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 is an important public health problem worldwide. In Poland the incidence rate decreased from 40,0 (in the year 1990) to 3,86 (in 2004) per 100,000 inhabitants. The goal of anti-chronic hepatitis B therapy is to prevent the progression of liver disease to cirrhosis which may effect in development of liver failure or HCC. The aims of treatment are: reduction of HBV viral load and normalization of ALT activity. Among HBeAg positive patients important marker is the loss of e antigenemia followed by seroconversion to anti-HBe positivity. Lamivudine is an oral nucleoside analogue with strong antiviral activity against hepatitis B virus. The objective of this study was to analyse the efficacy of lamivudine treatment of chronic hepatitis B patients positive for hepatitis B e antigen (HBeAg). 224 patients were treated in Hospital of Infectious Diseases in Warsaw in the years 2001-2002. Patients were treated for 48 weeks with 100 mg lamivudine once daily (50 mg in case of renal failure). Results obtained at the end of therapy: loss of HBeAg was observed in 33,4% and seroconversion to anti-HBe in 15,1% patients, normalization of ALT activity was noticed in 53,4% patients, inhibition of HBV DNA replication was observed in 37,9% patients. The results are comparable with known randomized clinical trials.
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PMID:[Results of 48 weeks lamivudine treatment of patients with chronic hepatitis B and HBeAg (+)]. 1696 76

Although preventable by vaccination, hepatitis B infection is common, affecting more than 350 million individuals worldwide. Chronic hepatitis B infection is associated with the complications of chronic liver disease including cirrhosis and hepatocellular carcinoma. Current agents designed to target hepatitis B are hindered by the development of resistance, poor tolerability or limited efficacy and a demand for new agents and strategies continues. This review focuses on telbivudine, a novel agent in the fight against hepatitis B.
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PMID:Novel anti-hepatitis B agents: A focus on telbivudine. 1698 73

Chronic hepatitis B virus infection afflicts 400 million people worldwide and untreated will progress to cirrhosis in 15-40% of individuals, with an associated increased risk for the development of hepatocellular carcinoma. The 'inactive carrier state' carries a benign prognosis with a very low risk of cirrhosis or hepatocellular carcinoma. However, the hepatitis B e antigen (HBeAg)-positive chronic hepatitis state is an active disease state with increased risk for progressing to cirrhosis and hepatocellular carcinoma. The HBeAg-negative mutant variety of chronic hepatitis B has been associated with a higher incidence of cirrhosis at initial presentation and more frequent progression to hepatocellular carcinoma compared with the wild-type hepatitis B. Five medications are currently approved by the US FDA for the treatment of chronic hepatitis B: interferon-alpha, lamivudine, adefovir dipivoxil, entecavir and peginterferon-alpha-2a. Interferon-alpha therapy has been shown to increase the rate of HBeAg and hepatitis B DNA loss with a small chance of hepatitis B surface antigen loss, but has significant adverse effects and is ineffective against the HBeAg-negative mutant. Lamivudine is a safely used, orally administered drug with good efficacy, but is associated with the development of a lamivudine-resistant (Lam-R) mutant in a large proportion of patients after long-term therapy. High relapse rates after lamivudine therapy make this medication less effective in the HBeAg-negative mutant also. Adefovir dipivoxil is a safely used, orally administered drug, which is effective against the Lam-R mutant. Adefovir dipivoxil is effective against the wild-type and HBeAg-negative hepatitis B and has a very low incidence of resistance development. Entecavir is a highly potent and selective new oral drug against hepatitis B. It has demonstrated no resistance development in treatment-naive patients, but a low incidence of resistance in patients infected with prior Lam-R mutants. Peginterferon-alpha-2a is administered once weekly and has improved efficacy compared with standard interferon-alpha and lamivudine. However, it has a similar adverse-effect profile to standard interferon-alpha. Pharmacoeconomic studies have demonstrated a cost benefit in treating chronic hepatitis B patients compared with no therapy. However, results have been conflicting, with earlier studies showing a cost advantage of lamivudine over interferon-alpha and a more recent, comprehensive study favouring interferon-alpha monotherapy in HBeAg-negative patients and adefovir dipivoxil 'salvage' after lamivudine resistance development in HBeAg-positive patients.
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PMID:Natural course, therapeutic options and economic evaluation of therapies for chronic hepatitis B. 1704 Jan 14

Chronic hepatitis B progresses to cirrhosis in the majority of immunosuppressed patients. The outcome of long-term antiviral therapy in HBV-infected organ transplant recipients is unknown. In 1996, we included 20 heart transplant (HT) recipients in a pilot trial to treat chronic hepatitis B with famciclovir. At that time, bridging fibrosis or cirrhosis was evident in 15 individuals (75%). From 1998 onwards, patients were switched to lamivudine in case of primary or secondary virological nonresponse to famciclovir. Adefovir or tenofovir became available at our centre for HT recipients in 2002. After 103 months, one patient was still on famciclovir showing a complete virological response. Sixteen patients were switched to lamivudine after 0.5-4 years of famciclovir therapy. Six of those showed a long-term response to lamivudine therapy lasting for up to 7 years. Lamivudine resistance developed in the remaining 10 patients (63%), in 4 of them successful rescue therapy (adefovir n = 3, tenofovir n = 1) could be initiated. Only one hepatocellular carcinoma developed, which was successfully treated by locoregional ablative therapy. Nine patients died (45%), with lamivudine-resistance-related liver failure as the cause of death in five cases. Significant improvement of Ishak fibrosis scores could be demonstrated in six of the seven patients with more than two sequential liver biopsies available. Long-term antiviral therapy of chronic hepatitis B can lead to regression of liver cirrhosis in patients after organ transplantation, unless viral resistance occurs. This study demonstrates the urgent need for further antivirals to overcome antiviral resistance.
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PMID:Improved outcome of chronic hepatitis B after heart transplantation by long-term antiviral therapy. 1705 72

Methods for diagnosing hepatic fibrosis have progressed significantly over the last few years--notably with the appearance of minimally invasive biological tests (which avoid the need for liver needle biopsy but nevertheless require a blood sample). Hepatic ultrasonic transient elastography (Fibroscan) is a new diagnostic method for hepatic fibrosis: it is totally noninvasive and gives an immediate result. Here, we review the currently available data on the use of the Fibroscan. Today's main field of application is chronic, viral hepatitis C, with areas under the receiver operation characteristic curve of 0.79-0.83, 0.90-0.91 and 0.91-0.97 for the diagnosis of F2, F3 and F4 fibrosis (defined according to the Metavir classification system), respectively. Furthermore, the Fibroscan enables the noninvasive diagnosis of cirrhosis (regardless of the latter's aetiology), with positive and negative predictive values of 70-95% and 77-95%, respectively. Chronic viral hepatitis B, HIV-hepatitis C virus and HIV-hepatitis B virus coinfections, alcohol-related liver diseases and intrahepatic cholestatic diseases are the device's other main fields of application in hepatology. Today, the Fibroscan is a reliable alternative for the noninvasive diagnosis of hepatic fibrosis. Various diagnostic strategies and performing cost/benefit analyses are now necessary, to assess fully the value of hepatic elastography relative to biological tests for hepatic fibrosis.
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PMID:Noninvasive diagnosis of liver fibrosis by ultrasonic transient elastography (Fibroscan). 1709 82

Chronic hepatitis B (CHB) is one of the leading causes of morbidity and mortality worldwide. Although various drugs are available for the treatment of CHB, emergence of the hepatitis B e antigen (HBeAg)-negative mutant variant, specifically in Asia, the Middle East and southern Europe, is creating a new challenge as this variant is less responsive to available treatments. HBeAg-negative CHB rapidly progresses to cirrhosis and its related complications. This review discusses the available literature on the approved and under-trial treatment options and their respective efficacies for HBeAg-negative CHB.
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PMID:Management of patients with HBeAg-negative chronic hepatitis B. 1726 76

Chronic hepatitis B virus infection causes nearly all the deaths from this virus. As the initial infection occurs without symptoms and decades prior to the onset of cirrhosis and liver cancer, these consequences are rarely recognized as being caused by the virus. Consequently, its public health importance is under-recognized. Safe and effective vaccines have now been available for over 20 years. Concerns have been raised regarding the mercury preservative in vaccines leading to potential toxicity. But the evidence to date does not support any association of hepatitis B vaccine with serious adverse consequences. Protecting infants through immunization is the most effective control strategy. By 2005, over 80% of countries had implemented routine infant immunization. In countries with relatively low rates of hepatitis B virus infection, some have argued to defer immunization until later life. However, these arguments focus on the more visible acute infection. The possible future cost from a single infant infection argues for universal infant hepatitis B immunization--given the very high costs of treating its consequences (e.g., liver transplant) and the very low price of the vaccine.
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PMID:Should hepatitis B vaccine be used for infants? 1728 Apr 76

Chronic hepatitis B virus (HBV) infection is a serious health issue worldwide. The presence of HBV replication markers--hepatitis B e antigen (HBeAg) or HBV DNA--is associated with continuing hepatitis activity or intermittent hepatitis flares and subsequent disease progression, including hepatic decompensation and development of liver cirrhosis or hepatocellular carcinoma (HCC). Long-term (>10 years) prospective studies in patients >30 years of age have shown that HBeAg seropositivity is associated with increased risk of disease progression, and the risk of cirrhosis and HCC begins to increase at an HBV DNA level of 10(4) copies/ml. Therefore, elimination of HBV, or at least sustained or maintained suppression of HBV, is the key to reducing hepatitis and thereby halting or preventing disease progression. Therapy with interferon-alpha or a direct antiviral agent has been shown to reduce the risk of cirrhosis and prevent further disease worsening. In both the woodchuck hepatitis model and in HBV patients, maintained suppression of HBV replication by a direct antiviral agent may reduce the progression to HCC. However, the efficacy of current antiviral therapy is still far from satisfactory. The ability to achieve a high rate of sustained or maintained HBV suppression with a low risk of drug resistance would be the ultimate goal in the treatment of chronic HBV infection.
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PMID:Hepatitis B virus replication and liver disease progression: the impact of antiviral therapy. 1731 Aug 11

Chronic hepatitis B is caused by persistent infection with the hepatitis B virus (HBV), a unique DNA virus that replicates through an RNA intermediate produced from a stable covalently closed circular DNA molecule. Viral persistence appears to be due to inadequate innate and adaptive immune responses. Chronic infection has a variable course after several decades resulting in cirrhosis in up to one-third of patients and liver cancer in a proportion of those with cirrhosis. Sensitive assays for HBV DNA levels in serum have been developed that provide important insights into pathogenesis and natural history. Therapy of hepatitis B is evolving. Peginterferon induces long-term remissions in disease in one-third of patients with typical hepatitis B e antigen (HBeAg) positive chronic hepatitis B, but a lesser proportion of those without HBeAg. Several oral nucleoside analogues with activity against HBV have been shown to be effective in suppressing viral levels and improving biochemical and histological features of disease in a high proportion of patients with and without HBeAg, at least in the short term. What is uncertain is which agent or combination of agents is most effective, how long therapy should last, and which criteria should be used to start, continue, switch or stop therapy. Long-term therapy with nucleoside analogues may be the most appropriate approach to treatment, but the expense and lack of data on long-term safety and efficacy make recommendations difficult. Clearly, many basic and clinical research challenges remain in defining optimal means of management of chronic hepatitis B.
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PMID:Management of hepatitis B: summary of a clinical research workshop. 1739 13

Chronic hepatitis B affects nearly 10% of HIV-infected patients. Thus, approximately four million people worldwide are HBV/HIV coinfected. Hepatitis B virus (HBV) infection is a dynamic disease and coinfection with HIV impacts directly on the outcome of HBV infection, considerably complicating its natural history, diagnosis, and management. Hepatic necroinflammation is lower in HBV/HIV coinfection, yet liver damage, especially fibrosis, progresses at a faster rate than in HBV monoinfection. With improved control of HIV disease with HAART, liver disease has emerged as one of the leading causes of death in patients with HIV Anti-HBV therapy should be considered for all HIV/HBV-coinfected patients with evidence of liver disease, irrespective of the CD4 cell count. In coinfected patients not requiring HAART, HBV therapy should be based on agents with no HIV activity such as adefovir. In contrast, in patients with CD4 counts less than 350 cells/microl, the use of agents with dual anti-HIV and anti-HBV activity should be considered. Combination therapy should ideally be used to avoid or delay the development of antiviral resistance. Regular monitoring of patients is imperative to recognize reactivation and subsequent need for treatment, and to identify drug resistance and viral breakthrough early. Similar close monitoring is required for patients presenting with advanced HIV infection and reduced functional hepatic reserve due to HBV-related cirrhosis. Effective antiviral treatment can precipitate immune reconstitution disease resulting in serious hepatic flare and precipitating liver decompensation. Clearly, more data are needed to more effectively treat HIV/HBV coinfection.
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PMID:Treatment of HIV/HBV coinfection: clinical and virologic issues. 1747 12


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