liver transplantation

Chan, Henry Lik‐Yuen; Chui, A.K.K; Lau, W. Y.; Chan, Francis K.L.; Wong, Moses; Tse, Chi‐Shing; Rao, A.R.; Wong, John; Sung, Joseph J.Y.

doi:10.1002/jmv.10185

Cited by 80 publications

(75 citation statements)

References 20 publications

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“…In our laboratory, HBV DNA was measured by Taqman realtime polymerase chain reaction assay validated against the EUROHEP standard with a linear range of detection from 20 to 2 Â 10 8 IU/mL. 23 The patients were followed up once every 3 to 6 months. During each visit, patients' symptoms, clinical events, drug history and adherence were recorded.…”

Section: Methodsmentioning

confidence: 99%

Entecavir treatment reduces hepatic events and deaths in chronic hepatitis B patients With liver cirrhosis

et al. 2013

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Entecavir is a potent antiviral agent with high genetic barrier to resistance, hence it is currently recommended as first-line antiviral therapy for chronic hepatitis B (CHB). The aim of this study was to investigate the efficacy of entecavir on clinical outcomes and deaths. It was a retrospective-prospective cohort study based on two cohorts of patients. The entecavir cohort included consecutive CHB patients who had received entecavir 0.5 mg/day for at least 12 months. The historical control cohort included untreated patients recruited since 1997 who underwent routine clinical care. The primary outcome was the 5-year cumulative probability of hepatic events, defined as any cirrhotic complications, hepatocellular carcinoma (HCC), and/or liver-related mortality. A total of 1,446 entecavir-treated patients (72% men; age, 51 6 12 years; follow-up, 36 6 13 months) and 424 treatment-naïve patients (65% men; age, 41 6 13 years; follow-up, 114 6 31 months) were studied. Overall, there was no difference in hepatic events between the entecavir and control cohorts. Among patients with liver cirrhosis (482 entecavir-treated, 69 treatment-naïve), entecavir-treated patients had reduced risks of all clinical outcomes when compared with treatment-naïve patients with cirrhosis after adjusted for model for end-stage liver disease score: hepatic events (hazard ratio [HR], 0.51; 95% confidence interval [CI], 0.34-0.78; P 5 0.002), HCC (HR, 0.55; 95% CI, 0.31-0.99; P 5 0.049), liver-related mortality (HR, 0.26; 95% CI, 0.13-0.55; P < 0.001), and all-cause mortality (HR, 0.34; 95% CI, 0.18-0.62; P < 0.001). Entecavir-treated patients with cirrhosis who failed to achieve undetectable hepatitis B virus DNA (105/482 [22%]) had comparable risk of hepatic events as the untreated patients. Conclusion: Entecavir therapy reduces the risks of hepatic events, HCC, liver-related and all-cause mortality of CHB patients with liver cirrhosis in 5 years, particularly among those who had maintained viral suppression. (HEPATOLOGY 2013;58:1537-1547 C hronic hepatitis B (CHB) is the leading cause of liver cirrhosis and hepatic events, including various cirrhotic complications and hepatocellular carcinoma (HCC) in Asia. 1 A high level of hepatitis B virus (HBV) DNA has been consistently shown to be an independent risk factor for the development of cirrhosis and HCC. 2,3 Antiviral therapy is effective in suppressing HBV DNA and reducing the risk of hepatic events and HCC. 4,5 Lamivudine, the first generation oral nucleoside analogue was shown to reduce the incidence of hepatic events in patients with advanced fibrosis or compensated cirrhosis by 50%. 6 However, the clinical benefit may be negated by lamivudine resistance and virologic relapse after cessation of treatment. 6,7 Therefore, lamivudine is no longer the firstline antiviral therapy for CHB. Instead, nucleos(t)ide analogues with high genetic barrier to resistancenamely, entecavir and tenofovir disoproxil fumarateare recommended by international guidelines. [8][9][10] Entecavir is a more potent ...

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Section: Methodsmentioning

confidence: 99%

Entecavir treatment reduces hepatic events and deaths in chronic hepatitis B patients With liver cirrhosis

et al. 2013

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“…HBV genotyping was determined by PCR amplification and restriction fragment length polymorphism as described previously (4). All samples with inconclusive findings were confirmed by bidirectional sequencing of the HBV surface gene and compared to the published sequences in GenBank (9).…”

Section: Methodsmentioning

confidence: 99%

Evaluation of Impact of Serial Hepatitis B Virus DNA Levels on Development of Hepatocellular Carcinoma

Chan

Wong

et al. 2009

J Clin Microbiol

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We aimed to investigate the impact of hepatitis B virus (HBV) DNA on the development of hepatocellular carcinoma (HCC). We conducted a case/control study based on 506 chronic HBV patients followed up since 1997. Forty-one patients developed HCC, and each of them was age and gender matched with two simultaneously recruited controls without HCC. HBV DNA was measured at the initial visit, at yearly intervals, and at the last visit. Patient age at the time of HCC development was 55 ؎ 9 years. Forty-nine (40%) patients experienced antiviral treatment. The median time from diagnosis to the development of HCC was 17 months, and the control patients were followed for 92 months. At the trough level (defined as lowest level among all studied visits), more (27 patients; 66%) HCC patients had HBV DNA levels of >10,000 copies/ml than the controls (17 patients; 21%). The area under the receiver operating characteristic curve of the trough log HBV DNA level for HCC was 0.79 (95% confidence interval [CI], 0.69 to 0.89). Trough log HBV DNA (odds ratio, 11.4; 95% CI, 3.6 to 37.6; P < 0.0001) and liver cirrhosis (odds ratio, 11.4; 95% CI, 3.6 to 36.2; P < 0.0001) levels were independently associated with HCC after an adjustment for age, gender, antiviral treatment, and HBV genotype. The difference in the trough HBV DNA level was more obvious among untreated patients (5.7 ؎ 1.4 log copies/ml in HCC patients versus 3.2 ؎ 1.3 log copies/ml in control patients; P < 0.0001) than among those who had received antiviral treatment (3.0 ؎ 1.4 log copies/ml in HCC patients versus 2.5 ؎ 0.9 log copies/ml in control patients; P ‫؍‬ 0.38). A high trough HBV DNA level was associated with a higher risk of HCC. Whether antiviral treatment could prevent HCC was uncertain.

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“…Hepatitis B virus DNA was quantified in the sera of patients with chronic hepatitis B (CHB) infection, as previously described (30,31 ). Concentrations Ͼ10 000 copies/mL were considered evidence for active viral replication (32 ).…”

Section: Assessment Of Liver Functionmentioning

confidence: 99%

Aberrant Concentrations of Liver-Derived Plasma Albumin mRNA in Liver Pathologies

Chan

Wong

Mok³

et al. 2010

Clinical Chemistry

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Factors associated with viral breakthrough in lamivudine monoprophylaxis of hepatitis B virus recurrence after liver transplantation

Cited by 80 publications

References 20 publications

Entecavir treatment reduces hepatic events and deaths in chronic hepatitis B patients With liver cirrhosis

Entecavir treatment reduces hepatic events and deaths in chronic hepatitis B patients With liver cirrhosis

Evaluation of Impact of Serial Hepatitis B Virus DNA Levels on Development of Hepatocellular Carcinoma

Aberrant Concentrations of Liver-Derived Plasma Albumin mRNA in Liver Pathologies

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