Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic hepatitis B virus (HBV) infection is the primary risk factor for the development of hepatocellular carcinoma worldwide. After decades of chronic hepatitis, about 30-40% of patients progress into liver cirrhosis, and of them, around 1-5% subsequently develop hepatocellular carcinoma (HCC) annually. Since the carcinogenic process involves the interplay between the hepatitis virus and the host hepatocytes, both genomes contribute to the final pathogenic outcome, either individually or synergistically. Studying the genetic factors predisposing hepatocarcinogenesis in both host and viral genomes will help illuminate the critical carcinogenic mechanisms, and create molecular targets for future therapy. In this article, we thus review the epidemiology of HBV-related HCC and viral factors involved in hepatocarcinogenesis.
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PMID:Hepatitis B virus-related hepatocellular carcinoma: epidemiology and pathogenic role of viral factors. 1747 93

Chronic hepatitis B virus (HBV) infection affects > 350 million individuals worldwide. Chronic hepatitis B is associated with complications of end-stage liver disease, including cirrhosis and hepatocellular carcinoma. HBV replication is the best predictor of liver disease progression to cancer, and antiviral therapy may diminish or halt this unfavorable outcome. Six drugs have been approved for the treatment of chronic hepatitis B: interferon-alpha(2b), pegylated interferon-alpha(2a), lamivudine, adefovir, entecavir and telbivudine. Most agents designed to target hepatitis B are hindered by the development of resistance, poor tolerability or limited efficacy; therefore, new agents and treatment strategies are needed. Telbivudine is the latest approved anti-HBV agent; it is an orally administered nucleoside analog that selectively inhibits HBV replication. It has demonstrated potent activity against HBV in Phase III clinical studies, with good tolerance, lack of mitochondrial toxicity and no dose-limiting side effects.
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PMID:Telbivudine: a new option for the treatment of chronic hepatitis B. 1747 11

Chronic hepatitis B is the most common cause of cirrhosis and liver cancer worldwide. Approximately 45% of the world's population lives in regions where chronic hepatitis B virus (HBV) infection is endemic, including most of Asia and the Pacific Islands, Africa, and the Middle East. Nearly one fourth of the population of San Francisco was born in Asia and the Pacific Islands. In 2006, the San Francisco Department of Public Health (SFDPH) received reports consistent with probable chronic HBV infection for 2,238 persons. To characterize persons with reported confirmed chronic HBV infection in San Francisco in 2006, SFDPH collected additional data on a subset of 567 cases reported to the SFDPH chronic hepatitis B registry. Eighty-four percent of the persons were Asians/Pacific Islanders (A/PIs), 80% of whom were foreign born. Fewer than half had been referred to a gastroenterologist/hepatologist for evaluation at the time of reporting. Persons with chronic HBV infection can benefit from medical care by providers with expertise in viral hepatitis. In addition, close contacts of infected persons should be screened and offered vaccination if found to be susceptible to HBV infection. Culturally appropriate counseling for and follow-up of persons with chronic HBV infection and their contacts could help reduce the transmission of HBV infection.
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PMID:Characteristics of persons with chronic hepatitis B--San Francisco, California, 2006. 1749 91

Chronic hepatitis B virus (HBV) infection is a significant public health problem in the United States, with 1.25 million people infected with the virus. The long-term risks of chronic HBV infection include cirrhosis and hepatocellular carcinoma, which occur in 15% to 30% of those infected at birth or early in life and may lead to liver transplantation or death. During the past few years, the development and increased availability of oral antiviral agents have made treatment simpler, safer, and more tolerable for these patients. This article focuses on 3 of these drugs--lamivudine, adefovir, and entecavir--and their use in patients with chronic HBV infection and advanced hepatic fibrosis or cirrhosis.
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PMID:Chronic hepatitis B with advanced fibrosis or cirrhosis: impact of antiviral therapy. 1759 74

Chronic hepatitis B remains a treatment challenge despite the availability of new nucleoside analogs. This is due to the persistence of viral infection during therapy, which exposes the patient to the risk of developing antiviral drug resistance. Therefore, new polymerase inhibitors are needed to manage resistance to existing drugs and new trials of combination therapy are required to delay drug resistance. In the future, antiviral agents targeting other steps of the viral life cycle will be needed to achieve antiviral synergy and prevent antiviral drug resistance. Immune modulators are also expected to enhance antiviral response and to achieve sustained response. Discovery of new antiviral drugs and design of new treatment strategies are, therefore, needed to manage this disease, which is still the main cause of cirrhosis and hepatocellular carcinoma worldwide.
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PMID:Emerging drugs for hepatitis B. 1760 97

Chronic hepatitis B virus (HBV) infection is the most common cause of hepatic fibrosis and hepatocellular carcinoma (HCC), mainly as a result of chronic necroinflammatory liver disease. A characteristic feature of chronic hepatitis B infection, alcoholic liver disease and nonalcoholic fatty liver disease (NAFLD) is hepatic steatosis. Hepatic steatosis leads to an increase in lipid peroxidation in hepatocytes, which, in turn, activates hepatic stellate cells (HSCs). HSCs are the primary target cells for inflammatory and oxidative stimuli, and these cells produce extracellular matrix components. Chronic hepatitis B appears to progress more rapidly in males than in females, and NAFLD, cirrhosis and HCC are predominately diseases that tend to occur in men and postmenopausal women. Premenopausal women have lower hepatic iron stores and a decreased production of proinflammatory cytokines. Hepatic steatosis has been observed in aromatase-deficient mice, and has been shown to decrease in animals after estradiol treatment. Estradiol is a potent endogenous antioxidant which suppresses hepatic fibrosis in animal models, and attenuates induction of redox sensitive transcription factors, hepatocyte apoptosis and HSC activation by inhibiting a generation of reactive oxygen species in primary cultures. Variant estrogen receptors are expressed to a greater extent in male patients with chronic liver disease than in females. These lines of evidence suggest that the greater progression of hepatic fibrosis and HCC in men and postmenopausal women may be due, at least in part, to lower production of estradiol and a reduced response to the action of estradiol. A better understanding of the basic mechanisms underlying the sex-associated differences in hepatic fibrogenesis and carciogenesis may open up new avenues for the prevention and treatment of chronic liver disease.
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PMID:Female hepatology: favorable role of estrogen in chronic liver disease with hepatitis B virus infection. 1770

Chronic hepatitis B or C can cause severe liver diseases such as liver cirrhosis and hepatocellular carcinoma (HCC). Both viral infections together especially hepatitis c virus infection (HCV) are the mayor indication for liver transplantation in Western Europe and the United States. Recurrence of hepatitis B virus (HBV) or HCV infection after orthotopic liver transplantation (OLT) plays a key role for the outcome after liver transplantation concerning patient and graft survival rates. Allograft dysfunctions, cirrhosis of the allograft and graft failure are major complications after recurrent viral hepatitis. The survival after liver transplantation for HBV-related liver disease changed dramatically during the last two decades with results today comparable with non-HBV-related liver transplantations. Availability of immunoprophylaxis with hepatitis B immunoglobulin (HBIG) as well as nucleoside/nucleotide analogues like lamivudine or adefovir in the pre- and post-transplant setting conferred to significant better results due to an efficient prophylaxis and the possibility of therapy of HBV reinfection of the allograft. New drugs such as entecavir, tenofovir and telbivudine for the treatment of chronic hepatitis B infections may offer even more opportunities in the transplant setting. In contrast, despite recent achievements in the treatment of HCV infection with pegylated interferons and ribavirin, patients with HCV cirrhosis or after liver transplantation are difficult to treat. Sustained virological response (SVR) rates in prophylactic and therapeutic approaches of HCV reinfection after OLT are only low compared to the pre-cirrhotic HCV infection. Moreover, best treatment duration and dosage of recurrent HCV infection with pegylated interferon in combination with ribavirin remains to be defined.
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PMID:Prophylaxis and treatment of recurrent viral hepatitis after liver transplantation. 1789 Feb 61

Chronic hepatitis B is probably the major cause of cirrhosis and hepatocellular carcinoma. The detection of the hepatitis B virus surface antigen (HBsAg) and HBV core protein, the e antigen (HBeAg), indicates infection with the hepatitis B virus and replication activity, respectively. Fructus schisandrae containing compound (KY88) may affect the elimination of HBV, strengthen the immune system, as well as stimulate liver cell regeneration. The present study was conducted to demonstrate the ability of KY88 in inhibiting hepatocellular carcinoma cell proliferation and secretions of HBsAg and HBeAg. The hepatocellular carcinoma cell line HB-8064 was treated by KY88 followed by the measurement of cell proliferation rate and secretions of HBsAg and HBeAg on days 1, 3, 5, and 7. A semi-quantitative RT-PCR method was used to quantify the expression of the mRNA. Seventy Sprague-Dawley rats were fed for 28days with purified KY88 for a toxicity test. The expression of surface and e antigens was lower when the cells were treated for a longer time with KY88 or when the doses were higher. One-way ANOVA analysis confirmed the mRNA content of HBsAg to be significantly less than control. The body weight did not show a significant difference compared to the control group. Fructus schisandrae-containing compound (KY88) was potentially effective in suppressing the proliferation of hepatocellular carcinoma cells. The decreased secretion and gene expression of HBsAg and HBeAg might restrict the growth of tumour masses.
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PMID:Fructus schisandrae (Wuweizi)-containing compound inhibits secretion of HBsAg and HBeAg in hepatocellular carcinoma cell line. 1790 89

Chronic hepatitis B virus (HBV) infection leads to long-term sequelae such as cirrhosis and hepatocellular carcinoma. Antiviral therapy aims at controlling the viral replication and thus, decreasing the likelihood of such complications. In this study, we evaluated the dynamics of biochemical and virological parameters over 10 years of antiviral therapy in a Thai patient with chronic HBeAg-negative HBV infection, who had relapsed after two courses of interferon alfa treatment. Lamivudine administration initially led to a significant reduction in alanine aminotransferase (ALT) and HBV DNA levels, but a subsequent emergence of YIDD mutants caused an ALT flare and a virus breakthrough. A 4-log HBV DNA decrease and normalization of the ALT level were achieved within 3 months of adefovir monotherapy without any relapse during follow-up exceeding 20 months. Thus, careful monitoring during treatment and knowledge of cross-resistance to antiviral salvage therapy are crucial for the management of patients with chronic hepatitis B.
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PMID:Dynamics of HBV DNA levels, HBV mutations and biochemical parameters during antiviral therapy in a patient with HBeAg-negative chronic hepatitis B. 1803 7

Chronic hepatitis B virus (HBV) infection is one of the leading causes of liver cirrhosis and hepatocellular carcinoma (HCC). Current treatment strategies of HBV infection including the use of interferon (IFN)-alpha and nucleotide analogues such as lamivudine and adefovir have met with only partial success. Therefore, it is necessary to develop more effective antiviral therapies that can clear HBV infection with fewer side effects. RNA interference (RNAi), by which a small interfering RNA (siRNA) induces the gene silence at a post-transcriptional level, has the potential of treating HBV infection. The successful use of chemically synthesized siRNA, endogenous expression of small hairpin RNA (shRNA) or microRNA (miRNA) to silence the target gene make this technology towards a potentially rational therapeutics for HBV infection. However, several challenges including poor siRNA stability, inefficient cellular uptake, widespread biodistribution and non-specific effects need to be overcome. In this review, we discuss several strategies for improving the anti-HBV therapeutic efficacy of siRNAs, while avoiding their off-target effects and immunostimulation. There is an in-depth discussion on the (1) mechanisms of RNAi, (2) methods for siRNA/shRNA production, (3) barriers to RNAi-based therapies, and (4) delivery strategies of siRNA for treating HBV infection.
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PMID:RNAi for treating hepatitis B viral infection. 1807 1


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