In addition, the outcome of our patient population within the different BCLC stages matches exactly the published survival data for the BCLC classification.3 Furthermore, the independence of CRP from treatment allocation in the training and the validation cohort upon multivariate analysis and the reproducibility of our findings at a second independent timepoint see more confirmed the validity of our data. Prospective studies are needed to study the impact of CRP levels on response and outcome to specific antitumor treatments like TACE or sorafenib therapy. In summary, our study identified serum

CRP as a novel, noninvasive, inexpensive, objective, available, and widely applicable prognostic marker for patients with HCC, irrespective of tumor stage and Child-Pugh class and therapy. Thus, we recommend collecting serum CRP in future clinical trials, in particular in the setting of intermediate or advanced-stage HCC. The causal role of CRP in tumor progression merits further investigations in preclinical studies. We thank Professor Harald Heinzl for excellent statistical consulting. Additional Supporting Information may be found in the online version of this article. “
“As the main iron storage site in the body and the main source of IWR-1 the iron-regulatory hormone, hepcidin, the liver plays a pivotal role in iron

homeostasis. A variable degree of hepatic iron accumulation has long been recognized in a number of chronic liver diseases. Both alcoholic and non-alcoholic steatohepatitis display increased iron deposits in the liver, with an hepatocellular, mesenchymal, or mixed pattern, and recent reports have documented a concomitant aberrant hepcidin expression that could be linked to different coincidental Ketotifen pathogenic events (e.g. the etiological agent itself,

necroinflammation, metabolic derangements, genetic predisposition). The present study reviews the pathogenic mechanisms of iron accumulation in steatohepatitis during alcoholic and non-alcoholic liver disease and the role of excess iron in chronic disease progression. “
“The epidemic of obesity has been associated with a significant increase in nonalcoholic fatty liver disease (NAFLD). The pathogenesis of NAFLD in this setting is predicated on the premise that obesity-related insulin resistance is responsible for the development of hepatic steatosis. Our current understanding holds that in some patients, the increased free fatty acid (FFA) flux to the liver and decreased hepatic FFA oxidation results in lipotoxicity and progression to hepatocyte ballooning, lobular inflammation, and pericellular fibrosis—the histopathologic hallmarks of nonalcoholic steatohepatitis (NASH). To this end, investigators have predominantly focused on therapies that improve insulin resistance.