Efficacy evaluation of 104-week telbivudine therapy in HBeAg-positive chronic hepatitis B / 中国感染与化疗杂志

Objective To evaluate the efficacy of telbivudine in HBeAg-positive chronic hepatitis B (CHB) patients by comparing the efficacy of initial telbivudine therapy in treatment-naive patients with sequential telbivudine therapy in patients with poor response to adefovir.Methods A total of 90 HBeAg-positive CHB patients were assigned to receive sequential telbivudine therapy following poor response to adefovir dipivoxil (n=45),or initial telbivudine therapy in antiviral treatment-naive patients (n=45).All patients were treated with telbivudine 600 mg daily for 104 weeks.The efficacy was evaluated in terms of liver function tests,serum HBV markers,HBV DNA and antiviral drug resistance.Results Telbivudine showed good overall efficacy after treatment for 104 weeks in terms of alanine aminotransferase normalization rate (91.1％),HBV DNA negative conversion rate (80.0％),HBeAg loss rate (57.8％),and HBeAg/HBeAb seroconversion rate (30.0％).The HBV DNA negative conversion rate in initial treatment group was significantly higher than that in sequential treatment group (P＜0.05).However,among the patients with early response,the efficacy did not show significant difference between groups (P＞0.05).The patients with early response showed significantly better efficacy than those without early response,in terms of higher HBV DNA negative conversion rate,higher HBeAg loss rate and HBeAg/ HBeAb seroconversion rate (P＜0.000 1 or P＜0.05),but lower virological breakthrough rate (P＜0.05).Conclusions Telbivudine has shown reliable efficacy in CHB patients.Initial telbivudine therapy is better than sequential therapy in CHB patients with poor response to adefovir.However,for patients with early response to telbivudine,no statistical difference is found between initial and sequential therapy in long-term treatment efficacy (104 weeks).The patients receiving sequential telbivudine therapy should be monitored closely for early antiviral response to optimize treatment.

Rebrote virológico en el tratamiento de hepatitis B con entecavir: ¿resistencia? / Virological breakthrough in treating hepatitis B with entecavir: It means resistance?

Paciente varón de 45 años natural de Lima, casado con antecedentes de , múltiples parejas sexuales y operado de fimosis, que debuta con eritema nodoso y diagnosticado de hepatitis B crónica en Agosto del 2008, en controles por consultorio se realiza diagnóstico de cirrosis hepática child A y hepatocarcinoma. Inicia tratamiento para la hepatitis B con Entecavir 0,5mg y luego se realiza hepatectomía del segmento V, En Febrero 2009 en controles de imágenes se evidencia recidiva de hepatocarcinoma en el segmento VI (lesión de 14mm) con AFP de 68 ng/dl, se realiza etanolización, con evolución final favorable. Durante el seguimiento no se observa evidencia de recidiva de HCC, continua con Entecavir 0,5 mg /d y en abril 2010, luego de 72 semanas de tratamiento con adecuada adherencia al tratamiento presenta rebrote virológico (carga viral positiva de 646 UI/dl), y se decide agregar a la terapia Tenofovir. Actualmente paciente con buena evolución con última carga viral de Abril del 2012 negativa recibiendo terapia doble para VHB. Reportamos el caso por ser uno de los primeros en nuestro país de resistencia probable a Entecavir y donde se pone de manifiesto la necesidad de examenes complementarios que confirmen dicha sospecha.

A 45 year- old - married man, with several sexual partners, initiated symptoms with nodosum erythema and in August 2008, is diagnosed of chronic hepatitis due to hepatitis B virus (HBV). Later he was diagnosed of Child A cirrhosis and hepatocarcinoma. He began HBV treatment with Entecavir 0,5 mg; then he underwent a V segment hepatectomy. In February 2009 he presented a relapse with a tumor of 14 mm on VI segment with AFP values of 68 ng/dl, so he underwent an ethanolization with good evolution. During the follow up, he has not presented evidence of relapse of hepatocarcinoma and continued with Entecavir 0,5 mg/d. In April 2010, after 72 weeks of therapy with good compliance, the patient presented a virological breakthrough (viral load 646 UI/dl) and Tenofovir was added to his therapy. Nowadays the patient is receiving double therapy for HBV and his last viral load, April 2012, was negative. This could be the first case in our country of a probable resistance to Entecavir; complementary tests are needed in order to rule out this suspicion.

Efficacy of Lamivudine in Patients with Hepatitis B e Antigen-Negative Chronic Liver Diseases / 대한간학회지

BACKGROUND/AIMS: Lamivudine therapy is effective in inhibiting HBV replications in patients with HBeAg-negative chronic liver disease. However, the sustained response rate appears to be particularly poor, because the vast majority of patients relapse soon after cessation of therapy. The aim of this study was to evaluate the efficacy of lamivudine, the breakthrough rate, and the relapse rate of discontinuing therapy after response in patients with HBeAg-negative chronic liver disease. METHODS: Fifty-nine patients with HBeAg-negative chronic liver disease who have received lamivudine for at least 6 months, were studied. The mean duration of treatment was 14 months. Complete response was defined as undetectable serum HBV DNA by bDNA and normalization of ALT levels. Once HBV DNA disappearance and ALT normalization were observed, lamivudine therapy was continued for at least two additional months. The mean follow-up after cessation of treatment was 6 (1-22) months. RESULTS: Fifty-six patients were undetectable HBV DNA. The cumulative HBV DNA loss rates at 3 months and 5 months were 90% and 95%, respectively. The ALT normalization was observed in 52 patients. The cumulative ALT normalization rates at 6 months and 10 months were 78% and 86%, respectively. The complete response was observed in 52 patients. The cumulative rates of complete response at 10 months and 18 months were 80% and 88%, respectively. A predictive factor for complete response was only the duration of lamivudine treatment. Virological breakthrough was observed in 5 (8.5%). Thirty-four patients stopped taking lamivudine after 7.7 (2-15) months of the additional therapy. Seventeen of those patients (50%) experienced relapse. The cumulative relapse rates at 3 months, 6 months and 10 months were 24%, 47%, and 66%, respectively. The only predictive factor for relapse was the duration of additional lamivudine treatment after response. CONCLUSIONS: Lamivudine was an effective treatment of HBeAg negative chronic liver disease. Relapse, however, was usually observed after cessation of lamivudine. Our results showed that long-term lamivudine therapy is required in order to decrease the high relapse rates in patients with HBeAg-negative chronic liver disease.