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Background and Aims: This study aimed to determine the safety and efficacy of atezolizumab + bevacizumab therapy in hepatocellular carcinoma patients receiving anti‐platelet agents or anticoagulants. Methods: Patients were divided into those using (IM out) and those not using (IM in) anti‐platelet agents or anticoagulants, who violated the exclusion criteria of the IMbrave150 trial, and were retrospectively examined. Results: The study included 185 patients (IM in: 157; IM out: 28). For first‐line treatment, progression‐free survival was 184 days for IM in and 266 days for IM out (p =.136). Overall survival was 603 days for IM in and not reached for IM out (p =.265), with no significant between‐group difference. Similarly, there were no significant between‐group differences in progression‐free survival or overall survival for later‐line treatment. Haemorrhagic adverse events of ≥grade 3 were observed in 11 IM in patients and 3 IM out patients. No significant factors associated with haemorrhagic adverse events of ≥grade 3 were identified in the multivariate analysis including IM out classification, whose p value was.547. Regarding thrombotic/embolic adverse events in the IM out group, one case of exacerbation of portal vein thrombosis was observed. No deaths were directly attributable to bleeding events or exacerbations of thrombosis. Conclusion: Atezolizumab + bevacizumab therapy shows similar safety and efficacy in patients receiving and those not receiving anti‐platelet agents or anticoagulants; therefore, it can be considered for patients with hepatocellular carcinoma receiving anti‐platelet agents or anticoagulants. [ABSTRACT FROM AUTHOR]

Aim: Little is known about the appropriate use of peginterferon-α-2b (PEG IFN-α-2b) or ribavirin (RBV) in genotype 1 chronic hepatitis C (CH-C) patients with complete early virological response (cEVR). Female patients, especially the older, are known to experience inferior treatment outcomes. Method: A total of 150 CH-C patients with cEVR treated for 48 weeks ( n = 104) or 52-64 weeks ( n = 46) with PEG IFN-α-2b and RBV combination therapy were retrospectively analyzed to evaluate the benefits of extended treatment. Results: In the 48-week group, patients without a sustained virological response (SVR) were more often female ( P = 0.004) and had received a significantly lower total RBV dose ( P = 0.003) than those with SVR. The SVR rate in these female patients was similar to males with hepatitis C virus (HCV) RNA negativity at treatment week 8 ( P = 0.413); however, it was lower than that in males with HCV RNA negativity at treatment week 12 ( P = 0.005). In the 52-64-week group, although the total RBV dose (mg/kg) after treatment week 48 was less in females than in males ( P = 0.027), the SVR rate in females was equivalent to that in males ( P = 0.604). Conclusion: Genotype 1 CH-C patients treated with PEG IFN-α-2b and RBV combination therapy without SVR were more often female and had received a lower total RBV dose than males. The smaller SVR rate in female patients with cEVR compared to males may be overcome by extending treatment even if the RBV dose is lowered due to anemia. [ABSTRACT FROM AUTHOR]

Aim: Hepatic steatosis is one of the factors limiting the virological response to interferon-based antiviral therapy for chronic hepatitis C (CH-C) patients infected with genotype 1, while contradictory results have been reported for genotype 2. We aimed to clarify the effect of hepatic steatosis on therapeutic outcome and cumulative positivity of serum HCV RNA in CH-C patients infected with genotype 2 treated by peginterferon (PEG-IFN)α2b and ribavirin (RBV) combination therapy. Methods: A total of 74 treatment-naïve non-cirrhotic CH-C patients infected with genotype 2 who received PEG-IFNα2b and RBV according to the standard regimen were divided into hepatic steatosis 0-10% and >10% groups. The clinical backgrounds, sustained virological response (SVR) rates and cumulative positivity of serum HCV RNA were compared between the two groups. Results: Among the 74 patients, 61 (82.4%) had hepatic steatosis 0-10% and 13 (17.6%) had hepatic steatosis >10%. Scores of homeostasis model assessment-insulin resistance and hepatic fibrosis were higher in patients with hepatic steatosis >10% than hepatic steatosis 0-10% ( P = 0.040 and 0.042, respectively). Non-SVR was more frequent in patients with hepatic steatosis >10% than hepatic steatosis 0-10% ( P = 0.003). Cumulative positivity of serum HCV RNA was significantly higher in patients with hepatic steatosis >10% than hepatic steatosis 0-10% ( P = 0.004). Conclusions: In CH-C patients infected with genotype 2 treated by PEG-IFNα2b and RBV combination therapy, hepatic steatosis >10% was associated with increased insulin resistance, advanced hepatic fibrosis and higher cumulative positivity of serum HCV RNA, which lead to a higher risk of non-SVR. [ABSTRACT FROM AUTHOR]

Aims/Background: This study was undertaken in order to characterize the liver injury induced by transcatheter arterial chemoembolization therapy (TACE) for hepatocellular carcinoma (HCC) and to elucidate mechanisms involved in the growth of mononuclear phagocytes in injured human liver in vivo. Patients and Methods: The serum levels of macrophage-colony stimulating factor (M-CSF) along with clinical parameters were examined in 43 patients with HCC who underwent TACE. Ten patients who underwent angiography alone served as controls. Results: Serum M-CSF increased and peaked on the third day after TACE showing significant correlations ( p<0.001, respectively) with the increases in serum alanine aminotransferase (ALT) and type IV collagen-7S (IVcol-7S). The lipopolysaccharide-stimulated production of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α in peripheral whole blood increased and peaked on the first or on the third day after TACE. In effective cases of TACE, significantly ( p<0.05) greater increases in serum M-CSF were noted as compared with those in ineffective cases. Discussion: The serum levels of M-CSF increased after TACE in correlation with hepatic inflammation and necrosis and increased production of IL-1β, TNF-α, and IL-6 in peripheral whole blood. These results suggest a mechanism by which hepatic injury enhances the production of M-CSF via a cytokine cascade, which results in the proliferation of liver macrophages in vivo. [ABSTRACT FROM AUTHOR]