This study shows that a combination therapy of peginterferon and ribavirin is highly effective for chronic HCV infection, producing a high SVR and ETR.

Aim: This study's aim was to determine the accuracy of the spleen stiffness value acquired using acoustic radiation force impulse (ARFI) technology, to predict the presence of esophageal varices (EVs) in patients with liver cirrhosis of various etiologies. Material and methods: Of the 366 enrolled patients, 192 had hepatitis B virus, 74 had hepatitis C virus, and 100 had alcohol-related cirrhosis. All patients underwent biochemical tests, gastrointestinal endoscopy, and liver and spleen elastography by ARFI. We evaluated the correlation between the presence of EVs and factors including liver and spleen stiffness measured by ARFI, biochemical tests, and other noninvasive measurements, such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), platelet count (PLT), spleen diameter (SD), PLT to SD ratio, AST to ALT ratio (AAR) score, the AST to PLT ratio index (APRI) score. Result: A univariate analysis revealed that the AAR score, APRI score, PLT, PLT/SD ratio, and spleen elastography variables were all independently associated with EVs (p<0.05). On multivariate analysis, only spleen elastography was associated with EVs (p=0.001). However, in cases of alcohol-induced liver cirrhosis, spleen stiffness was not reliable for the prediction of EVs. Conclusion: Spleen elastography measured using ARFI may serve as a non-invasive method for determining the presence of EVs. However, it is not an appropriate predictor for EVs in alcoholic cirrhosis.

Hepatic iron overload (HIO) is a hallmark of nonalcoholic fatty liver disease (NAFLD) with a poor prognosis. Recently, the role of hepatic erythrophagocytosis in NAFLD is emerging as a cause of HIO. We undertook various assays using human NAFLD patient pathology samples and an in vivo nonalcoholic steatohepatitis (NASH) mouse model named STAMTM. To make the in vitro conditions comparable to those of the in vivo NASH model, red blood cells (RBCs) and platelets were suspended and subjected to metabolic and inflammatory stresses. An insert-coculture system, in which activated THP-1 cells and RBCs are separated from HepG2 cells by a porous membrane, was also employed. Through various analyses in this study, the effect of cilostazol was examined. The NAFLD activity score, including steatosis, ballooning degeneration, inflammation, and fibrosis, was increased in STAMTM mice. Importantly, hemolysis occurred in the serum of STAMTM mice. Although cilostazol did not improve lipid or glucose profiles, it ameliorated hepatic steatosis and inflammation in STAMTM mice. Platelets (PLTs) played an important role in increasing erythrophagocytosis in the NASH liver. Upregulated erythrophagocytosis drives cells into ferroptosis, resulting in liver cell death. Cilostazol inhibited the augmentation of PLT and RBC accumulation. Cilostazol prevented the PLT-induced increase in ectopic erythrophagocytosis in in vivo and in vitro NASH models. Cilostazol attenuated ferroptosis of hepatocytes and phagocytosis of RBCs by THP-1 cells. Augmentation of hepatic erythrophagocytosis by activated platelets in NASH exacerbates HIO. Cilostazol prevents ectopic erythrophagocytosis, mitigating HIO-mediated ferroptosis in NASH models.

Aim: This study's aim was to determine the accuracy of the spleen stiffness value acquired using acoustic radiation force impulse (ARFI) technology, to predict the presence of esophageal varices (EVs) in patients with liver cirrhosis of various etiologies. Material and methods: Of the 366 enrolled patients, 192 had hepatitis B virus, 74 had hepatitis C virus, and 100 had alcohol-related cirrhosis. All patients underwent biochemical tests, gastrointestinal endoscopy, and liver and spleen elas-tography by ARFI. We evaluated the correlation between the presence of EVs and factors including liver and spleen stiffness measured by ARFI, biochemical tests, and other noninvasive measurements, such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), platelet count (PLT), spleen diameter (SD), PLT to SD ratio, AST to ALT ratio (AAR) score, the AST to PLT ratio index (APRI) score. Result: A univariate analysis revealed that the AAR score, APRI score, PLT, PLT/SD ratio, and spleen elastography variables were all independently associated with EVs (p<0.05). On multivariate analysis, only spleen elastography was associated with EVs (p=0.001). However, in cases of alcohol-induced liver cirrhosis, spleen stiffness was not reliable for the prediction of EVs. Conclusion: Spleen elastography measured using ARFI may serve as a non-invasive method for determining the presence of EVs. However, it is not an appropriate predictor for EVs in alcoholic cirrhosis.

Warfarin is a widely used anticoagulant. Interindividual differences in drug response, a narrow therapeutic range and the risk of bleeding render warfarin difficult to use clinically. An 18-year-old woman with antiphospholipid syndrome received long-term warfarin therapy for a recurrent deep vein thrombosis. Six years later, she developed right flank pain. We diagnosed intrahepatic and subgaleal hemorrhages secondary to anticoagulation therapy. After stopping oral anticoagulation, a follow-up computed tomography showed improvement in the hemorrhage. After restarting warfarin because of a recurrent thrombosis, the intrahepatic hemorrhage recurred. We decided to start clopidogrel and hydroxychloroquine instead of warfarin. The patient has not developed further recurrent thrombotic or bleeding episodes. Intrahepatic hemorrhage is a very rare complication of warfarin, and our patient experienced intrahepatic and subgaleal hemorrhage although she did not have any risk factors for bleeding or instability of the international normalized ratio control.