They identified WNT5A as a factor positively regulating expressio

They identified WNT5A as a factor positively regulating expression of the hepatic ISGs. Moreover, they found that WNT5A increased HCV replication. This work links up-regulation of ISGs with stimulation of HCV replication. (Hepatology 2014;59:828–838.)

18F-fluoro-deoxy-glucose positron emission tomography/computerized tomography (PET/CT) is used routinely in oncologic workup. However, its accuracy in hepatocellular carcinoma (HCC) is limited and this test has not been endorsed by guidelines. This lack of accuracy suggests that HCC relies less on glycolysis than other tumors. It is then possible that another metabolite might be an adequate tracer. In a pilot study, Bieze et al. tested 18F-methyl-choline ABT-263 concentration PET/CT as an alternative tracer in 29 patients. This test displayed a sensitivity of 88% and a specificity of 100%. 18F-methyl-choline PET/CT revealed lesions that affected management in 15 patients. This is an important observation, which should revive the interest for PET/CT within the HCC community. (Hepatology 2014;59:996–1006.) A serum-ascites albumin gradient greater than 11 g/L generally suggests cirrhosis-induced ascites, with the most frequent exception being heart failure. Then, a protein concentration higher than 25 mg/L in ascites favors heart failure over cirrhosis. In an impressive selleck compound clinical study, Farias et al. propose serum B-type natriuretic

peptide (BNP) as a better marker for ascites resulting from heart failure. They compared serum-ascites albumin gradient, protein concentration in ascites, serum BNP, and ascites BNP in a prospective group

of patients with new ascites resulting from heart failure, cirrhosis, and peritoneal Farnesyltransferase disease. Serum BNP was the most accurate measure for ascites related to heart failure: A value >364 pg/mL rules in heart failure and a value ≤182 rules out heart failure as the cause of ascites. This finding was confirmed in a validation cohort. Patients with a serum creatinine value above 2.5 mg/dL were excluded from this study, indicating that the value of serum BNP determination in patients with renal insufficiency remains to be investigated. In clinical practice, a diagnostic paracentesis likely remains indicated. (Hepatology 2014;59:1043–1051.) Alfa-fetoprotein (AFP) was already pronounced dead as a biomarker for HCC; obituaries have been written! Data from the HALT-C trial showed that AFP was not elevated in the months preceding the diagnosis of HCC in patients treated for chronic hepatitis C. Following a similar approach, Wong et al. report that AFP starts to increase 6 months before the diagnosis of HCC in a cohort of 1,531 entecavir-treated hepatitis B virus (HBV)-infected patients, followed for more than 4 years, among whom 57 patients developed HCC. Of note, surveillance sonography was done less frequently than the recommended 6-month interval.

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