Impact of Obesity and Heavy Alcohol Consumption on Hepatocellular Carcinoma Development after HCV Eradication with Antivirals.

Background And Aims: It remains unclear whether obesity increases the risk of hepatocellular carcinoma (HCC) in patients with chronic hepatitis C who achieved a sustained virological response (SVR) with antiviral therapy.

Methods: In this multicenter cohort study, we enrolled patients with chronic hepatitis C who achieved SVR with interferon (IFN)-based therapy (IFN group) or direct-acting antiviral (DAA) therapy (DAA group) between January 1, 1990, and December 31, 2018. The patients underwent regular surveillance for HCC.

Efficacy and safety of glecaprevir/pibrentasvir in patients with hepatitis C virus infection aged ≥75 years.

Aim: Opportunities to treat older patients with hepatitis C virus infection have increased. We investigated the efficacy and safety of glecaprevir/pibrentasvir in patients with HCV infection aged ≥75 years.

Methods: We retrospectively evaluated 131 patients with hepatitis C virus infection treated with glecaprevir/pibrentasvir at nine institutions in Japan.

Resistance mutations of hepatitis B virus in entecavir-refractory patients.

The emergence of resistance mutations in the reverse transcriptase gene of hepatitis B virus (HBV) is associated with treatment failure. Entecavir (ETV) is one of the most potent anti-HBV reagents; it has a very low resistance rate and is used as the first-line treatment for chronic hepatitis B. In this study, we isolated HBVs in 4 ETV-refractory patients (2 with viral breakthrough, 1 with partial virological response, and 1 with flare-up) and assessed ETV resistance using replication-competent 1.

Impact of resistance-associated variant dominancy on treatment in patients with HCV genotype 1b receiving daclatasvir/asunaprevir.

Sustained virological responses (SVR) by daclatasvir (DCV) and asunaprevir (ASV) therapy for genotype 1b hepatitis C virus (HCV) infected patients has been significantly affected by pre-existence of Y93 H resistance-associated variants (RAVs) in the non-structural protein 5A (NS5A) region. The aim of this study was to elucidate the dominancy of naturally occurring RAVs in viral quasispecies on treatment outcomes in patients with HCV. In total, 138 patients were prospectively selected from 152 patients treated with DCV and ASV, where evaluation of treatment outcomes at 12 weeks post-treatment was possible.

Acute hepatitis B of genotype H resulting in persistent infection.

A 47-year-old man presented with general fatigue and dark urine. The laboratory data showed increased levels of hepatic transaminases. The patient was positive for hepatitis B virus (HBV) markers and negative for anti-human immunodeficiency virus.

High levels of hepatitis B virus after the onset of disease lead to chronic infection in patients with acute hepatitis B.

Background: Some patients with acute hepatitis B virus (HBV) infection develop chronic infection. However, the method for identifying these patients has not been established.

Methods: We followed 215 Japanese patients with acute HBV infection until the clearance of hepatitis B surface antigen (HBsAg) or the development of chronic infection.

Short-term prolongation of pegylated interferon and ribavirin therapy for genotype 1b chronic hepatitis C patients with early viral response.

Aim: We tailored extended treatments using pegylated interferon (PEG IFN) and ribavirin (RBV) to viral responses after initiation of therapy and investigated the efficacy and safety of its therapy for chronic hepatitis C (CHC) patients.

Methods: Eighty-two genotype 1b CHC patients were enrolled in the present study. All patients received PEG IFN-alpha-2b and weight-based RBV therapy.

Effect of treatment with interferon alpha-2b and ribavirin in patients infected with genotype 2 hepatitis C virus.

Aim: Nearly 20% of chronic hepatitis C (CHC) patients with genotype 2 hepatitis C virus (HCV) infection are not curable, even by interferon (IFN)-ribavirin combination therapy. The aim of this study is to investigate the factors that determine the efficacy of combination therapy in patients with genotype 2 HCV infection.

Methods: Fifty patients with CHC who underwent a treatment of 6 MU IFN alpha-2b with ribavirin for 24 weeks were retrospectively analyzed.

Amino acid substitutions in the S region of hepatitis B virus in sera from patients with acute hepatitis.

Background: An increase in the number of acute hepatitis patients with hepatitis B virus (HBV) of non-indigenous genotypes may reduce the efficacy of vaccination against HBV.

Methods: We have determined the amino acid (aa) sequences in the major hydrophilic region (MHR) in the S region of HBV in patients with acute hepatitis B and compared those with the ones from HBV strains used for the production of HBV vaccines commercially available in Japan.

Results: Of 48 patients studied, 11 were infected with genotype A, 11 with genotype B and 26 with genotype C HBV.

Molecular epidemiology of hepatitis A virus in metropolitan areas in Japan.

Background: Transmission routes of hepatitis A virus (HAV) in Japan have changed. The present study investigated changes of transmission routes in relation to genetic drift.

Methods: All 60 patients who were admitted between 1993 and 2003 with a diagnosis of hepatitis A were retrospectively analyzed.

Risk factors for retinopathy associated with interferon alpha-2b and ribavirin combination therapy in patients with chronic hepatitis C.

Aim: To elucidate the frequency and risk factors for retinopathy in patients with chronic hepatitis C who are treated by interferon-ribavirin combination therapy.

Methods: We prospectively analyzed 73 patients with histologically confirmed chronic hepatitis C, who underwent combination therapy for 24 wk. Optic fundi were examined before, and 2, 4, 12 and 24 wk after the start of combination therapy.

Distinct geographic distributions of hepatitis B virus genotypes in patients with acute infection in Japan.

Genotypes of hepatitis B virus (HBV) were determined in 145 patients with acute hepatitis B from various districts in Japan to establish their geographic distribution and evaluating the influence on the clinical illness and outcome. Genotypes were A in 27 (19%) patients, B in 8 (5%), C in 109 (75%) and mixed with B and C in the remaining one (1%). Genotype A was more frequent in metropolitan than the other areas (21/69 (30%) vs.

Short-term lamivudine for the treatment of chronic hepatitis B.

Short-term lamivudine and its withdrawal were evaluated as regards an immunomodulatory therapy of chronic hepatitis B. Lamivudine was given for 3 or 6 months to 23 patients with chronic hepatitis B who were infected with hepatitis B virus (HBV) genotype C, including 15 with hepatitis B e antigen (HBeAg) and 8 without it. It decreased serum levels of alanine aminotransferase (ALT) and HBV DNA in HBeAg-positive patients.

Detection, using a novel method, of a high prevalence of cryoglobulinemia in persistent hepatitis C virus infection.

To elucidate precisely the prevalence and significance of cryoglobulinemia in hepatitis C, we examined the prevalence of serum cryoglobulin (CG) among 232 consecutive hepatitis C virus carriers (23 asymptomatic carriers, 164 with chronic hepatitis, 45 with cirrhosis), 30 consecutive hepatitis B virus carriers and 100 age- and sex-matched healthy volunteers. We used a gel-diffusion procedure that detects CG with greater sensitivity and specificity than the conventional precipitation method. Among the 232 patients, 166 were tested for the presence or absence of CG by the precipitation method also, which showed 60 (36.

Precore and core promoter mutations, hepatitis B virus DNA levels and progressive liver injury in chronic hepatitis B.

Background/aims: To elucidate the viral factors responsible for progressive liver injury in chronic hepatitis B.

Methods: We analyzed 179 persistently infected patients (21 asymptomatic carriers, 126 with chronic hepatitis and 32 with cirrhosis) with genotype C hepatitis B virus (HBV). HBeAg/anti-HBe, levels of HBV DNA, mutations in the basic core promoter (BCP) region at nucleotides 1762/1764 and mutation in the precore (preC) region at nucleotide 1896 were determined.