Congenital heart disease and the liver

Sumeet K. Asrani, Nina S. Asrani, Deborah K. Freese, Sabrina D. Phillips, Carole A. Warnes, Julie Heimbach, Patrick S. Kamath – 2 March 2012 – There are approximately 1 million adult patients with congenital heart disease (CHD) in the United States, and the number is increasing. Hepatic complications are common and may occur secondary to persistent chronic passive venous congestion or decreased cardiac output resulting from the underlying cardiac disease or as a result of palliative cardiac surgery; transfusion or drug‐related hepatitis may also occur.

Case‐control study of hepatitis B and hepatitis C in older adults: Do healthcare exposures contribute to burden of new infections?

Joseph F. Perz, Scott Grytdal, Suzanne Beck, Ana Maria Fireteanu, Tasha Poissant, Elena Rizzo, Katherine Bornschlegel, Ann Thomas, Sharon Balter, Jeremy Miller, R. Monina Klevens, Lyn Finelli – 2 March 2012 – Reports of hepatitis B virus (HBV) and hepatitis C virus (HCV) transmission associated with unsafe medical practices have been increasing in the United States. However, the contribution of healthcare exposures to the burden of new infections is poorly understood outside of recognized outbreaks.

A human claudin‐1–derived peptide inhibits hepatitis C virus entry

Youhui Si, Shufeng Liu, Xiuying Liu, Jana L. Jacobs, Min Cheng, Yuqiang Niu, Qi Jin, Tianyi Wang, Wei Yang – 1 March 2012 – Hepatitis C virus (HCV) entry is a complicated process that requires multiple host factors, such as CD81, scavenger receptor BI, claudin‐1 (CLDN1), and occludin. The interaction of virus and cellular entry factors represents a promising target for novel anti‐HCV drug development. In this study, we sought to identify peptide inhibitors for HCV entry by screening a library of overlapping peptides covering the four above‐mentioned entry factors.

Long‐term follow‐up of hemodynamic responders to pharmacological therapy after variceal bleeding

Salvador Augustin, Antonio González, Laia Badia, Laura Millán, Aranzazu Gelabert, Alejandro Romero, Antoni Segarra, María Martell, Rafael Esteban, Jaime Guardia, Joan Genescà – 1 March 2012 – Although it is assumed that hemodynamic responders to pharmacological therapy after a variceal hemorrhage are adequately protected from rebleeding, there is no evidence that either this response or its protective effect extend beyond the usual 2‐year follow‐up featured in available studies.

Fibrosis‐dependent mechanisms of hepatocarcinogenesis

David Y. Zhang, Scott L. Friedman – 1 March 2012 – Hepatocellular carcinoma (HCC) is a rising worldwide cause of cancer mortality, making the elucidation of its underlying mechanisms an urgent priority. The liver is unique in its response to injury, simultaneously undergoing regeneration and fibrosis. HCC occurs in the context of these two divergent responses, leading to distinctive pathways of carcinogenesis. In this review we highlight pathways of liver tumorigenesis that depend on, or are enhanced by, fibrosis.

Chronic inflammation, immune escape, and oncogenesis in the liver: A unique neighborhood for novel intersections

Jimmy K. Stauffer, Anthony J. Scarzello, Qun Jiang, Robert H. Wiltrout – 1 March 2012 – Sustained hepatic inflammation, driven by alcohol consumption, nonalcoholic fatty liver disease, and/or chronic viral hepatitis (hepatitis B and C), results in damage to parenchyma, oxidative stress, and compensatory regeneration/proliferation. There is substantial evidence linking these inflammation‐associated events with the increased incidence of hepatocellular carcinogenesis.

Long‐term risk of recurrent peptic ulcer bleeding in patients with liver cirrhosis: A 10‐year nationwide cohort study

Yao‐Chun Hsu, Jaw‐Town Lin, Tzu‐Ting Chen, Ming‐Shiang Wu, Chun‐Ying Wu – 1 March 2012 – Peptic ulcer bleeding leads to substantial morbidity and mortality in patients with liver cirrhosis, but their long‐term risk of recurrent bleeding remains elusive. This nationwide cohort study aimed to elucidate the association between cirrhosis and recurrent peptic ulcer bleeding by analyzing the Taiwan National Health Insurance Research Database.

Histopathology of de novo autoimmune hepatitis

Ananya Pongpaibul, Robert S. Venick, Sue V. McDiarmid, Charles R. Lassman – 29 February 2012 – De novo autoimmune hepatitis (DAIH) is a well‐recognized complication of pediatric liver transplantation (LT). The diagnosis is largely based on elevated liver function test results and the development of autoimmune antibodies. The histology of DAIH was first described in 1998. We present detailed histological data from the largest series to date of pretreatment and posttreatment biopsy samples from pediatric LT patients with DAIH.

The impaired immune regulation of autoimmune hepatitis is linked to a defective galectin‐9/tim‐3 pathway

Rodrigo Liberal, Charlotte R. Grant, Beth S. Holder, Yun Ma, Giorgina Mieli‐Vergani, Diego Vergani, Maria Serena Longhi – 28 February 2012 – In autoimmune hepatitis (AIH), liver‐damaging CD4 T cell responses are associated with defective CD4posCD25pos regulatory T cells (T‐regs). Galectin‐9 (Gal9), a β‐galactosidase–binding protein expressed by T‐regs, is key to their function, inhibiting T helper 1 immune responses by binding T cell immunoglobulin and mucin domain 3 (Tim‐3) on CD4 effector cells.

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