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        <title>Clinics in Liver Disease via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Clinics in Liver Disease' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Clinics+in+Liver+Disease&t=Clinics+in+Liver+Disease&s=Search&f=source]]></link>
        <lastBuildDate>Sun, 21 Mar 2010 15:07:52 +0100</lastBuildDate>
        <item>
            <title>Index</title>
            <link>http://www.medworm.com/index.php?rid=3206230&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109001032%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
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            <pubDate>Tue, 26 Jan 2010 14:22:07 +0100</pubDate>
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            <title>Management of Acute Hepatitis C</title>
            <link>http://www.medworm.com/index.php?rid=3206229&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000889%2Fabstract%3Frss%3Dyes</link>
            <description>This article examines the diagnosis of acute infection and critically appraises the various treatment regimens. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
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            <pubDate>Tue, 26 Jan 2010 14:22:07 +0100</pubDate>
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            <title>Health Care Workers as Source of Hepatitis B and C Virus Transmission</title>
            <link>http://www.medworm.com/index.php?rid=3206228&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000841%2Fabstract%3Frss%3Dyes</link>
            <description>Transmission of hepatitis B and C from health care workers to patients remains rare in developed medical care systems but may be more common in systems that are still developing. Since the 1970s, at least 69 health care workers infected with hepatitis B or C have been implicated in transmission of their infection. This likely underestimates the magnitude of the problem. In this article, risk factors associated with transmission are reviewed and infection prevention and control practices outlined. Management of infected providers is also discussed. National guidelines are compared, highlighting different countries' approaches to this complex challenge. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
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            <pubDate>Tue, 26 Jan 2010 14:22:07 +0100</pubDate>
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            <title>US Outbreak Investigations Highlight the Need for Safe Injection Practices and Basic Infection Control</title>
            <link>http://www.medworm.com/index.php?rid=3206227&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000853%2Fabstract%3Frss%3Dyes</link>
            <description>This article highlights the importance of basic infection control and the need for increased awareness of safe injection practices. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
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            <pubDate>Tue, 26 Jan 2010 14:22:07 +0100</pubDate>
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            <title>Infection Control Guidelines for Prevention of Health Care–Associated Transmission of Hepatitis B and C Viruses</title>
            <link>http://www.medworm.com/index.php?rid=3206226&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000865%2Fabstract%3Frss%3Dyes</link>
            <description>This article reviews patient-to-provider, patient-to-patient, and provider-to-patient transmission of hepatitis B and C in the health care setting. Current prevention strategies, precautions, and guidelines are discussed. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
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            <pubDate>Tue, 26 Jan 2010 14:22:07 +0100</pubDate>
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            <title>Health Care–Associated Hepatitis B and C Viruses: Legal Aspects</title>
            <link>http://www.medworm.com/index.php?rid=3206225&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS108932610900083X%2Fabstract%3Frss%3Dyes</link>
            <description>This article begins with an overview of the relevant sources of law and then explores legal duties and liability arising from two major categories of risk: occupational risks to health care providers and health care–associated risks to patients and other third parties. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
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            <pubDate>Tue, 26 Jan 2010 14:22:07 +0100</pubDate>
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            <title>Health Care–Associated Transmission of Hepatitis B &amp; C Viruses in Dental Care (Dentistry)</title>
            <link>http://www.medworm.com/index.php?rid=3206224&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000919%2Fabstract%3Frss%3Dyes</link>
            <description>This article describes the epidemiology of HBV and HCV and their particular risks to DHCP. Hepatitis B vaccination is discussed, as is postexposure management recommendations for both HBV and HCV. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
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            <pubDate>Tue, 26 Jan 2010 14:22:07 +0100</pubDate>
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            <title>Management of Acute Hepatitis B</title>
            <link>http://www.medworm.com/index.php?rid=3206223&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000944%2Fabstract%3Frss%3Dyes</link>
            <description>Acute hepatitis B virus (HBV) is a common cause of acute icteric hepatitis in adults. The vast majority of these patients resolve this acute infection and develop long-lasting immunity. In contrast, the vast majority of patients who develop chronic HBV have minimal symptoms and do not develop jaundice after becoming infected with HBV. These patients will frequently remain undiagnosed for years or decades. Approximately 1% of persons with acute HBV develop acute liver failure. Preventing acute HBV with vaccination is the best treatment. Although universal vaccination is now administered to newborns in many countries, the majority of adults have not been vaccinated and remain at risk. Because the majority of patients with acute HBV resolve this infection spontaneously, treatment with an oral...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
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            <pubDate>Tue, 26 Jan 2010 14:22:07 +0100</pubDate>
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            <title>Health Care–Associated Transmission of Hepatitis B and C in Oncology Care</title>
            <link>http://www.medworm.com/index.php?rid=3206222&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000877%2Fabstract%3Frss%3Dyes</link>
            <description>The risk of acquiring hepatitis B and C in the oncology setting was historically high and predominantly related to blood product administration in the prescreening era. With the development of progressively more sophisticated testing for hepatitis B and C, breaches in infection control have played an increasingly prominent role in disease transmission. Optimizing infection control in inpatient and outpatient oncology settings is essential in preventing the health care–associated transmission of hepatitis B and C to oncology patients. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
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            <pubDate>Tue, 26 Jan 2010 14:22:07 +0100</pubDate>
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            <title>Health Care–Associated Transmission of Hepatitis B and C Viruses in Endoscopy Units</title>
            <link>http://www.medworm.com/index.php?rid=3206221&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000932%2Fabstract%3Frss%3Dyes</link>
            <description>The risk for potential transmission of infectious agents during gastrointestinal (GI) endoscopy is concerning for patients and physicians. However, the instance of infection transmission remains rare after GI endoscopy procedures, with an estimated frequency of 1 in 1.8 million procedures. Endoscopy-related infection may occur when microorganisms are spread or transmitted from patient to patient by contaminated endoscopic or accessory equipments; from the GI tract through the bloodstream during endoscopy to susceptible organs or prostheses, or spread to adjacent tissues that are breached as a result of the endoscopy procedure; or from patients to endoscopy personnel and perhaps from endoscopy personnel to patients. Proper cleaning, disinfection, and reprocessing of endoscopies and accessor...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3206221</comments>
            <pubDate>Tue, 26 Jan 2010 14:22:07 +0100</pubDate>
            <guid isPermaLink="false">3206221</guid>        </item>
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            <title>Health Care–Associated Transmission of Hepatitis B and C Viruses in Hemodialysis Units</title>
            <link>http://www.medworm.com/index.php?rid=3206220&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000920%2Fabstract%3Frss%3Dyes</link>
            <description>This article summarizes the most recent information on epidemiology, clinical significance, and management of infection by hepatitis B and C viruses in this population. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3206220</comments>
            <pubDate>Tue, 26 Jan 2010 14:22:07 +0100</pubDate>
            <guid isPermaLink="false">3206220</guid>        </item>
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            <title>Molecular Epidemiology of Health Care–Associated Transmission of Hepatitis B and C Viruses</title>
            <link>http://www.medworm.com/index.php?rid=3206219&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000890%2Fabstract%3Frss%3Dyes</link>
            <description>The term “molecular epidemiology” has been ascribed to a host of different activities that involve gene-sequence analysis. Some examples of molecular epidemiology include modeling exercises of phylogenetic trees to reconstruct epidemics; studies of the evolution of hepatitis C virus (HCV); rates of nucleotide substitution in the hepatitis B virus (HBV) surface (S) gene; variations in the core promoter/pre-core/core region of HBV genotype C from different sources; analysis of HBV surface antigen mutations; molecular clock analyses of the short-term evolution of HCV; and analyses of clades and surface antigen polymorphisms of HBV. However, for most epidemiologists molecular epidemiology of viral hepatitis usually refers to studies of gene-sequence homology in HBV or HCV recovered from pe...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3206219</comments>
            <pubDate>Tue, 26 Jan 2010 14:22:07 +0100</pubDate>
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            <title>Occupational Exposure of Health Care Personnel to Hepatitis B and Hepatitis C: Prevention and Surveillance Strategies</title>
            <link>http://www.medworm.com/index.php?rid=3206218&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000828%2Fabstract%3Frss%3Dyes</link>
            <description>This article reviews the epidemiology of occupational exposures to hepatitis B and hepatitis C in health care personnel in hospital settings. The nature and likelihood of risk to health care personnel are evaluated along with estimates of seroconversion risk. The review focuses on prevention programs and available surveillance programs to aid in monitoring and reducing occupational exposures to blood-borne pathogens. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3206218</comments>
            <pubDate>Tue, 26 Jan 2010 14:22:07 +0100</pubDate>
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            <title>Epidemiology of Hepatitis B and C Viruses: A Global Overview</title>
            <link>http://www.medworm.com/index.php?rid=3206217&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000907%2Fabstract%3Frss%3Dyes</link>
            <description>This article reviews the prevalence, disease burden, genotype distribution, and transmission patterns of hepatitis B virus (HBV) and hepatitis C virus in the 6 World Health Organization regions. The global epidemiology of hepatitis B and C demonstrates a predominantly declining prevalence of the diseases. Improvement in the control of hepatitis B has been largely achieved with implementation of a more universal HBV vaccine program, although a large gap still remains in the effort toward global prevention of hepatitis B. The transmission of hepatitis C has been greatly impacted by mandatory screening of blood donors in most countries in the world, although intravenous drug use continues to be a major source of infection. Public education regarding the risks of exposure to infected paraphern...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3206217</comments>
            <pubDate>Tue, 26 Jan 2010 14:22:06 +0100</pubDate>
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        <item>
            <title>Preface</title>
            <link>http://www.medworm.com/index.php?rid=3206216&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000956%2Fabstract%3Frss%3Dyes</link>
            <description>Worldwide, a number of health care transmission outbreaks of infectious diseases, particularly hepatitis, in the past decade indicate startling evidence of an ongoing transmission of hepatitis in a health care setting. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3206216</comments>
            <pubDate>Tue, 26 Jan 2010 14:22:06 +0100</pubDate>
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            <title>Forthcoming issues</title>
            <link>http://www.medworm.com/index.php?rid=3206215&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109001020%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3206215</comments>
            <pubDate>Tue, 26 Jan 2010 14:22:06 +0100</pubDate>
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        <item>
            <title>Contents</title>
            <link>http://www.medworm.com/index.php?rid=3206214&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109001019%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3206214</comments>
            <pubDate>Tue, 26 Jan 2010 14:22:06 +0100</pubDate>
            <guid isPermaLink="false">3206214</guid>        </item>
        <item>
            <title>Index</title>
            <link>http://www.medworm.com/index.php?rid=2873597&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000737%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2873597</comments>
            <pubDate>Fri, 09 Oct 2009 09:29:11 +0100</pubDate>
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            <title>Non-Alcoholic Fatty Liver Disease: Is Bariatric Surgery the Answer?</title>
            <link>http://www.medworm.com/index.php?rid=2873596&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000646%2Fabstract%3Frss%3Dyes</link>
            <description>As the worldwide obesity epidemic continues to increase, the prevalence of non-alcoholic fatty liver disease (NAFLD) and specifically non-alcoholic steatohepatitis (NASH) will become increasingly prominent. NASH will surpass chronic hepatitis C infection as the primary indication for orthotopic liver transplantation in the near future. With the evolution of surgical techniques, bariatric surgery is currently recognized as the most effective method for achieving sustained weight loss and reversing numerous comorbidities in severely obese individuals. This review focuses on the potential risks and benefits of bariatric surgery in subjects with NAFLD and explores its role in the management of NASH in the obese patient. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2873596</comments>
            <pubDate>Fri, 09 Oct 2009 09:29:11 +0100</pubDate>
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            <title>Pharmacologic Therapy of Non-Alcoholic Steatohepatitis</title>
            <link>http://www.medworm.com/index.php?rid=2873595&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000531%2Fabstract%3Frss%3Dyes</link>
            <description>This article discusses this therapy, with particular emphasis on pharmacologic therapy. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2873595</comments>
            <pubDate>Fri, 09 Oct 2009 09:29:11 +0100</pubDate>
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            <title>Lifestyle Modification as the Primary Treatment of NASH</title>
            <link>http://www.medworm.com/index.php?rid=2873594&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000580%2Fabstract%3Frss%3Dyes</link>
            <description>This article reviews the rationale and data behind recommending lifestyle changes to prevent and reverse NASH, focusing specifically on changes that lead to increased physical activity in sedentary patients, changes in dietary habits, and decreased calorie consumption to achieve gradual and sustained weight loss in those who are overweight or obese. In a culture that values avoiding even minimal exertion these are not easy changes to make. Ultimately, the success of care providers in helping patients to recognize and overcome these barriers depends on a patient's motivation, but clinicians can be more persuasive and able to bolster this motivation when armed with a conviction based on data that establish this to be the best course of action for patients with NASH. (Source: Clinics in Liver...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2873594</comments>
            <pubDate>Fri, 09 Oct 2009 09:29:11 +0100</pubDate>
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            <title>NASH and HCC</title>
            <link>http://www.medworm.com/index.php?rid=2873593&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000592%2Fabstract%3Frss%3Dyes</link>
            <description>Primary liver cancer is the fifth most common malignancy worldwide and the third leading cause of cancer mortality. Non-alcoholic fatty liver disease is the most common cause of chronic liver disease in the United States encompassing a spectrum of entities marked by hepatic steatosis in the absence of significant alcohol consumption. Although simple steatosis follows a generally benign course, the more aggressive form, non-alcoholic steatohepatitis, can progress to cirrhosis and result in complications including hepatocellular carcinoma. A significant number of cases of hepatocellular carcinoma remain cryptogenic without known underlying chronic liver disease. It is increasingly recognized that non-alcoholic steatohepatitis likely accounts for a substantial portion of cryptogenic hepatocel...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2873593</comments>
            <pubDate>Fri, 09 Oct 2009 09:29:11 +0100</pubDate>
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            <title>Fatty Liver and Liver Transplantation</title>
            <link>http://www.medworm.com/index.php?rid=2873592&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000622%2Fabstract%3Frss%3Dyes</link>
            <description>This article addresses some of these challenges. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2873592</comments>
            <pubDate>Fri, 09 Oct 2009 09:29:10 +0100</pubDate>
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            <title>New Imaging Techniques for Non-Alcoholic Steatohepatitis</title>
            <link>http://www.medworm.com/index.php?rid=2873591&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000543%2Fabstract%3Frss%3Dyes</link>
            <description>No imaging modality has yet been proven to reliably differentiate simple hepatic steatosis from steatohepatitis. This review focuses on the predominant non-nuclear imaging modalities available to clinicians at the present time. The key feature of the techniques outlined in this review that demonstrate the most interesting results have one thing in common: imaging is not performed in a passive manner but is undertaken as a method to investigate functional differences between simple hepatic steatosis and steatohepatitis based upon the current working model for pathogenesis and progression. The purpose of this article is to review the strengths and weakness of current clinical and experimental imaging modalities for noninvasive detection of NAFLD, with an emphasis on NASH. (Source: Clinics in...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
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            <pubDate>Fri, 09 Oct 2009 09:29:10 +0100</pubDate>
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            <title>Predictors of Steatohepatitis and Advanced Fibrosis in Non-Alcoholic Fatty Liver Disease</title>
            <link>http://www.medworm.com/index.php?rid=2873590&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000634%2Fabstract%3Frss%3Dyes</link>
            <description>Non-alcoholic fatty liver disease is the most common cause of chronic liver disease in the United States. The development of non-alcoholic steatohepatitis increases the risk for cirrhosis and its complications. The gold standard for diagnosis is liver biopsy, the costs and risks of which make it impractical. Some demographic factors, blood tests, and imaging studies can be used to predict a higher risk of steatohepatitis or advanced fibrosis, but are of limited sensitivity and specificity. More accurate predictors and scoring systems would allow identifying who would benefit most from liver biopsy and monitor disease progression and response to therapy. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
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            <pubDate>Fri, 09 Oct 2009 09:29:10 +0100</pubDate>
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            <title>Endoplasmic Reticulum Stress and the Unfolded Protein Response</title>
            <link>http://www.medworm.com/index.php?rid=2873589&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000567%2Fabstract%3Frss%3Dyes</link>
            <description>This article reviews the pathways by which the UPR unfolds and its potential role in the development and progression of NAFLD. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2873589</comments>
            <pubDate>Fri, 09 Oct 2009 09:29:10 +0100</pubDate>
            <guid isPermaLink="false">2873589</guid>        </item>
        <item>
            <title>Apoptosis and Cytokines in Non-Alcoholic Steatohepatitis</title>
            <link>http://www.medworm.com/index.php?rid=2873588&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000555%2Fabstract%3Frss%3Dyes</link>
            <description>This article summarizes the process of apoptosis and roles of putative cytokines in progressive NAFLD. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2873588</comments>
            <pubDate>Fri, 09 Oct 2009 09:29:10 +0100</pubDate>
            <guid isPermaLink="false">2873588</guid>        </item>
        <item>
            <title>Role of Insulin Resistance and Lipotoxicity in Non-Alcoholic Steatohepatitis</title>
            <link>http://www.medworm.com/index.php?rid=2873587&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000610%2Fabstract%3Frss%3Dyes</link>
            <description>It is well established that the development of NAFLD and NASH are closely linked to an excess flow of free fatty acids (FFA) arising from dysfunctional/insulin resistant adipose tissue causing ectopic fat deposition in many organs. In the liver, when chronic lipid supply surpasses the metabolic ability to adapt it will induce hepatocellular damage as FFA are redirected into harmful pathways of non-oxidative metabolism with intracellular accumulation of toxic lipid-derived metabolites. Multiple mechanisms have been implicated including mitochondrial dysfunction, endoplasmic reticulum stress, and activation of multiple inflammatory pathways. Understanding the role of insulin resistance and lipotoxicity in NASH as part of a broader metabolic disorder is likely to assist practitioners in the s...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2873587</comments>
            <pubDate>Fri, 09 Oct 2009 09:29:10 +0100</pubDate>
            <guid isPermaLink="false">2873587</guid>        </item>
        <item>
            <title>Histopathology of Non-Alcoholic Fatty Liver Disease</title>
            <link>http://www.medworm.com/index.php?rid=2873586&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000609%2Fabstract%3Frss%3Dyes</link>
            <description>Current imaging methodologies can detect steatosis with increasing accuracy but cannot detect inflammation or pre-cirrhotic fibrosis or remodeling of the liver parenchyma. Imaging also cannot assess types or localization of hepatic steatosis. With the increased use of rodents to study NAFLD/NASH, careful analysis or reading highlights the fact that liver tissue evaluations reported in many of the popular animal models of NAFLD/NASH often do not imitate many of the significant aspects of the human disease, despite similar terminology applied by investigators. This review will focus on the findings in human disease. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2873586</comments>
            <pubDate>Fri, 09 Oct 2009 09:29:10 +0100</pubDate>
            <guid isPermaLink="false">2873586</guid>        </item>
        <item>
            <title>Epidemiology and Natural History of Non-Alcoholic Steatohepatitis</title>
            <link>http://www.medworm.com/index.php?rid=2873585&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000579%2Fabstract%3Frss%3Dyes</link>
            <description>This article describes the epidemiology and natural history of this disorder. It also describes current diagnostic and treatment methods and describes future implications NAFLD may have. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2873585</comments>
            <pubDate>Fri, 09 Oct 2009 09:29:10 +0100</pubDate>
            <guid isPermaLink="false">2873585</guid>        </item>
        <item>
            <title>Preface</title>
            <link>http://www.medworm.com/index.php?rid=2873584&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000658%2Fabstract%3Frss%3Dyes</link>
            <description>Our understanding of nonalcoholic fatty liver disease (NAFLD) has grown exponentially in the past 29 years since Ludwig and colleagues first described the histologic lesions that comprise a subset of NAFLD known as nonalcoholic steatohepatitis (NASH). A recent PubMed search using the term “nonalcoholic fatty liver disease” generated 1475 articles published since 1980, of which 1405 were published since the year 2000. Concern for this liver disease is validated, as NAFLD is becoming, if it has not already become, the number one chronic liver disease in this country and in many others around the world. As the prevalence of obesity and diabetes, both of which are characterized by impairment in insulin signaling, continues to rise, so will the prevalence of NAFLD. We as health care provide...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2873584</comments>
            <pubDate>Fri, 09 Oct 2009 09:29:10 +0100</pubDate>
            <guid isPermaLink="false">2873584</guid>        </item>
        <item>
            <title>Forthcoming issues</title>
            <link>http://www.medworm.com/index.php?rid=2873583&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000725%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2873583</comments>
            <pubDate>Fri, 09 Oct 2009 09:29:10 +0100</pubDate>
            <guid isPermaLink="false">2873583</guid>        </item>
        <item>
            <title>Contents</title>
            <link>http://www.medworm.com/index.php?rid=2873582&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000713%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2873582</comments>
            <pubDate>Fri, 09 Oct 2009 09:29:10 +0100</pubDate>
            <guid isPermaLink="false">2873582</guid>        </item>
        <item>
            <title>Index</title>
            <link>http://www.medworm.com/index.php?rid=2628164&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000476%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2628164</comments>
            <pubDate>Thu, 23 Jul 2009 10:59:09 +0100</pubDate>
            <guid isPermaLink="false">2628164</guid>        </item>
        <item>
            <title>Thrombopoietin Agonists for the Treatment of Thrombocytopenia in Liver Disease and Hepatitis C</title>
            <link>http://www.medworm.com/index.php?rid=2628163&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000385%2Fabstract%3Frss%3Dyes</link>
            <description>This article examines the nature of thrombocytopenia, ITP, and TPO. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2628163</comments>
            <pubDate>Thu, 23 Jul 2009 10:59:08 +0100</pubDate>
            <guid isPermaLink="false">2628163</guid>        </item>
        <item>
            <title>Monoclonal and Polyclonal Antibodies Against the HCV Envelope Proteins</title>
            <link>http://www.medworm.com/index.php?rid=2628162&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000373%2Fabstract%3Frss%3Dyes</link>
            <description>The potential for developing efficient and efficacious therapies for hepatitis C virus continues to improve. Insight into the molecular processes involved in attachment, entry, and fusion suggests that antibodies could potentially inhibit viral replication at any or all of these stages, and the attachment and entry stages present the best target for antibodies that can attack the virus. Monoclonal and polyclonal antibodies present an important therapeutic option in this area, and this article assesses current investigations of several antibodies. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2628162</comments>
            <pubDate>Thu, 23 Jul 2009 10:59:08 +0100</pubDate>
            <guid isPermaLink="false">2628162</guid>        </item>
        <item>
            <title>Caspase Inhibitors for the Treatment of Hepatitis C</title>
            <link>http://www.medworm.com/index.php?rid=2628161&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000336%2Fabstract%3Frss%3Dyes</link>
            <description>Decreasing hepatocyte injury and death is an attractive therapeutic target in chronic hepatitis C and other liver diseases. Apoptotic cell death is a critical mechanism responsible for liver injury in hepatitis C, and contributes to hepatic fibrogenesis. At the cellular level, apoptosis is executed by a family of cysteine proteases termed caspases. Caspase inhibitors have been developed to inhibit these proteases and attenuate cellular apoptosis in vivo. By reducing hepatocyte apoptosis these agents have the potential to serve as hepatoprotective agents, minimizing liver injury and fibrosis. Studies on a variety of animal models, and time-limited studies in human patients with hepatitis C suggest these are promising therapeutic agents. However, although these agents hold promise, their use...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2628161</comments>
            <pubDate>Thu, 23 Jul 2009 10:59:08 +0100</pubDate>
            <guid isPermaLink="false">2628161</guid>        </item>
        <item>
            <title>HCV NS5B Polymerase Inhibitors</title>
            <link>http://www.medworm.com/index.php?rid=2628160&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000270%2Fabstract%3Frss%3Dyes</link>
            <description>Chronic hepatitis C virus (HCV) infection affects approximately 4 million persons and is the major indication for liver transplantation in the United States. The current standard for treatment of HCV is pegylated interferon in combination with ribavirin. Despite significant advances in treatment, only approximately 50% of patients of treated patients clear HCV infection. Polymerase inhibitors, given their potent antiviral effects, represent a major contribution to the future of HCV treatment. Whether these new drugs will have a role in the treatment of the difficult patient (non-responders, those co-infected with HIV, decompensated liver disease and liver transplant recipients) remains to be determined. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2628160</comments>
            <pubDate>Thu, 23 Jul 2009 10:59:08 +0100</pubDate>
            <guid isPermaLink="false">2628160</guid>        </item>
        <item>
            <title>Telaprevir: Hope on the Horizon, Getting Closer</title>
            <link>http://www.medworm.com/index.php?rid=2628159&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000348%2Fabstract%3Frss%3Dyes</link>
            <description>In this report, the current experience using telaprevir to treat chronic HCV infection as monotherapy and in combination with other agents is reviewed. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2628159</comments>
            <pubDate>Thu, 23 Jul 2009 10:59:08 +0100</pubDate>
            <guid isPermaLink="false">2628159</guid>        </item>
        <item>
            <title>Boceprevir, an NS3 Protease Inhibitor of HCV</title>
            <link>http://www.medworm.com/index.php?rid=2628158&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS108932610900035X%2Fabstract%3Frss%3Dyes</link>
            <description>Hepatitis C virus (HCV) is a major cause of chronic liver disease leading to death from liver failure or hepatocellular carcinoma. Hepatitis C is the most common indication for liver transplantation worldwide and is a major cause of the increased incidence of hepatocellular cancer in the United States. The current paradigm for HCV treatment relies on pegylated interferon and ribavirin as agents that enhance endogenous mechanisms for viral clearance and are dependent on host factors. In patients with genotype 1 HCV infection, sustained viral response (SVR) rates remain suboptimal, with less than half of genotype 1–infected individuals going on to achieve SVR. This has led to a shift in the investigational focus for treatment of HCV toward specifically targeted antiviral therapy for HCV ag...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2628158</comments>
            <pubDate>Thu, 23 Jul 2009 10:59:08 +0100</pubDate>
            <guid isPermaLink="false">2628158</guid>        </item>
        <item>
            <title>Ribavirin Analogs</title>
            <link>http://www.medworm.com/index.php?rid=2628157&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000324%2Fabstract%3Frss%3Dyes</link>
            <description>Ribavirin is ineffective against hepatitis C virus as mono-therapy but is critical in attaining both early virologic response and sustained virologic response when combined with pegylated interferon. Ribavirin has significant dose-limiting toxicities, the most important of which is hemolytic anemia. Taribavirin is a ribavirin pro-drug, which targets the liver and has less incidence of anemia, and it may be a promising alternative to ribavirin in the future. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2628157</comments>
            <pubDate>Thu, 23 Jul 2009 10:59:08 +0100</pubDate>
            <guid isPermaLink="false">2628157</guid>        </item>
        <item>
            <title>Cyclophilin Inhibitors</title>
            <link>http://www.medworm.com/index.php?rid=2628156&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000282%2Fabstract%3Frss%3Dyes</link>
            <description>The percentage of patients chronically infected with hepatitis C virus (HCV) who have reached sustained antiviral response has increased since the introduction of the pegylated interferon-alpha (pIFNa) and ribavirin (RBV) treatment. However, the current standard pIFNa/RBV therapy not only has a low success rate (about 50%) but is often associated with serious side effects. Thus, there is an urgent need for the development of new anti-HCV agents. Cyclophilin (Cyp) inhibitors are among the most promising of the new anti-HCV agents under development. Recent clinical studies demonstrate that Cyp inhibitors are potent anti-HCV drugs, with a novel mechanism of action and efficacy profiles that make them attractive candidates for combination with current and future HCV treatments. (Source: Clinic...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2628156</comments>
            <pubDate>Thu, 23 Jul 2009 10:59:08 +0100</pubDate>
            <guid isPermaLink="false">2628156</guid>        </item>
        <item>
            <title>Hepatitis C Virus Infection and Immunomodulatory Therapies</title>
            <link>http://www.medworm.com/index.php?rid=2628155&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000361%2Fabstract%3Frss%3Dyes</link>
            <description>Hepatitis C virus (HCV) infection remains a large-scale and significant health concern. The combination of subcutaneously administered pegylated interferon and oral ribavirin is the FDA-approved regimen for the treatment of chronic HCV infection. Combination therapy may result in a sustained virologic response leading to HCV eradication, with a reduction in risk for cirrhosis, hepatic decompensation, and hepatocellular carcinoma.9,10 However, the combination of PEG-IFN and ribavirin does not universally result in cure in all patients who undergo treatment. In this article, the authors discuss immunomodulatory therapies and clinical trials in the treatment of HCV infection. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2628155</comments>
            <pubDate>Thu, 23 Jul 2009 10:59:08 +0100</pubDate>
            <guid isPermaLink="false">2628155</guid>        </item>
        <item>
            <title>Antisense Inhibitors, Ribozymes, and siRNAs</title>
            <link>http://www.medworm.com/index.php?rid=2628154&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000300%2Fabstract%3Frss%3Dyes</link>
            <description>The current standard of care for the treatment of hepatitis C virus infection, pegylated interferon-α and ribavirin, is costly, associated with significant side effects, and effective in only 50% of patients. There is therefore a need for the development of novel antiviral therapies. One such approach involves the application of gene silencing technologies, including antisense oligonucleotides, ribozymes, RNA interference, and aptamers. However, despite great scientific advances over the past decade, and promising in vitro data, several significant challenges continue to limit the translation of this technology to the clinical setting. This review provides a concise update of the current literature. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2628154</comments>
            <pubDate>Thu, 23 Jul 2009 10:59:08 +0100</pubDate>
            <guid isPermaLink="false">2628154</guid>        </item>
        <item>
            <title>Antifibrotics for Chronic Hepatitis C</title>
            <link>http://www.medworm.com/index.php?rid=2628153&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000312%2Fabstract%3Frss%3Dyes</link>
            <description>Development and testing of antifibrotic agents for the treatment of chronic hepatitis C have generally been targeted toward hepatic stellate cells, transforming growth factor-β, the inflammatory response, or extracellular matrix accumulation. Although several agents such as interferon-γ, long-term pegylated interferon, and caspase inhibitors have been studied, none have proved to be effective to date. There is a clear need for drugs that inhibit or reverse hepatic fibrosis as these would be immediately applicable to patients for whom antiviral therapy has failed or who have contraindications to antiviral therapy such as those with decompensated liver disease or renal failure. A major impediment in the development of new drugs in this field has been the inability to identify appropriate h...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2628153</comments>
            <pubDate>Thu, 23 Jul 2009 10:59:08 +0100</pubDate>
            <guid isPermaLink="false">2628153</guid>        </item>
        <item>
            <title>Novel Interferons for Treatment of Hepatitis C Virus</title>
            <link>http://www.medworm.com/index.php?rid=2628152&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000294%2Fabstract%3Frss%3Dyes</link>
            <description>The current standard of care for treatment of hepatitis C is pegylated interferon and ribavirin. Despite the large number of new oral agents under development, interferon will likely remain the backbone of future therapy. Interferon has unique antiviral and immunomodulatory properties, which have been critical in limiting resistance to protease inhibitors and improving efficacy. Hence, optimizing pharmacokinetics and promoting adherence to interferon dosing regimens will become even more critical as new regimens enter the clinical arena. This review highlights novel interferons under development that may offer therapeutic advantages over the formulations currently available. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2628152</comments>
            <pubDate>Thu, 23 Jul 2009 10:59:08 +0100</pubDate>
            <guid isPermaLink="false">2628152</guid>        </item>
        <item>
            <title>Preface</title>
            <link>http://www.medworm.com/index.php?rid=2628151&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000397%2Fabstract%3Frss%3Dyes</link>
            <description>The current standard of care for chronic hepatitis C therapy is a combination of pegylated interferon and ribavirin. Eradication of the hepatitis C virus (HCV) has been proved to be possible in roughly half of all patients treated; however, viral eradication rates are superior in patients with viral genotypes 2 and 3 compared with genotype 1 patients. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2628151</comments>
            <pubDate>Thu, 23 Jul 2009 10:59:08 +0100</pubDate>
            <guid isPermaLink="false">2628151</guid>        </item>
        <item>
            <title>Forthcoming issues</title>
            <link>http://www.medworm.com/index.php?rid=2628150&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000464%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2628150</comments>
            <pubDate>Thu, 23 Jul 2009 10:59:08 +0100</pubDate>
            <guid isPermaLink="false">2628150</guid>        </item>
        <item>
            <title>Contents</title>
            <link>http://www.medworm.com/index.php?rid=2628149&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000452%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2628149</comments>
            <pubDate>Thu, 23 Jul 2009 10:59:08 +0100</pubDate>
            <guid isPermaLink="false">2628149</guid>        </item>
        <item>
            <title>Index</title>
            <link>http://www.medworm.com/index.php?rid=2419208&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000221%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2419208</comments>
            <pubDate>Fri, 01 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2419208</guid>        </item>
        <item>
            <title>Care of the Cirrhotic Patient</title>
            <link>http://www.medworm.com/index.php?rid=2419207&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000087%2Fabstract%3Frss%3Dyes</link>
            <description>Timely surveillance for varices and hepatocellular carcinoma, prophylaxis against spontaneous bacterial peritonitis (SBP) improve survival in patients awaiting transplantation. Early diagnosis of minimal or overt hepatic encephalopathy can delay life threatening complications, reduce need for hospitalization, and potentially improve survival pending liver transplantation. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2419207</comments>
            <pubDate>Fri, 01 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2419207</guid>        </item>
        <item>
            <title>Hepatitis Vaccination and Prophylaxis</title>
            <link>http://www.medworm.com/index.php?rid=2419206&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000075%2Fabstract%3Frss%3Dyes</link>
            <description>This article discusses current recommendations for vaccination and other forms of prophylaxis aimed at minimizing the clinical effects of these viruses. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2419206</comments>
            <pubDate>Fri, 01 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2419206</guid>        </item>
        <item>
            <title>Management of Autoimmune and Cholestatic Liver Disorders</title>
            <link>http://www.medworm.com/index.php?rid=2419205&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000130%2Fabstract%3Frss%3Dyes</link>
            <description>The management of autoimmune and cholestatic liver disorders is a challenging area of hepatology. Autoimmune and cholestatic liver diseases represent a comparatively small proportion of hepatobiliary disorders, yet their appropriate management is of critical importance for patient survival. In this article, management strategies are discussed, including the indications and expectations of pharmacologic therapy, endoscopic approaches, and the role of liver transplantation. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2419205</comments>
            <pubDate>Fri, 01 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2419205</guid>        </item>
        <item>
            <title>Drug-Induced Hepatotoxicity or Drug-Induced Liver Injury</title>
            <link>http://www.medworm.com/index.php?rid=2419204&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000105%2Fabstract%3Frss%3Dyes</link>
            <description>Drug-induced hepatotoxicity is underreported and underestimated in the United States. It is an important cause of acute liver failure. Common classes of drugs causing drug-induced hepatotoxicity include antibiotics, lipid lowering agents, oral hypoglycemics, psychotropics, antiretrovirals, acetaminophen, and complementary and alternative medications. Hepatotoxic drugs often have a signature or pattern of liver injury including patterns of liver test abnormalities, latency of symptom onset, presence or absence of immune hypersensitivity, and the course of the reaction after drug withdrawal. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2419204</comments>
            <pubDate>Fri, 01 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2419204</guid>        </item>
        <item>
            <title>Management of Alcoholic Liver Disease</title>
            <link>http://www.medworm.com/index.php?rid=2419203&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000051%2Fabstract%3Frss%3Dyes</link>
            <description>Understanding alcohol addiction and abstinence is key to treating alcoholic liver disease, since abstinence leads to improvement in all forms of alcoholic liver damage. Although pharmacotherapy for alcoholism, using agents such as naltrexone, acamprosate, topiramate, and baclofen, is an exciting field, few studies have included patients with liver disease or cirrhosis. To treat alcoholic liver injury, corticosteroids have become the standard of care in patients with severe alcoholic hepatitis. In contrast, the role of pharmacotherapy to treat alcoholic fibrosis is unclear, with failure to observe a benefit in randomized, placebo-controlled clinical trials of colchicine, S-adenosylmethionine (SAMe), or phosphatidylcholine. Liver transplantation remains an option in selected patients with li...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2419203</comments>
            <pubDate>Fri, 01 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2419203</guid>        </item>
        <item>
            <title>Nonalcoholic Fatty Liver Disease: A Practical Approach to Evaluation and Management</title>
            <link>http://www.medworm.com/index.php?rid=2419202&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000117%2Fabstract%3Frss%3Dyes</link>
            <description>Non-alcoholic fatty liver disease (NAFLD) has become one of the most common forms of chronic liver disease in the Western world. The rise in NAFLD is thought to be associated with the prevalence of metabolic syndrome. NASH is a subtype of NAFLD that may progress to cirrhosis and end stage liver disease. Although there are no approved treatment regimens for NAFLD or NASH, a number of different interventions are being tested. Meanwhile, most experts advocate that components of metabolic syndrome should be effectively treated. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2419202</comments>
            <pubDate>Fri, 01 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2419202</guid>        </item>
        <item>
            <title>Modern Diagnosis and Management of Hepatocellular Carcinoma</title>
            <link>http://www.medworm.com/index.php?rid=2419201&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000099%2Fabstract%3Frss%3Dyes</link>
            <description>The incidence of hepatocellular carcinoma (HCC) is rising, and the number of patients with HCC is expected to more than double over the next 1 to 2 decades. HCC meets the criteria for establishment of a surveillance program. Patients with cirrhosis, regardless of the cause, are at the highest risk for developing HCC and this is the population in which surveillance should be performed. (Alpha-fetoprotein and hepatic ultrasonography are the currently recommended surveillance tests. If a surveillance test is abnormal, there is a need for a recall test for diagnostic evaluation of HCC. Triple-phase imaging is recommended for evaluation at recall, with MRI being more sensitive and specific. Novel genetic markers can improve the histologic diagnosis of early HCC. The Barcelona staging classifica...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2419201</comments>
            <pubDate>Fri, 01 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2419201</guid>        </item>
        <item>
            <title>Surgery in the Patient with Liver Disease</title>
            <link>http://www.medworm.com/index.php?rid=2419200&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS108932610900004X%2Fabstract%3Frss%3Dyes</link>
            <description>The advent of liver transplantation has greatly improved the long-term survival of patients with decompensated cirrhosis, and surgery is now performed more frequently in patients with advanced liver disease. The estimation of perioperative mortality is limited by the retrospective nature of and biased patient selection in the available clinical studies. The overall experience is that, in patients with cirrhosis, use of the Child classification and Model for End-Stage Liver Disease (MELD) score provides a reasonably precise estimation of perioperative mortality. Careful preoperative preparation and monitoring to detect complications early in the postoperative course are essential to improve outcomes. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2419200</comments>
            <pubDate>Fri, 01 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2419200</guid>        </item>
        <item>
            <title>Approach to a Liver Mass</title>
            <link>http://www.medworm.com/index.php?rid=2419199&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000063%2Fabstract%3Frss%3Dyes</link>
            <description>Incidentally discovered liver masses are becoming more common with the increasing application and power of imaging techniques for the evaluation of abdominal conditions. Although such masses are often benign, conclusive diagnoses must be established in order to provide appropriate patient care. Various imaging modalities can be utilized to accurately diagnose such masses without resort to more invasive diagnostic measures. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2419199</comments>
            <pubDate>Fri, 01 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2419199</guid>        </item>
        <item>
            <title>The Hospitalized Patient with Abnormal Liver Function Tests</title>
            <link>http://www.medworm.com/index.php?rid=2419198&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000129%2Fabstract%3Frss%3Dyes</link>
            <description>Evaluation of abnormal liver function tests (LFTs) in the hospitalized patient is typically more urgent than the outpatient setting. This process is best organized into four steps. The first step is to determine whether the abnormal LFTs are associated with the illness resulting in the admission to the hospital or preceded the present illness. The second is to determine the etiology of the underlying liver disease. The third step is to evaluate the severity of the liver dysfunction and determine if acute liver failure (ALF) or acute decompensation of chronic liver failure is present. The final step is to look for the presence of associated complications—either those of ALF or chronic liver failure as appropriate. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2419198</comments>
            <pubDate>Fri, 01 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2419198</guid>        </item>
        <item>
            <title>The Asymptomatic Outpatient with Abnormal Liver Function Tests</title>
            <link>http://www.medworm.com/index.php?rid=2419197&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000038%2Fabstract%3Frss%3Dyes</link>
            <description>Traditionally, the constellation of biochemistry tests including liver enzymes, total bilirubin, and hepatic synthetic measures (prothrombin time (PT) and serum albumin level) are referred to as liver function tests (LFTs). Abnormal LFTs can be encountered during primary health care visits, routine blood donation, and insurance screening. A reported 1% to 4% of asymptomatic patients exhibit abnormal LFTs, leading to a sizeable number of annual consultations to a gastroenterology and/or hepatology practice. A cost-effective and systematic approach is essential to the interpretation of abnormal LFTs. A review of pattern of abnormal LFTs, detailed medical history, and a comprehensive physical examination help establish a foundation for further individualized testing. Further investigation oft...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2419197</comments>
            <pubDate>Fri, 01 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2419197</guid>        </item>
        <item>
            <title>Preface</title>
            <link>http://www.medworm.com/index.php?rid=2419196&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000142%2Fabstract%3Frss%3Dyes</link>
            <description>A consequence of the rapid advances in the science and practice of hepatology has been an expanding number of diagnostic tests and therapeutic interventions. Although these new modalities have transformed the care of patients with liver disease, effective use of invasive, and often expensive, diagnostics is crucial. (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2419196</comments>
            <pubDate>Fri, 01 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2419196</guid>        </item>
        <item>
            <title>Forthcoming issues</title>
            <link>http://www.medworm.com/index.php?rid=2419195&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS108932610900021X%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2419195</comments>
            <pubDate>Fri, 01 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2419195</guid>        </item>
        <item>
            <title>Contents</title>
            <link>http://www.medworm.com/index.php?rid=2419194&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.liver.theclinics.com%2Farticle%2FPIIS1089326109000208%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2419194</comments>
            <pubDate>Fri, 01 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2419194</guid>        </item>
        <item>
            <title>Human NOTES Cholecystectomy: Transgastric Hybrid Technique.</title>
            <link>http://www.medworm.com/index.php?rid=2177215&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19198959%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: NOTES hybrid transgastric cholecystectomy can be performed safely in human patients. This procedure is still technically challenging given the current instrumentation that is available. In order to perform a pure NOTES transgastric cholecystectomy, a safe blind access method, improved retraction, endoscopic hemostatic clips, and reliable closure methods need to be developed.
    PMID: 19198959 [PubMed - as supplied by publisher] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2177215</comments>
            <pubDate>Sat, 07 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2177215</guid>        </item>
        <item>
            <title>Preface.</title>
            <link>http://www.medworm.com/index.php?rid=2120522&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19150303%26dopt%3DAbstract</link>
            <description>Authors: Caldwell SH, Sanyal AJ
    
    PMID: 19150303 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2120522</comments>
            <pubDate>Thu, 22 Jan 2009 06:23:41 +0100</pubDate>
            <guid isPermaLink="false">2120522</guid>        </item>
        <item>
            <title>The coagulation cascade in cirrhosis.</title>
            <link>http://www.medworm.com/index.php?rid=2120521&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19150304%26dopt%3DAbstract</link>
            <description>Authors: Monroe DM, Hoffman M
    The coagulation &quot;cascade&quot; model accurately represents the mechanisms of the prothrombin time and activated partial thromboplastin time tests. However, these tests and the &quot;cascade&quot; model do not accurately reflect the risk of hemorrhage or thrombosis in vivo. In hepatic insufficiency, a balanced reduction in the levels of most of pro- and anticoagulant proteins produced in the liver does not impair thrombin generation until levels are quite low. However, the ability of the coagulation system to tolerate or recover from an insult is markedly impaired in liver disease. This allows the coagulation system to be more easily tipped into a state favoring either hemorrhage or thrombosis.
    PMID: 19150304 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2120521</comments>
            <pubDate>Thu, 22 Jan 2009 06:23:37 +0100</pubDate>
            <guid isPermaLink="false">2120521</guid>        </item>
        <item>
            <title>The platelet and platelet function testing in liver disease.</title>
            <link>http://www.medworm.com/index.php?rid=2120520&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19150305%26dopt%3DAbstract</link>
            <description>This article outlines the role of platelet abnormalities and possibilities for platelet function testing in patients who have liver disease.
    PMID: 19150305 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2120520</comments>
            <pubDate>Thu, 22 Jan 2009 06:23:34 +0100</pubDate>
            <guid isPermaLink="false">2120520</guid>        </item>
        <item>
            <title>Hyperfibrinolysis in liver disease.</title>
            <link>http://www.medworm.com/index.php?rid=2120519&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19150306%26dopt%3DAbstract</link>
            <description>Authors: Ferro D, Celestini A, Violi F
    The incidence of hyperfibrinolysis in patients with cirrhosis is still debated. The reasons for this uncertainty probably lie in the lack of appropriate laboratory tests for its evaluation. There is a relative consensus, however, that hyperfibrinolysis can complicate the clinical course of liver cirrhosis, especially in cases of moderate to severe liver failure. Hyperfibrinolysis correlates positively with the severity of underlying liver disease, and low-grade systemic fibrinolysis is found in 30% to 46% of patients who have end-stage liver disease. Accelerated intravascular coagulation with secondary hyperfibrinolysis has been reported in patients who have liver failure. Hyperfibrinolysis may delay primary hemostasis, thereby aggravating varicea...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2120519</comments>
            <pubDate>Thu, 22 Jan 2009 06:23:29 +0100</pubDate>
            <guid isPermaLink="false">2120519</guid>        </item>
        <item>
            <title>Superimposed coagulopathic conditions in cirrhosis: infection and endogenous heparinoids, renal failure, and endothelial dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=2120518&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19150307%26dopt%3DAbstract</link>
            <description>Authors: Smalberg JH, Leebeek FW
    In this article, the authors discuss three pathophysiologic mechanisms that influence the coagulation system in patients who have liver disease. First, bacterial infections may play an important role in the cause of variceal bleeding in patients who have liver cirrhosis, affecting coagulation through multiple pathways. One of the pathways through which this occurs is dependent on endogenous heparinoids, on which the authors focus in this article. Secondly, the authors discuss renal failure, a condition that is frequently encountered in patients who have liver cirrhosis. Finally, they review dysfunction of the endothelial system. The role of markers of endothelial function in cirrhotic patients, such as von Willebrand factor and endothelin-1, is discusse...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2120518</comments>
            <pubDate>Thu, 22 Jan 2009 06:23:25 +0100</pubDate>
            <guid isPermaLink="false">2120518</guid>        </item>
        <item>
            <title>Heparin-like Effect in Liver Disease and Liver Transplantation.</title>
            <link>http://www.medworm.com/index.php?rid=2120517&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19150308%26dopt%3DAbstract</link>
            <description>Authors: Senzolo M, Cholongitas E, Thalheimer U, Riddell A, Agarwal S, Mallett S, Ferronato C, Burroughs AK
    Liver cirrhosis is characterized by impairment of primary and secondary hemostasis but it is not clear how this impairment is related to the bleeding problems seen in cirrhosis. This delicate hemostatic balance can be perturbed by numerous conditions, such as variceal bleeding, renal failure, or infection/sepsis, which may lead to worsening of coagulation status to date. The role of endogenous heparinoids (glycosaminoglycans) in the coagulopathy of patients who have cirrhosis has been demonstrated by thromboelastography with the addition of heparinase I in patients who have recent variceal bleeding and infection. The heparin-like effect has also been demonstrated to be part of th...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2120517</comments>
            <pubDate>Thu, 22 Jan 2009 06:23:22 +0100</pubDate>
            <guid isPermaLink="false">2120517</guid>        </item>
        <item>
            <title>Tests of coagulation in liver disease.</title>
            <link>http://www.medworm.com/index.php?rid=2120516&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19150309%26dopt%3DAbstract</link>
            <description>Authors: Tripodi A
    The complex coagulation defect secondary to chronic liver disease is considered responsible for the bleeding problems that often are associated with the disease. Accordingly, clinicians order laboratory tests to assess the risk of bleeding and rely on these results to make decisions about the management of the associated coagulation disturbances. Recent data, however, indicate that the abnormality of coagulation in stable cirrhosis is more a myth than a reality and may help explain why the prolonged global coagulation tests are poor predictors of bleeding in this setting. Alternative tests more closely mimicking what occurs in vivo should be developed and investigated in appropriate clinical trials to determine their value in the management of bleeding in cirrhosis.
...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2120516</comments>
            <pubDate>Thu, 22 Jan 2009 06:23:19 +0100</pubDate>
            <guid isPermaLink="false">2120516</guid>        </item>
        <item>
            <title>The international normalized ratio of prothrombin time in the model for end-stage liver disease score: a reliable measure.</title>
            <link>http://www.medworm.com/index.php?rid=2120515&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19150310%26dopt%3DAbstract</link>
            <description>Authors: Kamath PS, Kim WR
    The Model for End-stage Liver Disease (MELD) has been demonstrated to be an excellent predictor of survival in patients who have end-stage liver disease. It is derived from the international normalized ratio (INR) of prothrombin time, serum creatinine, and serum total bilirubin. The major use of the MELD score is to prioritize allocation of organs for liver transplant among patients who have chronic liver disease. Virtually every study that has looked at the MELD score as a predictor of survival has demonstrated that the MELD score using the INR with international sensitivity index calibrated for patients on warfarin has a 'c' statistic of approximately 0.8, indicating excellent discrimination.
    PMID: 19150310 [PubMed - in process] (Source: Clinics in Live...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2120515</comments>
            <pubDate>Thu, 22 Jan 2009 06:23:16 +0100</pubDate>
            <guid isPermaLink="false">2120515</guid>        </item>
        <item>
            <title>International Normalized Ratio of Prothrombin Time in the Model for End-stage Liver Disease Score: An Unreliable Measure.</title>
            <link>http://www.medworm.com/index.php?rid=2120514&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19150311%26dopt%3DAbstract</link>
            <description>Authors: Arjal R, Trotter JF
    The current basis for deceased donor liver allocation is the Model for End-stage Liver Disease (MELD) score, which is an objective means of predicting 90-day patient survival. Although the MELD system is a vast improvement over the prior allocation scheme, published studies have refuted the United Network for Organ Sharing statement that &quot;the MELD and PELD [Pediatric End-stage Liver Disease] formulas are simple, objective and verifiable and yield consistent results whenever the score is calculated.&quot; In particular, wide inter-laboratory variation exists in the most heavily weighted MELD determinant, the international normalized ratio (INR). Whether this variation impacts the equitable distribution of deceased donor livers is unclear. However, the current tec...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2120514</comments>
            <pubDate>Thu, 22 Jan 2009 06:23:12 +0100</pubDate>
            <guid isPermaLink="false">2120514</guid>        </item>
        <item>
            <title>Blood products, volume control, and renal support in the coagulopathy of liver disease.</title>
            <link>http://www.medworm.com/index.php?rid=2120513&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19150312%26dopt%3DAbstract</link>
            <description>Authors: Argo CK, Balogun RA
    Plasma-based products are commonly used in patients who have chronic liver disease to treat perceived coagulopathy despite unproven efficacy and potentially severe risks, such as transfusion-related acute lung injury, which carries a high mortality rate. Moreover, volume expansion may acutely worsen portal hypertension and increase bleeding from the collateral portal vascular bed. Although factor replacement therapy may be warranted in selected situations, its use should be restricted because of the limitations of target tests, such as international normalized ratio, which poorly reflects presence of bleeding diatheses in patients who have cirrhosis. Renal replacement therapies are frequent adjuncts in patients who have cirrhosis and are acutely decompensat...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2120513</comments>
            <pubDate>Thu, 22 Jan 2009 06:23:07 +0100</pubDate>
            <guid isPermaLink="false">2120513</guid>        </item>
        <item>
            <title>The Role of Anti-Fibrinolytics, rFVIIa and Other Pro-Coagulants: Prophylactic Versus Rescue?</title>
            <link>http://www.medworm.com/index.php?rid=2120512&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19150313%26dopt%3DAbstract</link>
            <description>This article discusses the use of activated factor VIIa and anti-fibrinolytic agents to treat coagulopathy in the setting of liver disease and the potential advantages and disadvantages of these alternatives, and the limitations of the current literature. This article also compares the limitations, risks, and potential benefits of prophylactic therapy to prevent bleeding before invasive procedures with rescue therapy for spontaneous and postprocedure bleeding, and describes the relative advantages and disadvantages of these two approaches.
    PMID: 19150313 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2120512</comments>
            <pubDate>Thu, 22 Jan 2009 06:23:03 +0100</pubDate>
            <guid isPermaLink="false">2120512</guid>        </item>
        <item>
            <title>Coagulopathy of acute liver failure.</title>
            <link>http://www.medworm.com/index.php?rid=2120511&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19150314%26dopt%3DAbstract</link>
            <description>Authors: Munoz SJ, Stravitz RT, Gabriel DA
    Coagulopathy is an essential component of the acute liver failure (ALF) syndrome and reflects the central role of liver function in hemostasis. ALF is a syndrome characterized by the development of hepatic encephalopathy and coagulopathy within 24 weeks of the onset of acute liver disease. Coagulopathy in this setting is a useful prognostic tool in ALF and a dynamic indicator of the hepatic function. If severe, it can be associated with bleeding and is commonly a major obstacle to the performance of invasive procedures in patients with ALF. This review focuses on the epidemiology, pathophysiology, presentation, evaluation, and management of coagulopathy in ALF.
    PMID: 19150314 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2120511</comments>
            <pubDate>Thu, 22 Jan 2009 06:23:00 +0100</pubDate>
            <guid isPermaLink="false">2120511</guid>        </item>
        <item>
            <title>Hypercoagulation in liver disease.</title>
            <link>http://www.medworm.com/index.php?rid=2120510&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19150315%26dopt%3DAbstract</link>
            <description>Authors: Northup PG
    The coagulopathy of liver disease is complex and often unpredictable. Despite clear evidence of an increased tendency for bleeding in patients who have cirrhosis, many circumstances also promote local and systemic hypercoagulable states. The consequences of hypercoagulability include the obvious morbidity and mortality of portal vein thrombosis, deep vein thrombosis, and pulmonary embolism, but possibly also include other end-organ syndromes, such as portopulmonary hypertension, hepatorenal syndrome, and spontaneous bacterial peritonitis. A more subtle contribution also could be responsible for progression of early fibrosis to decompensated cirrhosis. Future research is needed to elucidate specific mechanistic pathways that might lead to local hypercoagulation and t...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2120510</comments>
            <pubDate>Thu, 22 Jan 2009 06:22:53 +0100</pubDate>
            <guid isPermaLink="false">2120510</guid>        </item>
        <item>
            <title>Parenchymal extinction: coagulation and hepatic fibrogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=2120509&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19150316%26dopt%3DAbstract</link>
            <description>This article discusses the evidence for a role for coagulation cascade activity in hepatic fibrogenesis and explores the proposed pathogenic mechanisms including the downstream events of thrombin activation. Interference with either the generation of thrombin or its downstream activity may reduce hepatic fibrosis. Also examined are the implications for future therapeutic intervention.
    PMID: 19150316 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2120509</comments>
            <pubDate>Thu, 22 Jan 2009 06:22:44 +0100</pubDate>
            <guid isPermaLink="false">2120509</guid>        </item>
        <item>
            <title>Portal vein thrombosis and budd-Chiari syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=2120508&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19150317%26dopt%3DAbstract</link>
            <description>Authors: Bittencourt PL, Couto CA, Ribeiro DD
    Venous thrombosis results from the convergence of vessel wall injury and/or venous stasis, known as local triggering factors, and the occurrence of acquired and/or inherited thrombophilia, also known as systemic prothrombotic risk factors. Portal vein thrombosis (PVT) and Budd-Chiari syndrome (BCS) are caused by thrombosis and/or obstruction of the extrahepatic portal veins and the hepatic venous outflow tract, respectively. Several divergent prothrombotic disorders may underlie these distinct forms of large vessel thrombosis. While cirrhotic PVT is relatively common, especially in advanced liver disease, noncirrhotic and nontumoral PVT is rare and BCS is of intermediate incidence. In this article, we review pathogenic mechanisms and curren...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2120508</comments>
            <pubDate>Thu, 22 Jan 2009 06:22:34 +0100</pubDate>
            <guid isPermaLink="false">2120508</guid>        </item>
        <item>
            <title>Bleeding in liver surgery: prevention and treatment.</title>
            <link>http://www.medworm.com/index.php?rid=2120507&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19150318%26dopt%3DAbstract</link>
            <description>Authors: Alkozai EM, Lisman T, Porte RJ
    Intraoperative blood loss and transfusion of blood products are negatively associated with postoperative outcome after liver surgery. Blood loss can be minimized by surgical methods, including vascular clamping techniques, the use of dissection devices, and the use of topical hemostatic agents. Preoperative correction of coagulation tests with blood products has not been shown to reduce intraoperative bleeding and it may, in fact, enhance the bleeding risk. Maintaining a low central venous pressure has been shown to be effective in reducing blood loss during partial liver resections, and volume contraction rather than prophylactic transfusion blood products seems justified in patients undergoing major liver surgery. Although antifibrinolytic drug...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2120507</comments>
            <pubDate>Thu, 22 Jan 2009 06:22:20 +0100</pubDate>
            <guid isPermaLink="false">2120507</guid>        </item>
        <item>
            <title>Coagulation disorders and bleeding in liver disease: future directions.</title>
            <link>http://www.medworm.com/index.php?rid=2120506&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19150319%26dopt%3DAbstract</link>
            <description>Authors: Caldwell SH, Sanyal AJ
    Much has changed since the characterization of the wide spectrum of abnormalities in the coagulation system in patients who have acute and chronic liver disease. With inherent limitations of conventional laboratory measures of coagulation in liver disease, it is now incumbent on us to explore how best to apply (or withhold) specific agents in specific situations. This will clearly require well focused translational research to understand and bring into sharp focus the various problems present, from dysfibrinogen to endogenous heparinoids, to uremia, to hyperfibrinolysis and even to unrecognized hypercoagulable conditions. The challenge lies ahead.
    PMID: 19150319 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2120506</comments>
            <pubDate>Thu, 22 Jan 2009 06:21:54 +0100</pubDate>
            <guid isPermaLink="false">2120506</guid>        </item>
        <item>
            <title>Preface. Hepatic fibrosis: pathogenesis, diagnosis, and emerging therapies.</title>
            <link>http://www.medworm.com/index.php?rid=2045434&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18984462%26dopt%3DAbstract</link>
            <description>Authors: Friedman SL
    
    PMID: 18984462 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2045434</comments>
            <pubDate>Sat, 01 Nov 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2045434</guid>        </item>
        <item>
            <title>Preface.</title>
            <link>http://www.medworm.com/index.php?rid=1938015&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18984462%26dopt%3DAbstract</link>
            <description>Authors: Friedman SL
    
    PMID: 18984462 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1938015</comments>
            <pubDate>Sat, 01 Nov 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1938015</guid>        </item>
        <item>
            <title>The global impact of hepatic fibrosis and end-stage liver disease.</title>
            <link>http://www.medworm.com/index.php?rid=1938014&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18984463%26dopt%3DAbstract</link>
            <description>Authors: Lim YS, Kim WR
    Hepatic fibrosis is an integral part in the progression of chronic liver disease, ultimately leading to cirrhosis and hepatocellular carcinoma. Globally, alcohol consumption, hepatitis B (HBV) and hepatitis C (HCV) have been the main causes of cirrhosis. More recently, the increasing prevalence of obesity and the metabolic syndrome has resulted in increasing incidence of cirrhosis secondary to nonalcoholic fatty liver disease (NAFLD), especially in developed countries. Chronic liver disease and cirrhosis are important causes of morbidity and mortality in the world. Moreover, the burden of chronic liver disease is projected to increase, due in part to the increasing prevalence of end-stage liver disease and HCC secondary to NAFLD and HCV.
    PMID: 18984463 [PubM...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1938014</comments>
            <pubDate>Sat, 01 Nov 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1938014</guid>        </item>
        <item>
            <title>Genetic determinants in hepatic fibrosis: from experimental models to fibrogenic gene signatures in humans.</title>
            <link>http://www.medworm.com/index.php?rid=1938013&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18984464%26dopt%3DAbstract</link>
            <description>Authors: Weber S, Gressner OA, Hall R, Gr&amp;#xFC;nhage F, Lammert F
    Hepatic fibrosis, or scarring of the liver, is a nonspecific reaction to chronic liver injury. Hepatic fibrosis is commonly caused by exogenous factors such as viral hepatitis or alcohol abuse, but recent studies also indicate a genetic predisposition. Although some patients who have chronic liver diseases show only minor morphologic and functional alterations of the liver and are characterized by slow progression of disease with mild clinical symptoms, others develop pronounced hepatic fibrosis rapidly, culminating in cirrhosis, liver failure, or hepatocellular carcinoma, respectively. These well known differences in progression of hepatic fibrosis persist when controlling for age (at infection), gender, and exogenous f...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1938013</comments>
            <pubDate>Sat, 01 Nov 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1938013</guid>        </item>
        <item>
            <title>Cellular Sources of Extracellular Matrix in Hepatic Fibrosis.</title>
            <link>http://www.medworm.com/index.php?rid=1938012&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18984465%26dopt%3DAbstract</link>
            <description>Authors: Wells RG
    The deposition of increased and abnormal extracellular matrix is the hallmark of liver fibrosis. Hepatic stellate cells are well known as the major source of the fibrillar collagens and other components of the liver scar, but are now appreciated to be only one of many potentially fibrogenic cell populations in the diseased liver. Portal fibroblasts and circulating mesenchymal cells derived from the bone marrow are also important sources of matrix proteins in fibrosis. Recent data suggest that hepatocytes and biliary epithelial cells undergo an epithelial to mesenchymal transition, similarly assuming a fibrogenic phenotype. Sinusoidal endothelial cells and hepatocytes produce specific matrix proteins important in liver health and disease. The future challenge will be t...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1938012</comments>
            <pubDate>Sat, 01 Nov 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1938012</guid>        </item>
        <item>
            <title>Oxidative and nitrosative stress and fibrogenic response.</title>
            <link>http://www.medworm.com/index.php?rid=1938011&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18984466%26dopt%3DAbstract</link>
            <description>Authors: Urtasun R, de la Rosa LC, Nieto N
    Uncontrolled production of collagen I is the main feature of liver fibrosis. Following a fibrogenic stimulus such as alcohol, hepatic stellate cells (HSC) transform into an activated collagen-producing cell. In alcoholic liver disease, numerous changes in gene expression are associated with HSC activation, including the induction of several intracellular signaling cascades, which help maintain the activated phenotype and control the fibrogenic and proliferative state of the cell. Detailed analyses for understanding the molecular basis of the collagen I gene regulation have revealed a complex process involving reactive oxygen species (ROS) as key mediators. Less is known, however, about the contribution of reactive nitrogen species (RNS). In ad...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1938011</comments>
            <pubDate>Sat, 01 Nov 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1938011</guid>        </item>
        <item>
            <title>Stellate cell contraction: role, regulation, and potential therapeutic target.</title>
            <link>http://www.medworm.com/index.php?rid=1938010&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18984467%26dopt%3DAbstract</link>
            <description>Authors: Soon RK, Yee HF
    The contraction of hepatic stellate cells has been proposed to mediate fibrosis by regulating sinusoidal blood flow and extracellular matrix remodeling. Abundant data from diverse, yet complementary, experimental methods support a robust model for the regulation of contractile force generation by stellate cells. In this model, soluble factors associated with liver injury, including endothelin 1 and nitric oxide, are transduced primarily through Rho signaling pathways that promote the myosin II-powered generation of contractile force by stellate cells. The enhanced knowledge of the role and differential regulation of stellate cell contraction may facilitate the discovery of new and targeted strategies for the prevention and treatment of hepatic fibrosis.
    PMI...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1938010</comments>
            <pubDate>Sat, 01 Nov 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1938010</guid>        </item>
        <item>
            <title>Disease-specific mechanisms of fibrosis: hepatitis C virus and nonalcoholic steatohepatitis.</title>
            <link>http://www.medworm.com/index.php?rid=1938009&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18984468%26dopt%3DAbstract</link>
            <description>This article explores in depth the disease-specific mechanisms of fibrosis in hepatitis C and NASH, with a focus on recent developments.
    PMID: 18984468 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1938009</comments>
            <pubDate>Sat, 01 Nov 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1938009</guid>        </item>
        <item>
            <title>Cytokines and Renin-Angiotensin system signaling in hepatic fibrosis.</title>
            <link>http://www.medworm.com/index.php?rid=1938008&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18984469%26dopt%3DAbstract</link>
            <description>Authors: Moreno M, Bataller R
    Hepatic fibrosis is the result of a complex interplay between resident hepatic cells, infiltrating inflammatory cells, and a number of locally acting peptides called cytokines. Key mediators include transforming growth factor b1, vasoactive substances, adipokines, inflammatory cytokines and chemokines. Angiotensin II, the main effector of the renin-angiotensin system, is a true cytokine that plays a major role in liver fibrosis. Angiotensin II is locally synthesized in the injured liver and induces profibrogenic actions in hepatic stellate cells. Drugs blocking the renin-angiotensin system are promising antifibrotic agents. There are multiple signal transduction pathways involved in cytokine signaling. Drugs interfering intracellular pathways involved in i...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1938008</comments>
            <pubDate>Sat, 01 Nov 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1938008</guid>        </item>
        <item>
            <title>Relationships among stellate cell activation, progenitor cells, and hepatic regeneration.</title>
            <link>http://www.medworm.com/index.php?rid=1938007&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18984470%26dopt%3DAbstract</link>
            <description>Authors: Roskams T
    Hepatic stellate cells (HSC) play an important role in liver fibrogenesis. They are also key players in liver regeneration as part of the stem cell niche of hepatocytes and hepatic progenitor cells. They produce growth stimulating and inhibiting factors for these epithelial cell compartments. In addition, recent studies suggest a role for HSCs themselves for being progenitors of epithelial cells through a transitional mesenchymal phase.
    PMID: 18984470 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1938007</comments>
            <pubDate>Sat, 01 Nov 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1938007</guid>        </item>
        <item>
            <title>Immune interactions in hepatic fibrosis.</title>
            <link>http://www.medworm.com/index.php?rid=1938006&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18984471%26dopt%3DAbstract</link>
            <description>Authors: Holt AP, Salmon M, Buckley CD, Adams DH
    Liver cirrhosis is caused by iterative cycles of tissue injury, inflammation, and repair. Although most causes of acute hepatitis resolve without scarring, chronic hepatitis is associated with persistent inflammation and matrix remodeling, which leads to fibrosis and, eventually, cirrhosis. The mechanisms that govern wound healing involve interactions between the innate and adaptive immune systems and stromal cells within a microenvironment composed of cytokines, growth factors, and modified matricellular proteins. The immune system plays a central role in the regulation of fibrosis, tissue repair, and recovery that is vital for the maintenance of tissue homeostasis. Chronic inflammation and fibrosis are inextricably linked and the cellu...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1938006</comments>
            <pubDate>Sat, 01 Nov 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1938006</guid>        </item>
        <item>
            <title>Noninvasive assessment of liver fibrosis: serum markers, imaging, and other modalities.</title>
            <link>http://www.medworm.com/index.php?rid=1938005&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18984472%26dopt%3DAbstract</link>
            <description>This article outlines the various noninvasive markers, including blood tests, imaging, and novel technologies. It examines the principles behind their development, their diagnostic accuracy, and their evolution.
    PMID: 18984472 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1938005</comments>
            <pubDate>Sat, 01 Nov 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1938005</guid>        </item>
        <item>
            <title>Fibrosis and cirrhosis reversibility: clinical features and implications.</title>
            <link>http://www.medworm.com/index.php?rid=1938004&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18984473%26dopt%3DAbstract</link>
            <description>This article outlines differences between fibrosis and cirrhosis and discusses the reversibility of CLD and the regression of fibrosis and cirrhosis. The end-points of anti-fibrotic therapy are detailed.
    PMID: 18984473 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1938004</comments>
            <pubDate>Sat, 01 Nov 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1938004</guid>        </item>
        <item>
            <title>Fibrosis and cirrhosis reversibility - molecular mechanisms.</title>
            <link>http://www.medworm.com/index.php?rid=1938003&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18984474%26dopt%3DAbstract</link>
            <description>This article reviews recent discoveries relating to the cellular and molecular mechanisms that regulate fibrosis regression, with emphasis on studies that have used experimental in vivo models of liver disease. Apoptosis of hepatic myofibroblasts is discussed. The functions played by transcription factors, receptor-ligand interactions, and cell-matrix interactions as regulators of the lifespan of hepatic myofibroblasts are considered, as are the therapeutic opportunities for modulating these functions. Growth factors, proteolytic enzymes, and their inhibitors are discussed in detail.
    PMID: 18984474 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1938003</comments>
            <pubDate>Sat, 01 Nov 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1938003</guid>        </item>
        <item>
            <title>Current and future anti-fibrotic therapies for chronic liver disease.</title>
            <link>http://www.medworm.com/index.php?rid=1938002&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18984475%26dopt%3DAbstract</link>
            <description>This article emphasizes mechanisms underlying fibrogenesis and reviews available and future therapeutics.
    PMID: 18984475 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1938002</comments>
            <pubDate>Sat, 01 Nov 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1938002</guid>        </item>
        <item>
            <title>Hepatitis C virus. Preface.</title>
            <link>http://www.medworm.com/index.php?rid=1810965&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18625424%26dopt%3DAbstract</link>
            <description>Authors: Reddy KR, Kaplan DE
    
    PMID: 18625424 [PubMed - indexed for MEDLINE] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1810965</comments>
            <pubDate>Fri, 01 Aug 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1810965</guid>        </item>
        <item>
            <title>Preface.</title>
            <link>http://www.medworm.com/index.php?rid=1630420&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18625424%26dopt%3DAbstract</link>
            <description>Authors: Reddy KR, Kaplan DE
    
    PMID: 18625424 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1630420</comments>
            <pubDate>Thu, 17 Jul 2008 08:45:17 +0100</pubDate>
            <guid isPermaLink="false">1630420</guid>        </item>
        <item>
            <title>Optimizing the current therapy for chronic hepatitis C virus: peginterferon and ribavirin dosing and the utility of growth factors.</title>
            <link>http://www.medworm.com/index.php?rid=1630419&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18625425%26dopt%3DAbstract</link>
            <description>Authors: Shiffman ML
    Achieving a sustained virologic response depends on the patient achieving three sequential independent milestones: virologic response, maintaining this response throughout treatment, and not relapsing after treatment has been completed. The ability to achieve these milestones depends on the doses of interferon/peginterferon and ribavirin used and on whether treatment with these medications is adjusted, interrupted, or prematurely discontinued in response to adverse events. This review discusses strategies to optimize peginterferon and ribavirin dosing and the impact that growth factors may have on the ability to achieve a sustained virologic response.
    PMID: 18625425 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1630419</comments>
            <pubDate>Thu, 17 Jul 2008 08:45:15 +0100</pubDate>
            <guid isPermaLink="false">1630419</guid>        </item>
        <item>
            <title>Tailored treatment for hepatitis C.</title>
            <link>http://www.medworm.com/index.php?rid=1630418&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18625426%26dopt%3DAbstract</link>
            <description>Authors: Berg T
    Considering the high number of global cases of hepatitis C virus (HCV) infection (around 175 million), effective, individualized, tailored treatment approaches are imperative. In this respect, defining patients according to their initial response profiles was shown to have great impact on choosing the optimal treatment duration. The application of new more sensitive HCV RNA tests may further help to improve treatment individualization. In spite of the many relevant studies conducted in the past and at present, however, this problem is far from being resolved. Generally, it can be said that the presence of a rapid virologic response is a significant predictor of favorable outcome and permits an abbreviated treatment period. In contrast, patients who have a slow response ...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1630418</comments>
            <pubDate>Thu, 17 Jul 2008 08:45:11 +0100</pubDate>
            <guid isPermaLink="false">1630418</guid>        </item>
        <item>
            <title>Novel hepatitis C drugs in current trials.</title>
            <link>http://www.medworm.com/index.php?rid=1630417&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18625427%26dopt%3DAbstract</link>
            <description>Authors: Kronenberger B, Welsch C, Forestier N, Zeuzem S
    Almost half of the patients who have chronic hepatitis C cannot be cured with the current standard treatment. Recent progress in structure determination of HCV proteins and development of a subgenomic replicon system and a cell culture infectious HCV clone enabled the development of a specifically targeted antiviral therapy for hepatitis C (STAT-C). Many HCV-specific compounds are under investigation in preclinical and clinical trials. The development of agents in different classes may allow construction of antiviral combinations that enhance the effectiveness of antiviral treatment, reduce the duration of treatment, and, eventually, may even avoid the use of interferon-alfa.
    PMID: 18625427 [PubMed - in process] (Source: Clin...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1630417</comments>
            <pubDate>Thu, 17 Jul 2008 08:45:09 +0100</pubDate>
            <guid isPermaLink="false">1630417</guid>        </item>
        <item>
            <title>Noninvasive monitoring of hepatitis C fibrosis progression.</title>
            <link>http://www.medworm.com/index.php?rid=1630416&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18625428%26dopt%3DAbstract</link>
            <description>Authors: Kotlyar DS, Blonski W, Rustgi VK
    Noninvasive approaches in the diagnosis and monitoring of fibrosis are still evolving. Transient elastography is an inexpensive, rapid, and relatively accurate form of noninvasive monitoring, especially in severe fibrosis It is a nascent technology, however, and there is no clear indication that elastography is better than biopsy for less severe fibrosis. With improved resolution and longer term data, it may become a vital supplement. The combined use of transient elastography and biochemical markers seems to be the most promising noninvasive technique.
    PMID: 18625428 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1630416</comments>
            <pubDate>Thu, 17 Jul 2008 08:45:07 +0100</pubDate>
            <guid isPermaLink="false">1630416</guid>        </item>
        <item>
            <title>Hepatitis C infection and nonalcoholic Fatty liver disease.</title>
            <link>http://www.medworm.com/index.php?rid=1630415&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18625429%26dopt%3DAbstract</link>
            <description>This article focuses on the current understanding of the interplay between host and viral factors that are involved in the interaction between NAFLD and HCV.
    PMID: 18625429 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1630415</comments>
            <pubDate>Thu, 17 Jul 2008 08:45:01 +0100</pubDate>
            <guid isPermaLink="false">1630415</guid>        </item>
        <item>
            <title>Management Complexities of HIV/Hepatitis C Virus Coinfection in the Twenty-First Century.</title>
            <link>http://www.medworm.com/index.php?rid=1630414&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18625430%26dopt%3DAbstract</link>
            <description>Authors: Lo Re V, Kostman JR, Amorosa VK
    Because of shared routes of transmission, hepatitis C virus (HCV) coinfection is common among HIV-infected persons. Because of the effectiveness of antiretroviral therapy, chronic HCV has now emerged as a major cause of morbidity and mortality in this population. Because chronic HCV is highly prevalent among HIV-infected patients and has a rapid disease progression, antiviral therapy with pegylated interferon plus ribavirin is critical for the long-term survival of HIV/HCV-coinfected patients. In this article, the authors review the (1) epidemiology of HCV among HIV-infected individuals, (2) effect of HIV on the natural history of chronic HCV, (3) impact of antiretroviral therapy on HCV coinfection, and (4) management of chronic HCV in the HIV-i...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1630414</comments>
            <pubDate>Thu, 17 Jul 2008 08:44:58 +0100</pubDate>
            <guid isPermaLink="false">1630414</guid>        </item>
        <item>
            <title>Extrahepatic manifestations of hepatitis C virus infection.</title>
            <link>http://www.medworm.com/index.php?rid=1630413&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18625431%26dopt%3DAbstract</link>
            <description>This article describes the diagnosis and treatment of these diseases.
    PMID: 18625431 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1630413</comments>
            <pubDate>Thu, 17 Jul 2008 08:44:56 +0100</pubDate>
            <guid isPermaLink="false">1630413</guid>        </item>
        <item>
            <title>Hepatitis C and liver transplantation: enhancing outcomes and should patients be retransplanted.</title>
            <link>http://www.medworm.com/index.php?rid=1630412&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18625432%26dopt%3DAbstract</link>
            <description>This article reviews the literature on these topics and the work being done in each area to maximize outcomes in patients receiving transplants for HCV-related cirrhosis.
    PMID: 18625432 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1630412</comments>
            <pubDate>Thu, 17 Jul 2008 08:44:51 +0100</pubDate>
            <guid isPermaLink="false">1630412</guid>        </item>
        <item>
            <title>Hepatitis C virus infection and hepatocellular carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=1630411&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18625433%26dopt%3DAbstract</link>
            <description>Authors: Blonski W, Reddy KR
    Primary liver cancer is the sixth most common cancer in the world and the third most common cause of death attributable to cancer. Most primary liver cancers are hepatocellular carcinoma (HCC), accounting for 85% to 90% of cases. There is a trend of growing incidence of HCC in the United States. One of the most important risk factors for developing HCC is chronic hepatitis C virus (HCV) infection. Although several studies suggested the preventive effect of interferon from developing HCC in HCV-infected individuals, these findings need to be validated in large prospective and randomized trials.
    PMID: 18625433 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1630411</comments>
            <pubDate>Thu, 17 Jul 2008 08:44:47 +0100</pubDate>
            <guid isPermaLink="false">1630411</guid>        </item>
        <item>
            <title>Hepatitis C and innate immunity: recent advances.</title>
            <link>http://www.medworm.com/index.php?rid=1630410&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18625434%26dopt%3DAbstract</link>
            <description>Authors: Szabo G, Dolganiuc A
    Eradication of hepatitis C virus (HCV) infection requires a complex and coordinated interplay between innate and adaptive immune responses that, when it fails, leads to chronic infection. In this review, the innate immune mechanisms by which HCV is sensed and by which HCV undermines host defense are discussed. The critical role of dendritic cells in antigen presentation and T-cell activation in addition to type I interferon production and interference of HCV with innate immune cell functions are reviewed. Finally, current and emerging therapeutic approaches targeting innate immune pathways are evaluated.
    PMID: 18625434 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1630410</comments>
            <pubDate>Thu, 17 Jul 2008 08:44:38 +0100</pubDate>
            <guid isPermaLink="false">1630410</guid>        </item>
        <item>
            <title>Hepatitis C virus entry and neutralization.</title>
            <link>http://www.medworm.com/index.php?rid=1630409&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18625435%26dopt%3DAbstract</link>
            <description>Authors: Stamataki Z, Grove J, Balfe P, McKeating JA
    The processes of hepatitis C virus (HCV) entry and antibody-mediated neutralization are intimately linked. The high frequency of neutralizing antibodies (nAbs) that inhibit E2-CD81 interaction(s) suggests that this is a major target for the humoral immune response. The observation that HCV can transmit to naive cells by means of CD81-dependent and -independent routes in vitro awaits further investigation to assess the significance in vivo but may offer new strategies for HCV to escape nAbs. The identification of claudins in the entry process highlights the importance of cell polarity in defining routes of HCV entry and release, with recent experiments suggesting a polarized route of viral entry into cells in vitro. In this review, th...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1630409</comments>
            <pubDate>Thu, 17 Jul 2008 08:44:35 +0100</pubDate>
            <guid isPermaLink="false">1630409</guid>        </item>
        <item>
            <title>Host genetic factors and antiviral immune responses to hepatitis C virus.</title>
            <link>http://www.medworm.com/index.php?rid=1630408&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18625436%26dopt%3DAbstract</link>
            <description>Authors: Thio CL
    Human genome variations explain some of the heterogeneity in the immune response to antigenic stimuli. Such differences in response to hepatitis C virus (HCV) antigens can account for the ability of the immune response to clear HCV after an acute infection or to develop more rapidly progressive liver disease. Several studies have examined polymorphisms in several candidate immune-response genes for their relation to these HCV outcomes. Results of some of these studies complement knowledge gained from immunology studies, and others offer new insights into HCV biology. This review summarizes published studies on variation in immune-response genes and HCV outcomes.
    PMID: 18625436 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1630408</comments>
            <pubDate>Thu, 17 Jul 2008 08:44:32 +0100</pubDate>
            <guid isPermaLink="false">1630408</guid>        </item>
        <item>
            <title>Preface.</title>
            <link>http://www.medworm.com/index.php?rid=1422365&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18456177%26dopt%3DAbstract</link>
            <description>Authors: Heathcote EJ
    
    PMID: 18456177 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1422365</comments>
            <pubDate>Thu, 01 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1422365</guid>        </item>
        <item>
            <title>Presentation and Diagnosis of Primary Biliary Cirrhosis in the 21st Century.</title>
            <link>http://www.medworm.com/index.php?rid=1422364&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18456178%26dopt%3DAbstract</link>
            <description>This article reviews the presentation and diagnosis of PBC in the 21st century.
    PMID: 18456178 [PubMed - as supplied by publisher] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1422364</comments>
            <pubDate>Thu, 01 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1422364</guid>        </item>
        <item>
            <title>Antimitochondrial antibodies and other antibodies in primary biliary cirrhosis: diagnostic and prognostic value.</title>
            <link>http://www.medworm.com/index.php?rid=1422363&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18456179%26dopt%3DAbstract</link>
            <description>Authors: Muratori L, Granito A, Muratori P, Pappas G, Bianchi FB
    Antimitochondrial antibodies (AMA) are the serologic cornerstone in the diagnosis of primary biliary cirrhosis (PBC), even if they are not detectable in a proportion of patients, notwithstanding the most sensitive and sophisticated technologies used. To fill in the serologic gap in AMA-negative PBC, there is sound evidence to consider antinuclear antibody (ANA) patterns, such as anti-multiple nuclear dots and anti-membranous/rim-like, as PBC-specific surrogate hallmarks of the disease, and their detection can be considered virtually diagnostic. Furthermore, particular ANA specificities, such as anti-gp210, anti-p62, anticentromere antibodies, and anti-dsDNA, may provide additional diagnostic and prognostic information.
  ...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1422363</comments>
            <pubDate>Thu, 01 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1422363</guid>        </item>
        <item>
            <title>Natural history of primary biliary cirrhosis.</title>
            <link>http://www.medworm.com/index.php?rid=1422362&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18456180%26dopt%3DAbstract</link>
            <description>Authors: Mayo MJ
    Primary biliary cirrhosis is an insidious disease that progresses through the clinical phases: preclinical, asymptomatic, symptomatic, and liver insufficiency. The outlook of patients diagnosed with PBC has improved significantly over the past 2 decades because more patients are being diagnosed earlier in the disease process and being treated with UDCA. A need remains to better define and predict the course of symptomatic and asymptomatic patients on and off UDCA in order to better evaluate outcomes of clinical trials.
    PMID: 18456180 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1422362</comments>
            <pubDate>Thu, 01 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1422362</guid>        </item>
        <item>
            <title>Recent advances in the epidemiology of primary biliary cirrhosis.</title>
            <link>http://www.medworm.com/index.php?rid=1422361&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18456181%26dopt%3DAbstract</link>
            <description>Authors: Gross RG, Odin JA
    Since initial reports in the mid-1970s provided epidemiology data on primary biliary cirrhosis (PBC), many studies have characterized the variable frequency of this disease in diverse populations worldwide and sought to identify associated risk factors. Recent research confirms earlier work suggesting that the incidence and prevalence of PBC are on the rise, although geographic variation persists. Analysis of familial and geographic clustering supports the hypothesis that development and progression of the disease hinge on a complex interplay between genetic and environmental risk factors. International clinical data systems are needed to advance PBC epidemiologic research. Given this complexity, international clinical data systems are needed to advance PBC e...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1422361</comments>
            <pubDate>Thu, 01 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1422361</guid>        </item>
        <item>
            <title>Pathogenesis of primary biliary cirrhosis.</title>
            <link>http://www.medworm.com/index.php?rid=1422360&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18456182%26dopt%3DAbstract</link>
            <description>Authors: Jones DE
    Autoimmune phenomena have been recognized in primary biliary cirrhosis (PBC) for more than 50 years and the specificity of the characteristic responses directed at highly conserved mitochondrial antigens determined in detail over the past 20. Effecter autoreactive immune responses are characterized and potential mechanisms of breakdown of tolerance to self proposed. Elements of the clinical pattern of PBC, including the recurrence of the disease across HLA boundaries after liver transplantation, remain difficult to reconcile with a simple autoimmune model. Alternative (but not necessary mutually exclusive) pathogenetic models have been outlined, including a potential role for retroviral pathogens and directly cytopathic effects.
    PMID: 18456182 [PubMed - in process...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1422360</comments>
            <pubDate>Thu, 01 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1422360</guid>        </item>
        <item>
            <title>Antimitochondrial antibody-negative primary biliary cirrhosis.</title>
            <link>http://www.medworm.com/index.php?rid=1422359&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18456183%26dopt%3DAbstract</link>
            <description>Authors: Hirschfield GM, Heathcote EJ
    Primary biliary cirrhosis (PBC) is considered a classic autoimmune disease insofar as 95% of patients are seropositive for specific antimitochondrial antibodies (AMA). Yet it is still the case that the remaining 5% of patients have equivalent disease but test persistently AMA negative. Although variations exist in the immunologic profile of these patients, clinically there are no discernable differences, and although the diagnostic threshold is higher, the treatment and prognosis mirror that of classic disease. Previous terminology, therefore, has been abandoned in favor of the description, AMA-negative PBC.
    PMID: 18456183 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1422359</comments>
            <pubDate>Thu, 01 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1422359</guid>        </item>
        <item>
            <title>Animal models of primary biliary cirrhosis.</title>
            <link>http://www.medworm.com/index.php?rid=1422358&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18456184%26dopt%3DAbstract</link>
            <description>This article reviews the data on these animal models and places it in the perspective of human PBC and generic autoimmunity.
    PMID: 18456184 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1422358</comments>
            <pubDate>Thu, 01 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1422358</guid>        </item>
        <item>
            <title>Genetics and genomics of primary biliary cirrhosis.</title>
            <link>http://www.medworm.com/index.php?rid=1422357&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18456185%26dopt%3DAbstract</link>
            <description>Authors: Juran BD, Lazaridis KN
    The etiologic and pathogenic factors contributing to primary biliary cirrhosis (PBC) development, progression, response to treatment, and outcome remain a mystery. Recognition of the genomic regions harboring risk factors is hindered by the rarity and late onset of PBC. Recent advancements in genomics hold promise for understanding, prevention, and therapy of PBC. Large registries and biospecimen repositories of patients who have PBC, their family members, and controls are needed. Haplotype mapping-based association studies are necessary for defining genetic predisposition. Experimental data will provide the means for fine mapping studies, resequencing efforts, functional experimentation, and elucidation of gene-environment and gene-gene interaction.
   ...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1422357</comments>
            <pubDate>Thu, 01 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1422357</guid>        </item>
        <item>
            <title>Fatigue in primary biliary cirrhosis.</title>
            <link>http://www.medworm.com/index.php?rid=1422356&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18456186%26dopt%3DAbstract</link>
            <description>Authors: Newton JL
    The autoimmune liver disease, primary biliary cirrhosis (PBC), is associated with debilitating fatigue in a significant proportion of patients. The pathogenesis of fatigue in PBC is unclear, but preliminary studies suggest it has central mechanisms and may have peripheral manifestations. Studies are beginning to elucidate the biological associates of fatigue in PBC, particularly sleep disturbance and autonomic dysfunction. Comprehensive studies investigating the pathogenesis of fatigue in PBC are urgently needed as are large-scale prospective outcome studies.
    PMID: 18456186 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1422356</comments>
            <pubDate>Thu, 01 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1422356</guid>        </item>
        <item>
            <title>Pruritus in primary biliary cirrhosis: pathogenesis and therapy.</title>
            <link>http://www.medworm.com/index.php?rid=1422355&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18456187%26dopt%3DAbstract</link>
            <description>Authors: Bergasa NV
    Pruritus is a symptom experienced by patients who have primary biliary cirrhosis. It seems to result from pruritogens that (as a result of cholestasis) accumulate in plasma and other tissues, and which lead to altered neurotrasnmission. Administration of medications that change opioid neurotransmission (ie, opiate antagonists) results in relief of pruritus and its behavioral manifestation, scratching. Through unknown mechanisms, other centrally acting medications, including antidepressants, may have ameliorating effects on the pruritus of cholestasis. Stimulating endogenous detoxification pathways in the liver may also lead to the amelioration of pruritus. The removal of pruritogens through administration of nonabsorbable resins, nasobiliary drainage, biliary divers...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1422355</comments>
            <pubDate>Thu, 01 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1422355</guid>        </item>
        <item>
            <title>Osteoporosis in primary biliary cirrhosis: pathogenesis and treatment.</title>
            <link>http://www.medworm.com/index.php?rid=1422354&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18456188%26dopt%3DAbstract</link>
            <description>Authors: Par&amp;#xE9;s A, Gua&amp;#xF1;abens N
    Osteoporosis, characterized by loss of bone strength leading to fragility fractures, is a common event in patients who have primary biliary cirrhosis. Although its pathogenesis is not well known, it results mainly from low bone formation. There is no specific treatment, but bisphosphonates, especially alendronate, effectively increases bone mass and prevents bone loss. Despite these favorable effects on bone mass, no clear effects on decreasing the fracture rate are demonstrated, probably because of the low number of patients included in the trials. The potential usefulness of new agents requires further evaluation.
    PMID: 18456188 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1422354</comments>
            <pubDate>Thu, 01 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1422354</guid>        </item>
        <item>
            <title>Treatment of primary biliary cirrhosis: therapy with choleretic and immunosuppressive agents.</title>
            <link>http://www.medworm.com/index.php?rid=1422353&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18456189%26dopt%3DAbstract</link>
            <description>Authors: Silveira MG, Lindor KD
    Primary biliary cirrhosis (PBC) is a chronic cholestatic liver disease of presumed autoimmune etiology affecting predominantly middle-aged women; it is a slowly progressive disease causing loss of intrahepatic bile ducts, resulting in advanced fibrosis, cirrhosis, and liver failure. Many drugs have been studied for treatment, including agents with choleretic and immunosuppressive properties. Ursodeoxycholic acid (UDCA) has been evaluated most widely. After liver failure, the only effective treatment is liver transplantation. Effective therapy reduces the need for transplantation and improves life expectancy. For advanced liver disease or incomplete response to UDCA, new therapies to cure or retard the progression of disease in PBC are needed.
    PMID: 1...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1422353</comments>
            <pubDate>Thu, 01 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1422353</guid>        </item>
        <item>
            <title>Other potential medical therapies: the use of antiviral agents to investigate and treat primary ciliary cirrhosis.</title>
            <link>http://www.medworm.com/index.php?rid=1422352&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18456190%26dopt%3DAbstract</link>
            <description>Authors: Mason AL, Wasilenko ST
    A human betaretrovirus has been characterized in patients with primary biliary cirrhosis (PBC) and the related mouse mammary tumor virus linked with autoimmune biliary disease in the NOD.c3c4 mouse model. Translational studies have been performed in patients who have PBC to investigate the role of viral infection in disease. Patients treated with Combivir experienced significant improvements in hepatic biochemistry, clinical symptoms, and histology with evidence of reversal of ductopenia. Preliminary studies suggest that the NOD.c3c4 mouse model of PBC provides a good model to test safer and more potent drug regimens for future use in trials for patients who have PBC.
    PMID: 18456190 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1422352</comments>
            <pubDate>Thu, 01 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1422352</guid>        </item>
        <item>
            <title>Liver transplantation in primary biliary cirrhosis.</title>
            <link>http://www.medworm.com/index.php?rid=1422351&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18456191%26dopt%3DAbstract</link>
            <description>Authors: Milkiewicz P
    The proportion of patients who undergo liver transplantation for primary biliary cirrhosis (PBC) is steadily declining. This decline is partly from the increasing number of patients undergoing transplantation for other indications, but also perhaps because of the effect of ursodeoxycholic acid (UDCA) on the natural history of this condition. Nevertheless, patients who have PBC still constitute approximately 11% of all patients undergoing transplantation for cirrhosis. The prognosis after transplantation is excellent, with an approximately 80% 5-year survival reported by most large centres. Liver transplantation also significantly improves quality of life in survivors. The disease may recur after surgery in up to one third of patients, but recurrence has not been s...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1422351</comments>
            <pubDate>Thu, 01 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1422351</guid>        </item>
        <item>
            <title>Primary biliary cirrhosis: the future.</title>
            <link>http://www.medworm.com/index.php?rid=1422350&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18456192%26dopt%3DAbstract</link>
            <description>Authors: Hirschfield GM, Heathcote EJ
    Primary biliary cirrhosis is a progressive cholestatic liver disease of presumed autoimmune etiology. Patterns of disease are changing with earlier recognition and better access to investigation and treatment. With the convergence of animal, genetic, and clinical studies over the coming years, it is hoped that a greater understanding in the pathophysiology of the disease will translate into improved clinical endpoints for patients.
    PMID: 18456192 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1422350</comments>
            <pubDate>Thu, 01 May 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1422350</guid>        </item>
        <item>
            <title>Preface.</title>
            <link>http://www.medworm.com/index.php?rid=1206497&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18242494%26dopt%3DAbstract</link>
            <description>Authors: Jensen DM
    
    PMID: 18242494 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1206497</comments>
            <pubDate>Fri, 01 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1206497</guid>        </item>
        <item>
            <title>Mechanisms of cholestasis.</title>
            <link>http://www.medworm.com/index.php?rid=1206496&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18242495%26dopt%3DAbstract</link>
            <description>This article gives an overview of the molecular and cellular mechanisms of cholestasis. Topics reviewed include the pathomechanisms of hereditary cholestasis syndromes, such as progressive familial intrahepatic cholestasis, and hepatocellular transporter defects encountered in various acquired cholestatic disorders, such as intrahepatic cholestasis of pregnancy, drug-induced cholestasis, inflammatory cholestasis, primary sclerosing cholangitis, and primary biliary cirrhosis. In addition, current concepts regarding adaptive hepatocellular mechanisms counteracting cholestatic liver damage are discussed.
    PMID: 18242495 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1206496</comments>
            <pubDate>Fri, 01 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1206496</guid>        </item>
        <item>
            <title>Role of mitochondria in drug-induced cholestatic injury.</title>
            <link>http://www.medworm.com/index.php?rid=1206495&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18242496%26dopt%3DAbstract</link>
            <description>This article discusses the role of mitochondria in drug-induced cholestatic injury to the liver. The role of mitochondria in the cellular adaptation against the toxic effects of bile acids is discussed also.
    PMID: 18242496 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1206495</comments>
            <pubDate>Fri, 01 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1206495</guid>        </item>
        <item>
            <title>Medical treatment of cholestatic liver disease.</title>
            <link>http://www.medworm.com/index.php?rid=1206494&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18242497%26dopt%3DAbstract</link>
            <description>Authors: Paumgartner G, Pusl T
    In most cholestatic liver diseases the cause of the disease is not known and therapy can only be directed toward suppression of the pathogenetic processes and amelioration of the consequences of cholestasis. The recognition of adaptive-compensatory responses to cholestasis has become of major importance. They tend to minimize retention of bile acids and other potentially toxic solutes in the hepatocyte by limiting hepatocellular uptake, reducing bile acid synthesis, stimulating detoxification, and up-regulating alternative pathways for excretion. Some of the drugs used for the treatment of cholestatic liver diseases in an empiric way turned out to be modulators of nuclear receptors, which regulate these adaptive-compensatory responses. New drugs are being...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1206494</comments>
            <pubDate>Fri, 01 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1206494</guid>        </item>
        <item>
            <title>Role of methotrexate in the treatment of chronic cholestatic disorders.</title>
            <link>http://www.medworm.com/index.php?rid=1206493&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18242498%26dopt%3DAbstract</link>
            <description>This article examines the therapeutic potential of methotrexate (MTX) in the treatment of cholestatic liver disease, with specific reference to its use in primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC). In PBC patients, evidence suggests that a particular subset of patients may benefit, either biochemically or symptomatically, from the addition of MTX to their therapeutic regimen. How best to define these potential MTX responders remains unclear, but may warrant a &quot;therapeutic trial&quot; in some patients with more aggressive disease or in patients with refractory and disabling PBC-related symptoms. In contrast, PSC continues to be an immensely challenging disease to effectively treat, and the role of MTX for treating PSC patients remains dubious.
    PMID: 18242498 [P...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1206493</comments>
            <pubDate>Fri, 01 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1206493</guid>        </item>
        <item>
            <title>Cholestasis induced by total parenteral nutrition.</title>
            <link>http://www.medworm.com/index.php?rid=1206492&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18242499%26dopt%3DAbstract</link>
            <description>This article describes the definition, incidence, hepatic changes, histopathologic findings, risk factors, pathogenesis, and clinical implications of TPN-IC. The goal is to improve hospital and home management, quality of life, and prognosis of patients requiring parenteral nutrition.
    PMID: 18242499 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1206492</comments>
            <pubDate>Fri, 01 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1206492</guid>        </item>
        <item>
            <title>Intrahepatic cholestasis after liver transplantation.</title>
            <link>http://www.medworm.com/index.php?rid=1206491&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18242500%26dopt%3DAbstract</link>
            <description>Authors: Corbani A, Burroughs AK
    Biochemical cholestasis after liver transplantation is common and often has no clinical significance if biliary anastomosis strictures and leaks have been excluded. There is no agreed upon definition for severe cholestasis, but it is associated with a worse mortality. There has been little evaluation on risk factors, but these include cryoprecipitate and platelet transfusion intraoperatively, nonidentical blood group, suboptimal graft appearance, inpatient status before transplant, and bacteremia within the first month. Associated causes considered as early (&amp;lt;6 months) include ischemia-reperfusion injury, primary nonfunction, small-for-size graft syndrome, infection, drugs and acute cellular rejection. Late causes include hepatic artery thrombosis, c...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1206491</comments>
            <pubDate>Fri, 01 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1206491</guid>        </item>
        <item>
            <title>Cholangiocarcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=1206490&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18242501%26dopt%3DAbstract</link>
            <description>Authors: Blechacz BR, Gores GJ
    Cholangiocarcinoma is a primary hepatic malignancy originating from bile duct epithelium. It is the second most common primary hepatic neoplasia, and its incidence has increased within the last 3 decades. Although several risk factors have been identified, especially chronic biliary tract inflammation, most patients with cholangiocarcinoma have no identifiable risk factors. Recent developments in radiologic and molecular diagnostic methods have helped in the diagnosis of this disease. The only curative therapy is surgical resection or liver transplantation. For patients with advanced stage disease, survival remains limited. With growing understanding of the molecular and cellular etiology of this disease, new targeted therapies are being developed.
    PM...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1206490</comments>
            <pubDate>Fri, 01 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1206490</guid>        </item>
        <item>
            <title>Sepsis and cholestasis.</title>
            <link>http://www.medworm.com/index.php?rid=1206489&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18242502%26dopt%3DAbstract</link>
            <description>This article gives a comprehensive overview of the underlying molecular mechanisms of sepsis-associated cholestasis and jaundice, their clinical presentation, and diagnostic and therapeutic management.
    PMID: 18242502 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1206489</comments>
            <pubDate>Fri, 01 Feb 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1206489</guid>        </item>
        <item>
            <title>Anti-Mitochondrial Antibody-Negative Primary Biliary Cirrhosis.</title>
            <link>http://www.medworm.com/index.php?rid=1206488&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18242503%26dopt%3DAbstract</link>
            <description>Authors: Selmi C, Zuin M, Bowlus CL, Gershwin ME
    The recent development in the authors' laboratory of a sensitive bead assay able to detect AMA in 20% of otherwise AMA-negative sera seems to support the hypothesis that many AMA-negative cases of primary biliary cirrhosis (PCB) are secondary to limits in the methods used and do not represent an independent clinical entity. Clinical data demonstrate that patients without detectable serum AMA do not differ in their natural history from their seropositive counterparts. Anti-nuclear antibodies have been associated repeatedly with more severe disease and are helpful tools in the management of patients who have PBC, particularly those lacking AMA.
    PMID: 18242503 [PubMed - as supplied by publisher] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1206488</comments>
            <pubDate>Fri, 01 Feb 2008 05:00:00 +0100</pubDate>
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        <item>
            <title>Autoimmune Hepatitis and PSC Connection.</title>
            <link>http://www.medworm.com/index.php?rid=1206487&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18242504%26dopt%3DAbstract</link>
            <description>This article describes the connection between autoimmune hepatitis (AIH) and primary sclerosing cholangitis (PSC). The two conditions have chronicity, liver inflammation, and a positive autoimmune serology in common; they differ in terms of gender distribution and bile duct damage. There is evidence suggesting that AIH and PSC are immune-mediated diseases. PSC and AIH could lie within the spectrum of the same disease process. Future studies should determine how frequently AIH evolves to PSC.
    PMID: 18242504 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1206487</comments>
            <pubDate>Fri, 01 Feb 2008 05:00:00 +0100</pubDate>
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        <item>
            <title>Vanishing bile duct syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=1206486&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18242505%26dopt%3DAbstract</link>
            <description>This article reviews the multiple causes, postulated pathophysiology, clinical features, and treatment options for this syndrome.
    PMID: 18242505 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1206486</comments>
            <pubDate>Fri, 01 Feb 2008 05:00:00 +0100</pubDate>
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        <item>
            <title>Update on the treatment of the pruritus of cholestasis.</title>
            <link>http://www.medworm.com/index.php?rid=1206485&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18242506%26dopt%3DAbstract</link>
            <description>Authors: Bergasa NV
    The pruritus of cholestasis is a difficult clinical problem to manage. It can be severe and interfere with sleep. Clinical behavioral studies have confirmed that the pruritus is mediated at least in part by endogenous opioids. Other neurotransmitter systems may be involved in the mediation of pruritus. Work continues to identify the mechanisms that mediate the pruritus and to develop specific drugs to treat this often maddening symptom.
    PMID: 18242506 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1206485</comments>
            <pubDate>Fri, 01 Feb 2008 05:00:00 +0100</pubDate>
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        <item>
            <title>Preface.</title>
            <link>http://www.medworm.com/index.php?rid=1009019&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17981224%26dopt%3DAbstract</link>
            <description>Authors: Jacobson IM
    
    PMID: 17981224 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1009019</comments>
            <pubDate>Thu, 01 Nov 2007 04:00:00 +0100</pubDate>
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        <item>
            <title>Molecular virology of hepatitis B virus for clinicians.</title>
            <link>http://www.medworm.com/index.php?rid=1009018&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17981225%26dopt%3DAbstract</link>
            <description>This article reviews the molecular biology of the hepatitis B virus in an effort to explain its natural history from a molecular perspective. The life cycle of the virus, with special attention to virus replication, polypeptide production, and morphogenesis, is described. The way in which these steps may influence the natural history of viral pathogenesis, as well as the effectiveness of interventions, receives special consideration.
    PMID: 17981225 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1009018</comments>
            <pubDate>Thu, 01 Nov 2007 04:00:00 +0100</pubDate>
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        <item>
            <title>The role of the woodchuck model in the treatment of hepatitis B virus infection.</title>
            <link>http://www.medworm.com/index.php?rid=1009017&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17981226%26dopt%3DAbstract</link>
            <description>Authors: Kulkarni K, Jacobson IM, Tennant BC
    Experimental studies of animals with chronic hepadnavirus infection could provide valuable insight into optimal therapeutic strategies for individuals with chronic HBV infection. In this review, we focus on the contributions of the woodchuck model to our understanding of HBV biology and on its role in the development of antiviral drug. Furthermore, we consider the implications of studies focusing on the natural history of WHV infection for the management of HBV and the capacity of treatment to prevent complications of chronic hepatitis B infection.
    PMID: 17981226 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1009017</comments>
            <pubDate>Thu, 01 Nov 2007 04:00:00 +0100</pubDate>
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        <item>
            <title>The immunology of hepatitis B.</title>
            <link>http://www.medworm.com/index.php?rid=1009016&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17981227%26dopt%3DAbstract</link>
            <description>Authors: Vierling JM
    The hepatitis B virus (HBV) is an enveloped, hepatotrophic, oncogenic hepadnavirus that is noncytopathic for hepatocytes. HBV infection results in a variety of outcomes that are determined by the quality, quantity, and kinetics of the host innate and adaptive immune responses. Whether HBV infection is cleared or persists as a progressive or nonprogressive liver disease is determined by both viral and host factors. Replicative intermediates can persist in the liver under immunologic control after resolution of acute or chronic hepatitis B, conferring a risk for reactivation following a course of immunosuppression or chemotherapy.
    PMID: 17981227 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1009016</comments>
            <pubDate>Thu, 01 Nov 2007 04:00:00 +0100</pubDate>
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        <item>
            <title>Genotyping and genomic sequencing in clinical practice.</title>
            <link>http://www.medworm.com/index.php?rid=1009015&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17981228%26dopt%3DAbstract</link>
            <description>This article reviews the uses of NAT in the diagnosis and management of chronic hepatitis B.
    PMID: 17981228 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1009015</comments>
            <pubDate>Thu, 01 Nov 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1009015</guid>        </item>
        <item>
            <title>Long-Term Outcomes in Hepatitis B: The REVEAL-HBV Study.</title>
            <link>http://www.medworm.com/index.php?rid=1009014&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17981229%26dopt%3DAbstract</link>
            <description>This article reviews results from the REVEAL-HBV study, which found that hepatitis B virus DNA across a biologic gradient is very strongly predictive of the risk of disease progression and remains a strong predictor of risk after accounting for other important factors.
    PMID: 17981229 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1009014</comments>
            <pubDate>Thu, 01 Nov 2007 04:00:00 +0100</pubDate>
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        <item>
            <title>Surveillance for hepatocellular carcinoma and early diagnosis.</title>
            <link>http://www.medworm.com/index.php?rid=1009013&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17981230%26dopt%3DAbstract</link>
            <description>Authors: Sherman M
    Good management of patients at risk for the development of hepatocellular carcinoma includes regular ultrasound surveillance, and aggressive management of lesions detected at ultrasound. Good radiology and good pathology are essential to the appropriate management of these small lesions. With good quality testing it is possible to cure the majority of HCCs using minimally invasive techniques such as radiofrequency ablation. Such an approach has the potential to convert HCC from a disease in which incidence more or less equaled mortality to one in which cure is frequently possible.
    PMID: 17981230 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1009013</comments>
            <pubDate>Thu, 01 Nov 2007 04:00:00 +0100</pubDate>
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        <item>
            <title>Interferon therapy for chronic hepatitis B.</title>
            <link>http://www.medworm.com/index.php?rid=1009012&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17981231%26dopt%3DAbstract</link>
            <description>This article summarizes the results obtained with interferon alfa and pegylated interferon alfa, as monotherapy and in combination with lamivudine, in the treatment of chronic hepatitis B.
    PMID: 17981231 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1009012</comments>
            <pubDate>Thu, 01 Nov 2007 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1009012</guid>        </item>
        <item>
            <title>Oral antivirals for chronic hepatitis B.</title>
            <link>http://www.medworm.com/index.php?rid=1009011&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17981232%26dopt%3DAbstract</link>
            <description>This article reviews the durability of response, dose regimen, predictors of response, safety, and problems with resistance of these four agents and of promising agents currently in phase III clinical trials for the treatment of patients who have hepatitis B e antigen-positive and -negative chronic hepatitis B.
    PMID: 17981232 [PubMed - in process] (Source: Clinics in Liver Disease)</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1009011</comments>
            <pubDate>Thu, 01 Nov 2007 04:00:00 +0100</pubDate>
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            <title>Antiviral therapy of chronic hepatitis B: prevention of drug resistance.</title>
            <link>http://www.medworm.com/index.php?rid=1009010&amp;cid=s_33212_17_f&amp;fid=33212&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D17981233%26dopt%3DAbstract</link>
            <description>Authors: Fournier C, Zoulim F
    The emergence of viral resistance during treatment is becoming an important clinical issue for hepatitis B virus (HBV) antiviral therapy. Considerable progress has been achieved in the efficacy of treatment, with the development of new drugs that allow a sustained suppression of HBV replication, or at least maintain the viral load below a clinically relevant threshold. Although most drugs currently registered for the treatment of chronic hepatitis B are effective in suppressing viral load, long-term therapy is required to avoid viral reactivation and progression of liver disease. Because of the variability of the HBV genome, such long-term treatments are associated with the emergence of resistant viral strains, which may compromise the initial clinical ben...</description>
            <author>Clinics in Liver Disease</author>
            <type>journals</type>
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            <pubDate>Thu, 01 Nov 2007 04:00:00 +0100</pubDate>
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