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Management of Liver Diseases 2012
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Issue Highlights
HBV DNA suppression and HBsAg CLEARANCE IN HBeAg negative chronic hepatitis B patients on lamivudine therapy for over 5 yearsCurrent guidelines do not provide clear recommendations whether stable CHB patients on long-term lamivudine treatment without evidence for emerging resistance should be switched to a more potent anti-viral agent. This study reports on 191 Italian patients with HBeAg negative CHB who responded favorably to lamivudine for at least 5 years and continued intake of lamivudine for another median period of 36 months. Three years later, a favorable virologic response was still documented in 67% of them and 12% of responders cleared HBsAg. Although one third of patients developed resistance to lamivudine, the risk for viral breakthrough was lower as compared to a ~70% risk in the first 5 years. Results from this study provide some justification for continued lamivudine treatment in a sub-cohort of HBeAg negative CHB patients without emerging resistance in the frst 5 years of therapy.
Bacterial translocation and changes in the intestinal microbiome in mouse models of liver diseaseIntestinal dysbiosis and bacterial translocation (BT) are particularly relevant for fibrogenesis, inflammation, and possibly cancerogenesis in patients with advanced liver disease, but the underlying mechanisms are still partially unclear. In this study, increased intestinal permeability and bacterial translocation occurred one day following acute cholestatic and toxic liver injury in animal models. This was accompanied by decreased intestinal expression of the tight junction protein occludin. BT occured independently of any microbial changes in bile-duct-ligated (BDL) rats and preceded the occurrence of bacterial overgrowth in CCl4-induced liver injury. The bacterial spectrum remained unaltered in BDL but a dysbiosis was observed in CCl4-treated mice, suggesting that enteric microbiome differs with respect to the etiology of liver disease.
Special Sections
Snapshot
Macrophages: Central regulators of hepatic fibrogenesis and fibrosis resolution
Hepatic fibrosis is a bidirectional process with a significant reversible component, in which the hepatic stellate cell (HSC) activation has a central role. However, emerging evidence indicates that the hepatic macrophage is actually the master regulator of this dynamic fibrogenesis-fibrosis resolution paradigm. Macrophages are a source of soluble mediators which can act on the HSCs to induce a pro-fibrotic phenotype, such as TGF-ß, PDGF (a potent stimulator of myofibroblast proliferation), IL-1ß and TNF-a. Macrophages also have a pivotal role in fibrosis resolution, throughout mechanisms still not fully defined and likely to be multi-factorial. A greater understanding of these processes will enable the development of novel therapeutic strategies to accelerate fibrosis resolution.
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Liver transplantation for hepatocellular carcinoma in non-cirrhotic livers regardless of the number and size of tumours?14 May 2012
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EASL Recognition Awardee 2012 Prof. Helmer Ring-Larsen11 May 2012
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Hepatocyte-like cells differentiated from human induced pluripotent stem cells (iHLCs) are permissive to hepatitis C virus (HCV) infection: HCV study gets personal07 May 2012
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Two lymph nodes draining the mouse liver are the preferential site of DC migration and T cell activation27 April 2012
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Mouse organic solute transporter alpha deficiency alters FGF15 expression and bile acid metabolism27 April 2012
About EASL
In the forty plus years since EASL was founded, it has grown from a small organization that played host to 70 participants at its first meeting, to becoming the leading liver association in Europe. EASL attracts the foremost hepatology experts as members and has an impressive track record in promoting research in liver disease, supporting wider education and promoting changes in european liver policy.
For more information about EASL (http://www.easl.eu)
