Immune‐mediated hemolytic anemia in children after liver and small bowel transplantation

Piotr Czubkowski, Mike Williams, Seema Bagia, Deirdre Kelly, Girish Gupte – 5 April 2011 – Four children who underwent ABO‐compatible combined liver and small bowel transplantation developed severe immune‐mediated hemolytic anemia. The main management strategies were early and aggressive treatment with steroids, the introduction of rituximab (an anti‐CD20 monoclonal antibody), and the use of plasma exchange together with compatible but minimal blood transfusions. Three of the 4 children developed thrombi in the major vessels.

Down‐regulation of phosphatase and tensin homolog by hepatitis C virus core 3a in hepatocytes triggers the formation of large lipid droplets

Sophie Clément, Marion Peyrou, Andrea Sanchez‐Pareja, Lucie Bourgoin, Pierluigi Ramadori, David Suter, Manlio Vinciguerra, Kevin Guilloux, Stephanie Pascarella, Laura Rubbia‐Brandt, Francesco Negro, Michelangelo Foti – 4 April 2011 – Hepatitis C virus (HCV) perturbs the host's lipid metabolism and often results in hepatic steatosis. In nonalcoholic fatty liver disease, the intrahepatic down‐regulation of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a critical mechanism leading to steatosis and its progression toward fibrosis and hepatocellular carcinoma.

In vivo consequences of liver‐specific interleukin‐22 expression in mice: Implications for human liver disease progression

Ogyi Park, Hua Wang, Honglei Weng, Lionel Feigenbaum, Hai Li, Shi Yin, Sung Hwan Ki, Seong Ho Yoo, Steven Dooley, Fu‐Sheng Wang, Howard A. Young, Bin Gao – 4 April 2011 – Interleukin‐22 (IL‐22), which acts as either a proinflammatory or anti‐inflammatory cytokine in various disease models, is markedly up‐regulated in chronic liver diseases, including hepatitis B and C. In this report, we demonstrate a strong correlation between IL‐22 expression in the liver with active, inflammatory human liver disease.

Methodological concerns about a recent meta‐analysis of the influence of the I148M variant of patatin‐like phospholipase domain containing 3 on the susceptibility and histological severity of nonalcoholic fatty liver disease

Deficiency of liver adipose triglyceride lipase in mice causes progressive hepatic steatosis

Jiang Wei Wu, Shu Pei Wang, Fernando Alvarez, Stéphanie Casavant, Nicolas Gauthier, Lynda Abed, Krishnakant G. Soni, Gongshe Yang, Grant A. Mitchell – 4 April 2011 – Accumulation of cytoplasmic triacylglycerol (TG) underlies hepatic steatosis, a major cause of cirrhosis. The pathways of cytoplasmic TG metabolism are not well known in hepatocytes, but evidence suggests an important role in lipolysis for adipose triglyceride lipase (ATGL). We created mice with liver‐specific inactivation of Pnpla2, the ATGL gene.

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