38 Transcomplementation of HBx protein with hydrodynamic injection restored HBV infectivity in mice. Interestingly, all revertant viruses show a restored ability to express HBx.38 By infecting chimeric mice with genotype A, B and C, differing proliferative capacity has been shown between HBV genotypes.37 In mice infected for a relatively short time, there are no morphological changes in HBV infected mice livers in Small molecule library studies.13,36 In contrast, the occurrence of liver cell damage has been reported after long-term infection of chimeric mice with HBV39 or with specific strains of HBV;40 these findings are consistent with direct cytopathic effects of HBV under certain conditions. The biological properties of a newly

identified unique strain of HBV, genotype G, which replicates only in the presence of another genotype, were confirmed using the chimeric mouse.41 Infectivity of another

novel HBV strain, identified from a Japanese patient, that is divergent from known human and ape HBV has also been confirmed.42 Titration of HBV infectivity, which previously could only be carried out using chimpanzees, can be carried out effectively using chimeric mice.43 Taking advantage of the absence of human immune cells in the chimeric mice, Noguchi et al.44 showed that hypermutation of HBV increases in human hepatocytes under interferon treatment. Dandri et al. measured viral half-life in human and chimeric mice repopulated with wooly monkey hepatocytes.45 The results clearly showed that viral half-life is shortened by immunological

mechanisms in humans with low viral levels, but not in chimeric mice where functional AG-014699 research buy immunity is absent. Hiraga et al.46 showed an absence of interference between HBV and HCV. Evaluation of therapeutic agents is the most important role for this mouse model. Tsuge et al.13 assessed the effect of interferon and lamivudine using chimeric mice. Similarly, Dandri et al.47 showed the effects of adefovir using uPA/scid mice repopulated with tupaia hepatocytes, which also support replication of human HBV. Oga et al.48 identified a novel lamivudine-resistant variant that has an amino acid substitution outside of the YMDD motif. They showed that lamivudine was ineffective against the novel mutant MCE strain. It is thus apparent that this mouse/human liver chimeric model is ideal to study the susceptibility of mutant strains to various drugs, because mutant viruses can easily be made and infected into chimeric mice.13 The model has also been utilized to evaluate viral entry inhibitors derived from the large envelope protein.49 As observed in studies on HBV, HCV infection efficiency was poor and levels of viremia were low in mice where the repopulation rate of the mouse liver with human hepatocyte was low.17,50 As shown in Figure 3, human albumin levels in mouse serum were significantly higher in mice in which measurable viremia developed (Hiraga et al. unpublished data).

6%) were malnourished, 13,945 (4.4%) were obese, and 11,909 (3.8%) were morbidly obese. A total of 98,404 patients (31.1%) had at least one infection during hospitalization. Infection was most prevalent among malnourished patients (49.4%), followed by morbidly obese (40.9%), and then obese patients (32.2%). In multivariable analysis, malnutrition and morbid obesity predicted infection (Table 1). Among infected patients, risk factors for mortality included malnutrition (OR=2.10; 95% CI 2.022.20) and morbid obesity (OR=1.47;

95% CI 1.41-1.54). Regarding specific infections, malnourished patients had greatest prevalence of sepsis, UTI, LRI, SBP and CDI, while morbidly obese patients had highest prevalence of cellulitis. Prevalence of bacteremia was similar among all patient groups.

Conclusion: Malnutrition and morbid obesity are associated with infection acquisition in cirrhosis Daporinad in vitro and higher mortality among infected cirrhotics. The prevalence of specific infections also varies depending on nutritional status. Further study is MK-2206 mw needed regarding the impact and optimization of nutritional status in chronic liver disease. Disclosures: Tram T. Tran – Advisory Committees or Review Panels: Gilead, Bristol Myers Squibb; Consulting: Gilead, AbbVie, Janssen; Grant/Research Support: Bristol Myers Squibb; Speaking and Teaching: Bristol Myers Squibb, Gilead Vinay Sundaram – Advisory Committees or Review Panels: Salix, Gilead, Jansen; Speaking and Teaching: Salix The following people have nothing to disclose: Aung Kaung, Ken D. Nguyen, Amit Rajaram, Phillip Zakowski Aim: To determine what clinical factors contribute to the high mortality from septic shock among cirrhotics with spontaneous bacterial peritonitis (SBP). Methods: From the CATTS Database between 1996 and 2011, retrospective cohort study of all cirrhotic patients with septic shock and evidence of SBP (neu-trophils > 250 or positive tap). Results: Among 126 cirrhotics (mean age 55, 60% male),

in-hospital mortality was 82%. In comparing survivors (n=23) with non-survivors (n=103), 上海皓元医药股份有限公司 survivors had lower mean admission APACHE II (22 vs. 32), MELD (24 vs.34) and serum lactate (4.9 vs. 8.9, p<0.001 for all) and were less likely to have co-existent bloodstream infection (BSI) (22% vs. 50%, p=0.015). Survivors were more likely to receive appropriate initial antimicrobial therapy (100% vs. 75%, p=0.013) and receive therapy earlier (median 1.8 vs. 9.5 hours, p<0.001). Predicted death rates (regression) according to APACHE II score, lactate and time to antimicrobials are shown in Figure 1 . On multivariable analysis, APACHE II (Odds Ratio 1.45 (1.04-2.02, p=0.03), lactate (OR 2.34 (1.04-5.29), p=0.04) and time delay to appropriate antimicrobials (OR 1.86 per hour (1.10-3.14), p=0.02) were all significantly associated with increased mortality. Age, gender and presence of co-existent BSI did not impact outcome. This model performed well (c-statistic 0.98).

Finally, qHBsAg and qHBeAg were measured in stored samples, so a falsely low titer might have been seen because the natural BMS-777607 nmr decay of viral proteins led to error in the titers. In conclusion, we report a

systematic analysis of 2 years of serial qHBsAg and qHBeAg data for patients treated with ETV. The baseline level of qHBsAg and the on-treatment decline of qHBeAg in HBeAg(+) patients were proved to be highly useful in predicting VR and SR, respectively, and this lends support to the clinical utility of quantitative serological markers. In addition, these inexpensive and simple assays provide insight into the dynamic nature of

the association between qHBsAg, qHBeAg, and HBV DNA in patients receiving antiviral therapy; further studies are warranted to validate and explore their potential role. “
“Aim:  Dietary habits Erlotinib clinical trial are involved in the development of chronic inflammation; however, the impact of dietary profiles of hepatitis C virus carriers with persistently normal alanine transaminase levels (HCV-PNALT) remains unclear. The decision-tree algorithm is a data-mining statistical technique, which uncovers meaningful profiles of factors from a data collection. We aimed to investigate dietary profiles associated with HCV-PNALT using a decision-tree algorithm. Methods:  Twenty-seven HCV-PNALT and 41 patients with chronic hepatitis C were enrolled in this study. Dietary habit was assessed using a validated semiquantitative food frequency questionnaire. A decision-tree algorithm was created by dietary variables, and was medchemexpress evaluated by area under the receiver operating characteristic curve analysis (AUROC). Results:  In multivariate

analysis, fish to meat ratio, dairy product and cooking oils were identified as independent variables associated with HCV-PNALT. The decision-tree algorithm was created with two variables: a fish to meat ratio and cooking oils/ideal bodyweight. When subjects showed a fish to meat ratio of 1.24 or more, 68.8% of the subjects were HCV-PNALT. On the other hand, 11.5% of the subjects were HCV-PNALT when subjects showed a fish to meat ratio of less than 1.24 and cooking oil/ideal bodyweight of less than 0.23 g/kg. The difference in the proportion of HCV-PNALT between these groups are significant (odds ratio 16.87, 95% CI 3.40–83.67, P = 0.0005). Fivefold cross-validation of the decision-tree algorithm showed an AUROC of 0.6947 (95% CI 0.5656–0.8238, P = 0.0067). Conclusion:  The decision-tree algorithm disclosed that fish to meat ratio and cooking oil/ideal bodyweight were associated with HCV-PNALT.

HEP3002 is an ongoing, open-label, early access program of telaprevir (TVR) in 16 countries, for patients with genotype 1 hepatitis C infection with severe fibrosis or compensated cirrhosis. Methods: Liver biopsy or non-invasive tests (Fibroscan in 1040 patients) showing severe fibrosis or cirrhosis were required at entry.1587 patients were treated with TVR, pegylated interferon-alpha (P) and ribavirin (R, RBV) for 12 weeks, followed by PR. Use of iron supplements, erythropoietin (EPO) Selleckchem Belnacasan and blood transfusions was permitted. Grade 1-4 anemia

included the clinically significant adverse event terms (SSC) of anemia or hemoglobin (Hb) reduction. All analyses GSK2118436 solubility dmso were on the intent-to-treat (ITT) population, using 16 weeks of data. Continuous variables were used in the multivariate analyses to predict anaemia. Results: Mean age was 53 years and mean weight 78kg; 64% were male and 98% Caucasian, 66% had HCV RNA levels >800, 000 lU/mL, 47%/53% had severe fibrosis/cirrhosis, 22% had genotype 1a. Up to Week 16, 59% of patients developed grade 1-4 anemia, with 3 1% grade 3-4 cases; 630 patients (40%) dosereduced RBV, 332 (21%) received EPo157 (10%) were transfused, 14 (1%) received iron-based

products and 45 (3%) discontinued treatment because of anemia. Results by baseline disease stage are shown below. There were reductions in Hb below 10 g/dL in 48% of patients. In a multivariate analysis, the four strongest predictors of Hb <10 g/dL at any time on treatment were female sex (OR=1.69, 95% Cl 1.27-2.27, p=0.0004), age >65 years (OR=2.31, 95% Cl 1.46-3.65,

p=0.0003), low baseline Hb (OR=1.08, 95% Cl 1.06-1.09, p<0.0001) and higher weight-based dosing of RBV (OR=1.13, 95% Cl 1. 05-1.21, p=0.0005). Baseline Fibroscan test results were not a significant predictor of anemia. Conclusions: In this TVR early access program for patients with severe fibrosis or compensated cirrhosis, grade 3 or 4 anemia was reported in 31% of patients, but discontinuation of TVR for anemia 上海皓元 was rare (3%). Anemia was normally managed by RBV dose reduction, transfusion or the use of EPo. Type of anemia Definition F3 patients (n=746) F4 patients Grade 1 Hb 10-10.9 or 2.5-3.4g/dL decrease 81(11%) 76 (9%) Grade 2 Hb 9-9.9 g/dL or 3.5-4.4 g/dL decrease 116(16%) 169 (20%) Grade 3 Hb 7-8.9 or >4.5 g/dL decrease 188 (25%) 238 (29%) Grade 4 Hb <7 g/dL 26 (3%) 35 (4%) Discontinued TVR for anemia 14(2%) 31(4%) Anemia as serious AE 32 (4%) 43 (5%) Disclosures: Simone I.

HEP3002 is an ongoing, open-label, early access program of telaprevir (TVR) in 16 countries, for patients with genotype 1 hepatitis C infection with severe fibrosis or compensated cirrhosis. Methods: Liver biopsy or non-invasive tests (Fibroscan in 1040 patients) showing severe fibrosis or cirrhosis were required at entry.1587 patients were treated with TVR, pegylated interferon-alpha (P) and ribavirin (R, RBV) for 12 weeks, followed by PR. Use of iron supplements, erythropoietin (EPO) Ruxolitinib order and blood transfusions was permitted. Grade 1-4 anemia

included the clinically significant adverse event terms (SSC) of anemia or hemoglobin (Hb) reduction. All analyses BYL719 were on the intent-to-treat (ITT) population, using 16 weeks of data. Continuous variables were used in the multivariate analyses to predict anaemia. Results: Mean age was 53 years and mean weight 78kg; 64% were male and 98% Caucasian, 66% had HCV RNA levels >800, 000 lU/mL, 47%/53% had severe fibrosis/cirrhosis, 22% had genotype 1a. Up to Week 16, 59% of patients developed grade 1-4 anemia, with 3 1% grade 3-4 cases; 630 patients (40%) dosereduced RBV, 332 (21%) received EPo157 (10%) were transfused, 14 (1%) received iron-based

products and 45 (3%) discontinued treatment because of anemia. Results by baseline disease stage are shown below. There were reductions in Hb below 10 g/dL in 48% of patients. In a multivariate analysis, the four strongest predictors of Hb <10 g/dL at any time on treatment were female sex (OR=1.69, 95% Cl 1.27-2.27, p=0.0004), age >65 years (OR=2.31, 95% Cl 1.46-3.65,

p=0.0003), low baseline Hb (OR=1.08, 95% Cl 1.06-1.09, p<0.0001) and higher weight-based dosing of RBV (OR=1.13, 95% Cl 1. 05-1.21, p=0.0005). Baseline Fibroscan test results were not a significant predictor of anemia. Conclusions: In this TVR early access program for patients with severe fibrosis or compensated cirrhosis, grade 3 or 4 anemia was reported in 31% of patients, but discontinuation of TVR for anemia medchemexpress was rare (3%). Anemia was normally managed by RBV dose reduction, transfusion or the use of EPo. Type of anemia Definition F3 patients (n=746) F4 patients Grade 1 Hb 10-10.9 or 2.5-3.4g/dL decrease 81(11%) 76 (9%) Grade 2 Hb 9-9.9 g/dL or 3.5-4.4 g/dL decrease 116(16%) 169 (20%) Grade 3 Hb 7-8.9 or >4.5 g/dL decrease 188 (25%) 238 (29%) Grade 4 Hb <7 g/dL 26 (3%) 35 (4%) Discontinued TVR for anemia 14(2%) 31(4%) Anemia as serious AE 32 (4%) 43 (5%) Disclosures: Simone I.

70 Unlike many other enterically-transmitted

infections, person-to-person www.selleckchem.com/products/voxtalisib-xl765-sar245409.html transmission of HEV appears to be uncommon.71,72 Thus, secondary attack rates among household contacts of patients with hepatitis E are only 0.7% to 2.2%, as compared to 50% to 75% for hepatitis A. Even when multiple cases occur in a family, the time interval between cases is usually short, indicating a shared primary water-borne infection rather than person-to-person spread.71 Materno-fetal73 and transfusion-related transmission74 of HEV are well documented. However, the contribution of these routes to the overall disease burden appears to be small. In the US, Europe (including UK, France, the Netherlands, Austria, Spain and Greece), and developed countries of Asia-Pacific

(Japan, Taiwan, Hong Kong, Australia), hepatitis E is responsible for only occasional cases with acute viral hepatitis. Initially, most such cases were found to be related to travel to high-endemic areas. However, in recent years, solitary cases or small case series related to autochthonous (locally-acquired) hepatitis E in these regions have been reported.25–27 In the UK, a seasonal variation with peaks in spring beta-catenin inhibitor and summer has been reported.75 These rare autochthonous cases of hepatitis E in these areas are believed to be caused by zoonotic spread of infection from wild or domestic animals,75,76 since HEV isolates from them are genetically related to swine isolates.25–27 Experimental cross-species transmission of human isolates to pigs, and of swine HEV to primates supports this view.27,57 A cluster of Japanese cases among persons who had consumed inadequately-cooked deer meat a few weeks prior to the onset of illness has been reported.51 The genomic sequences of HEV isolated from these cases were identical to those from the left-over frozen meat, establishing food-borne transmission; these isolates also had a high (99.7%)

genomic sequence homology with those from a wild boar and another MCE wild deer from the forest where the implicated deer had been hunted, suggesting transmission between wild boars and deer.77 A proportion of commercial packets of pig liver sold in Japanese and US grocery stores have been shown to contain genotype 3 or 4 HEV.78,79 This finding, along with the reported association of sporadic hepatitis E cases with eating uncooked or undercooked pig livers in case-control studies, suggests that at least some autochthonous cases are related to consumption of contaminated meat. Contaminated shellfish has also been proposed as a potential vehicle. The reservoir of HEV responsible for maintaining the disease in hyperendemic populations has not been clearly determined. Protracted viremia and prolonged fecal shedding of HEV have been suggested; however, we found that viral shedding in feces lasts for only a short period.

An extralesional nontumoral sample was available in 30 cases; in addition, cases of low-grade dysplastic nodules (LGDNs; n = 15) and HGDNs (n = 16) were collected. All dysplastic nodules were confirmed to be nonmalignant because during follow-up (at least 12 months), they did not show evidence of malignant check details changes. The median ages, gender distributions, HCC grading, and chronic liver disease etiologies

of the two HCC groups are reported in Table 1. Five consecutive recuts from the original paraffin blocks were obtained in all cases and were stained with antibodies against GPC3, HSP70, GS, and CHC. Supporting Table 2 details the

reagents used in this study, the working dilutions, and the detection system. Immunocytochemical analysis was performed according to standard procedures. Samples stained for GPC3 and HSP70 were scored as positive when at least 10% of the tumoral population showed undisputed cytoplasmic/membrane (GPC3) or nucleoplasmic/cytoplasmic (HSP70) staining. GS immunoreactivity was scored as positive when at least 50% of the neoplastic cells showed nucleoplasmic/cytoplasmic staining. Positive controls included an HCC case as an external standard for GPC3 and nonneoplastic bile duct epithelium and perivenular nontumoral hepatocytes MK-2206 concentration as internal standards for HSP70 and GS, respectively. CHC-positive cases were considered to be those showing undisputed cytoplasmic antigen overexpression in more than 10% of the malignant hepatocytes in comparison with the surroundings, the latter being the extralesional sampling or nontumoral parenchyma adjacent to the core HCC.

Nonparenchymal cells such as endothelial cells were used as internal standards for CHC staining. The staining assessment was made by two pathologists (M.R. and L.D.T.) and was always based on antigen overexpression in the lesion versus the surroundings. medchemexpress These pathologists independently evaluated the specimens and applied the designated criteria. The results were then discussed between them, and concordance on agreed scores was achieved with a high k coefficient value (>0.80). To further address the issue of interobserver variability in the evaluation of CHC immunostaining, we trained both a junior pathologist and a senior pathologist with a small set of surgical specimens and liver biopsy samples. Then, the junior and senior pathologists independently evaluated all the cases of HCC and dysplastic nodules, and the results were compared to the previously agreed scores.

An extralesional nontumoral sample was available in 30 cases; in addition, cases of low-grade dysplastic nodules (LGDNs; n = 15) and HGDNs (n = 16) were collected. All dysplastic nodules were confirmed to be nonmalignant because during follow-up (at least 12 months), they did not show evidence of malignant Dinaciclib solubility dmso changes. The median ages, gender distributions, HCC grading, and chronic liver disease etiologies

of the two HCC groups are reported in Table 1. Five consecutive recuts from the original paraffin blocks were obtained in all cases and were stained with antibodies against GPC3, HSP70, GS, and CHC. Supporting Table 2 details the

reagents used in this study, the working dilutions, and the detection system. Immunocytochemical analysis was performed according to standard procedures. Samples stained for GPC3 and HSP70 were scored as positive when at least 10% of the tumoral population showed undisputed cytoplasmic/membrane (GPC3) or nucleoplasmic/cytoplasmic (HSP70) staining. GS immunoreactivity was scored as positive when at least 50% of the neoplastic cells showed nucleoplasmic/cytoplasmic staining. Positive controls included an HCC case as an external standard for GPC3 and nonneoplastic bile duct epithelium and perivenular nontumoral hepatocytes LY294002 solubility dmso as internal standards for HSP70 and GS, respectively. CHC-positive cases were considered to be those showing undisputed cytoplasmic antigen overexpression in more than 10% of the malignant hepatocytes in comparison with the surroundings, the latter being the extralesional sampling or nontumoral parenchyma adjacent to the core HCC.

Nonparenchymal cells such as endothelial cells were used as internal standards for CHC staining. The staining assessment was made by two pathologists (M.R. and L.D.T.) and was always based on antigen overexpression in the lesion versus the surroundings. MCE These pathologists independently evaluated the specimens and applied the designated criteria. The results were then discussed between them, and concordance on agreed scores was achieved with a high k coefficient value (>0.80). To further address the issue of interobserver variability in the evaluation of CHC immunostaining, we trained both a junior pathologist and a senior pathologist with a small set of surgical specimens and liver biopsy samples. Then, the junior and senior pathologists independently evaluated all the cases of HCC and dysplastic nodules, and the results were compared to the previously agreed scores.

An extralesional nontumoral sample was available in 30 cases; in addition, cases of low-grade dysplastic nodules (LGDNs; n = 15) and HGDNs (n = 16) were collected. All dysplastic nodules were confirmed to be nonmalignant because during follow-up (at least 12 months), they did not show evidence of malignant Cobimetinib purchase changes. The median ages, gender distributions, HCC grading, and chronic liver disease etiologies

of the two HCC groups are reported in Table 1. Five consecutive recuts from the original paraffin blocks were obtained in all cases and were stained with antibodies against GPC3, HSP70, GS, and CHC. Supporting Table 2 details the

reagents used in this study, the working dilutions, and the detection system. Immunocytochemical analysis was performed according to standard procedures. Samples stained for GPC3 and HSP70 were scored as positive when at least 10% of the tumoral population showed undisputed cytoplasmic/membrane (GPC3) or nucleoplasmic/cytoplasmic (HSP70) staining. GS immunoreactivity was scored as positive when at least 50% of the neoplastic cells showed nucleoplasmic/cytoplasmic staining. Positive controls included an HCC case as an external standard for GPC3 and nonneoplastic bile duct epithelium and perivenular nontumoral hepatocytes R788 cost as internal standards for HSP70 and GS, respectively. CHC-positive cases were considered to be those showing undisputed cytoplasmic antigen overexpression in more than 10% of the malignant hepatocytes in comparison with the surroundings, the latter being the extralesional sampling or nontumoral parenchyma adjacent to the core HCC.

Nonparenchymal cells such as endothelial cells were used as internal standards for CHC staining. The staining assessment was made by two pathologists (M.R. and L.D.T.) and was always based on antigen overexpression in the lesion versus the surroundings. MCE These pathologists independently evaluated the specimens and applied the designated criteria. The results were then discussed between them, and concordance on agreed scores was achieved with a high k coefficient value (>0.80). To further address the issue of interobserver variability in the evaluation of CHC immunostaining, we trained both a junior pathologist and a senior pathologist with a small set of surgical specimens and liver biopsy samples. Then, the junior and senior pathologists independently evaluated all the cases of HCC and dysplastic nodules, and the results were compared to the previously agreed scores.

Conclusions: The spliceosome factor SART1 is not IFN-inducible but is an IFN effector gene. SART1 exerts its anti-HCV action through direct transcriptional downregulation for some ISGs (e. g., IFIH1) and alternative splicing for others, including EIF4G3, G〇RASP2, and ZFAND6. SART1 does not have effects on IFN receptor or components. Taken together,

these data imp ulates ISGs in a non-classical manner. Disclosures: Raymond ī. Chung – Advisory Committees or Review Panels: Idenix; Consulting: Enanta; Grant/Research Support: Gilead, Merck, Mass Biologic, Gilead DAPT datasheet The following people have nothing to disclose: Wenyu Lin, Chuanlong Zhu, Jian Hong, Lei Zhao, Qikai Xu, Pattranuch Chusri, Nikolaus Jilg, Dahlene N. Fusco, Esperance A. Schaefer, Cynthia Brisac, Lee F. Peng “
“Aim:  To evaluate changes Lumacaftor in liver function parameters and risk factors 1 year after percutaneous radiofrequency ablation (RFA) therapy in patients with hepatocellular carcinoma (HCC). Methods:  Subjects in this retrospective study comprised 45 patients with HCC who underwent RFA therapy (RFA alone, n = 25; transcatheter arterial embolization therapy before RFA, n = 20) and showed no recurrence of HCC 1 year after RFA.

Serial changes in serum total bilirubin, albumin, prothrombin time and Child–Pugh score (CPs) were evaluated before and after RFA. In addition, Cox proportional hazards regression analysis was used to clarify risk factors for aggravation of liver function after RFA therapy. Results:  Serum albumin levels showed a significant decrease from before (3.6 ± 0.4 g/dL) to 12 months

after RFA therapy (3.2 ± 0.4 g/dL; P ≤ 0.05). CPs was significantly increased from before (6.4 ± 1.4) to both 6 months (6.8 ± 1.9; P ≤ 0.05) and 12 months after RFA (6.9 ± 2.0; P ≤ 0.05). Based on stepwise multivariate analysis, CPs of 9 or more before RFA was selected as a 上海皓元 significant risk factor for long-term aggravation of liver function after RFA. Conclusion:  Liver function parameters, particularly serum albumin level, gradually and dominantly decreased in HCC patients with grade B and C according to the CPs classification over the course of 1 year after RFA therapy. A CPs of 9 or more represents a major risk factor for the aggravation of liver function after RFA therapy. “
“Aim:  Non-alcoholic steatohepatitis (NASH) patients frequently have hypertension, which is considered to be an important predictive factor for the subsequent development of hepatic fibrosis. The renin-angiotensin system is also known to contribute to the progression of NASH. Various types of functional single-nucleotide polymorphisms (SNPs) involved in the development of NASH have been proposed. Angiotensinogen (AGT) gene SNPs related to cardiovascular diseases have been reported. We aimed to evaluate the involvement of the AGT gene haplotype in Japanese NASH patients.