Antiviral therapy delays esophageal variceal bleeding in hepatitis B virus-related cirrhosis
Chang-Zheng Li, Qing-Shan Li, Jun-Hong Yan, Department of Gastroenterology and Hepatology, Institute of Hepatobiliary and Gastrointestinal Diseases, Chinese Second Artillery General Hospital, Beijing 100088, China. World Journal of Gastroenterology
(Impact Factor: 2.37).
10/2013; 19(40):6849-56. DOI: 10.3748/wjg.v19.i40.6849
To investigate the effect of antiviral therapy with nucleoside analogs in hepatitis B virus (HBV)-related cirrhosis and esophageal varices.
Eligible patients with HBV-related cirrhosis and esophageal varices who consulted two tertiary hospitals in Beijing, China, the Chinese Second Artillery General Hospital and Chinese PLA General Hospital, were enrolled in the study from January 2005 to December 2009. Of 117 patients, 79 received treatment with different nucleoside analogs and 38 served as controls. Bleeding rate, change in variceal grade and non-bleeding duration were analyzed. Multivariate Cox proportional hazard regression was used to identify factors related to esophageal variceal bleeding.
The bleeding rate was decreased in the antiviral group compared to the control group (29.1% vs 65.8%, P < 0.001). Antiviral therapy was an independent factor related to esophageal bleeding in multivariate analysis (HR = 11.3, P < 0.001). The mean increase in variceal grade per year was lower in the antiviral group (1.0 ± 1.3 vs 1.7 ± 1.2, P = 0.003). Non-bleeding duration in the antiviral group was prolonged in the Kaplan-Meier model. Viral load rebound was observed in 3 cases in the lamivudine group and in 1 case in the adefovir group, all of whom experienced bleeding. Entecavir and adefovir resulted in lower bleeding rates (17.2% and 28.6%, respectively) than the control (P < 0.001 and P = 0.006, respectively), whereas lamivudine (53.3%) did not (P = 0.531).
Antiviral therapy delays the progression of esophageal varices and reduces bleeding risk in HBV-related cirrhosis, however, high-resistance agents tend to be ineffective for long-term treatment.
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ABSTRACT: Hepatocellular carcinoma (HCC) is a major health problem worldwide, representing one of the leading causes of death. Chronic hepatitis B virus (HBV) infection (CHB) is the most important etiologic factor of this tumor, accounting for the development of more than 50% of the cases in the world. Primary prevention of HCC is possible by hepatitis B vaccination conferring protection from HBV infection. However, according to the World Health Organization Hepatitis B Fact sheet N° 204 (update of July 2014) globally there exists a large pool of > 240 million people chronically infected with HBV who are at risk for development of HCC. These individuals represent a target population for secondary prevention both of cirrhosis and of HCC. Since ongoing HBV replication in CHB is linked with the progression of the underlying liver disease to cirrhosis as well as with the development of HCC, effective antiviral treatment in CHB has also been evaluated in terms of secondary prevention of HCC. Currently, most patients with active CHB are subjected to long term treatment with the first line nucleos(t)ide analogues entecavir and tenofovir. These compounds are of high antiviral potency and have a high barrier to HBV resistance compared to lamivudine, adefovir dipivoxil and even telbivudine. Many studies have shown that patients under antiviral treatment, especially those in virological remission, develop less frequently HCC compared to the untreated ones. However, the risk for development of HCC cannot be eliminated. Therefore, surveillance for the development of HCC of patients with chronic hepatitis B must be lifelong or until a time in the future when new treatments will be able to completely eradicate HBV from the liver particularly in the early stages of CHB infection. In this context, the aim of this review is to outline the magnitude of the risk for development of HCC among patients with CHB, in the various phases of the infection and in relation to virus, host and environmental factors as evaluated in the world literature. Moreover, the benefits of antiviral treatment of CHB with nucleos/tide analogs, which have changed the natural history of the disease and have reduced but not eliminated the risk of HCC are also reviewed.
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ABSTRACT: Variceal bleeding is the most serious complication of portal hypertension. All cirrhotic patients should be screened endoscopically for varices which are present in about 30% of compensated and 60% of decompensated patients at diagnosis. In patients without varices, endoscopy surveillance should be continued every 2 years. Patients with high-risk varices (moderate or large in size, or with red color signs, or in Child-Pugh C patients) should be treated with a nonselective β-blocker to prevent bleeding (propranolol, nadolol or carvedilol). Endoscopic banding ligation is also effective for the prevention of first bleeding, and it is the first choice in patients with contraindications or intolerance to β-blockers. Acute variceal hemorrhage still has a high mortality rate (around 15%) and requires intensive care management and conservative blood transfusion policy. Treatment is based on the combined use of vasoactive drugs, endoscopic band ligation and prophylactic antibiotics. Failures are best managed by transjugular intrahepatic portosystemic shunt (TIPS). Balloon tamponade or specifically designed covered esophageal stents can be used as a bridge to definitive therapy in unstable patients. Early, preemptive TIPS might be the first choice in patients at high risk of failure (Child-Pugh B with active bleeding or Child-Pugh C up to 13 points). Patients surviving a variceal bleeding are at high risk of rebleeding. A combination of β-blockers and endoscopic band ligation is the most effective therapeutic approach. Preliminary data suggest that the addition of simvastatin increases survival in these patients. © 2015 S. Karger AG, Basel.
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