As the cause of gastrointestinal bleeding remained obscure, she was offered a wireless video capsule enteroscopy study (Given Imaging PillCamTM SB). The capsule was noted to enter the small intestine after 11 minutes and the recording ended approximately 8 hours later failing to show any evident bleeding source. Passage of the capsule in the colon was not demonstrated. Fourteen days after, the patient PLX3397 cell line was asymptomatic but since she did not notice passage per anum of the capsule, a plain abdominal x ray was performed and diagnosis of retained capsule was made (Figure 1).

Repeat small bowel barium enema demonstrated slow transit of contrast at the capsule impaction site. After surgical consultation, diagnostic laparoscopy was scheduled. Laparoscopy revealed a short concentric small

bowel stricture without lymphadenopathy. The remainder of the bowel and peritoneal cavity were normal. Small bowel resection containing the capsule with primary anastomosis was performed (Figure 2). The postoperative course was uneventful. Histopathologic evaluation of the resected bowel diagnosed a pT3N0M0 small bowel intestinal type adenocarcinoma. The term capsule retention is defined by a capsule remaining in the digestive tract for at least 14 days. The frequency of this complication depends mostly on the clinical indication for the capsule enteroscopy, and varies from less than 1% in patients with obscure gastrointestinal bleeding to 13% in Crohn’s disease. Most often capsule retention remains asymptomatic but acute small bowel obstruction and perforation may occur. Capsule

retention has been described to occur with strictures due to non-steroidal anti-inflammatory drugs (NSAID), VX-809 mw Crohn’s disease, small bowel tumors, radiation enteritis, and post-surgical anastomotic strictures. Retention may result in surgery in patients in whom medical treatment for Crohn’s disease or NSAID enteropathy would have sufficed. Therefore, in patients with known Crohn’s disease and/or inappropriate NSAID use, a “wait and see” policy may avoid unnecessary abdominal surgery. If a history of inflammatory bowel disease can be excluded, then capsule retention should Anidulafungin (LY303366) be considered a clear-cut surgical indication. Contributed by “
“A 47-year-old man diagnosed with human immunodeficiency virus (HIV) infection 3 months previously presented with 1-month’s history of inguinal tenderness associated with skin lesions. He had not been commenced on highly active antiretroviral therapy (HAART). The skin lesion was approximately 5 cm in diameter and biopsies were consistent with Kaposi’s sarcoma (KS). His CD4 count was 52 cells/µL and his HIV RNA viral load was 7.8 × 105 copies/mL. His hemoglobin was 11.4 g/dL and fecal occult blood test was positive. Colonoscopy was performed to and revealed submucosal nodules with a deep red color in the cecum (Figure 1). After indigo carmine dye chromoendoscopy, the center of the lesions appeared to be slightly depressed (Figure 1).

PUBMED, MEDLINE, EMBASE and the Cochrane Database were searched for articles published from 1990 to December 2012. Our results showed that the presence of high viral load significantly increased overall HCC recurrence risk after curative therapy. Pooled data from four studies on the recurrence rate among patients with genotype C infection compared with genotype B showed an increased risk of recurrence. Basal core promoter (BCP) mutation was associated with a significant risk in the recurrence of HCC. The pooled estimate of treatment effect was significantly

in favor of a preventive effectiveness of antiviral therapy. The present study suggested that HCC patients with high viral load, genotype C and BCP mutation had a significantly higher risk of recurrence. Antiviral therapy has potential beneficial effects

PLK inhibitor after the curative treatment of HCC in terms of tumor recurrence. “
“The etiology of see more biliary atresia (BA) is unknown. Given that patterns of anomalies might provide etiopathogenetic clues, we used data from the North American Childhood Liver Disease Research and Education Network to analyze patterns of anomalies in infants with BA. In all, 289 infants who were enrolled in the prospective database prior to surgery at any of 15 participating centers were evaluated. Group 1 was nonsyndromic, isolated BA (without major malformations) (n = 242, 84%), Group 2 was BA and at least medroxyprogesterone one malformation considered major as defined by the National Birth Defects Prevention Study but without laterality defects (n = 17, 6%). Group 3 was syndromic, with laterality defects (n = 30, 10%). In the population as a whole, anomalies (either major

or minor) were most prevalent in the cardiovascular (16%) and gastrointestinal (14%) systems. Group 3 patients accounted for the majority of subjects with cardiac, gastrointestinal, and splenic anomalies. Group 2 subjects also frequently displayed cardiovascular (71%) and gastrointestinal (24%) anomalies; interestingly, this group had genitourinary anomalies more frequently (47%) compared to Group 3 subjects (10%). Conclusion: This study identified a group of BA (Group 2) that differed from the classical syndromic and nonsyndromic groups and that was defined by multiple malformations without laterality defects. Careful phenotyping of the patterns of anomalies may be critical to the interpretation of both genetic and environmental risk factors associated with BA, allowing new insight into pathogenesis and/or outcome. (Hepatology 2013;58:1724–1731) The etiology of biliary atresia (BA) is unknown. In a large series of European infants reported by Davenport et al.,[1] infants with BA were catalogued by two different presentations: acquired/perinatal/nonsyndromic (∼90%) versus embryonal/syndromic (∼10%).

5B). The other two major phosphorylated MAPKs (phosphorylated stress-activated protein kinase/c-Jun N-terminal kinase [p-SAPK/JNK] and p38 MAPK) only increased insignificantly after heat treatment (Supporting Fig.4). Phosphorylation levels returned to baseline at day 12 after heat treatment. Notably, expression of heat shock protein selleck chemicals llc (HSP)27, 70, and 90 was significantly increased at day 5 post–heat treatment temperature dependently and also reverted to baseline levels at day 12 (Supporting Fig. 5). Liver specimens from 64 HCC patients, 20 patients with cirrhosis, and

30 subjects with CHC without cirrhosis were examined for Shc expression (Fig. 5C). Shc staining was absent in healthy liver, but dramatically increased in HCC tissue, whereas samples with CHC without cirrhosis showed an intermediate expression (P < 0.0005 for HCV cirrhosis versus HCC and for HCV without cirrhosis versus HCV click here cirrhosis; Fig. 5D). Next, we formed two groups with high and lower Shc-LIs (≥65% or <65%; n = 54 and n = 30, respectively) in patients with advanced fibrosis (without and with HCC). When comparing both

groups by Kaplan-Meier’s analysis, OS rate of patients with Shc-LI ≥65% was significantly lower than with Shc-LI <65% (P = 0.0316; Fig. 5E). When Shc-LI (%) in these patients was compared with hematological parameters associated with hepatocarcinogenesis (alpha-fetaprotein [AFP]-L3%, AFP, and protein induced by vitamin K absence/antagonist-II [PIVKA-II]) and liver function (alanine aminotransferase, aspartate

aminotransferase, total bilirubin, alkaline phosphate, gamma-glutamyl transpeptidase, ALB, and platelet count) in all samples (Supporting Table 3), a strong correlation was only found with AFP-L3 (%) (r = 0.5312; P < 0.0001). However, no strong correlation between Shc-LI and the other parameters was observed. Expression of both phosphorylated Shc-variants, p46- and p52-Shc, was assessed by semiquantitative western blotting in homogenized lysates of human liver specimens (Fig. 5F). Although p52-Shc was strongly expressed in both cirrhosis and HCC specimens (p = 0.0374 and p = 0.0054, respectively), p46-Shc was detected only in HCC, whereas no p66-Shc could be Hydroxychloroquine ic50 detected in any samples. In all HCC samples, phosphorylated p46-Shc expression was much stronger than phosphorylated p52-Shc expression (P = 0.0313). Five days after heat treatment (50˚C), HEPG2 cells were exposed to the Erk1/2 inhibitor, U0126, whereas HEPG2 cells kept at 37˚C served as controls. Notably, effective Erk1/2 inhibition, as evidenced by complete suppression of Erk1/2 phosphorylation (Fig. 6A), blunted enhanced proliferation (Fig. 6B) and essentially normalized (or reduced) all parameters related to EMT, except for significantly reduced, but still elevated, CK19 and COL1A1 (Figs. 4 and 6C,D).

Myeloid-derived suppressor cells (MDSCs) are another BMDC population whose diagnostic and prognostic significance has been recently investigated in HCC patients. MDSCs, which comprise both immature and mature elements of the mononuclear and polymorphonuclear myeloid lineages, are often expanded in the blood and lymphoid organs of cancer patients and are thought to promote tumor progression primarily by suppressing see more antitumor immunity and promoting tumor angiogenesis.7 Hoechst et al. found that the frequency of mononuclear CD14+/human leukocyte antigen/DR–/low (HLA-DR–/low)

MDSCs, but not total CD14+ monocytes, was significantly increased in the blood of HCC patients, compared to healthy controls.8 CD14+HLA-DR–/low MDSCs were found to stimulate the expansion of immunosuppressive CD4+CD25+FOXP3+ check details regulatory T cells8 and to inhibit the activity of natural killer (NK) cells9 when cocultured ex vivo with T

or NK cells, respectively. These data highlight the clinical significance of mononuclear MDSCs as a diagnostic biomarker of HCC and provide evidence for their involvement in immunosuppression associated with HCC progression. HCC is a highly vascularized tumor, and the progression of early lesions to overt HCC is associated with the appearance of a prominent arterial blood supply.10,11 The antiangiogenic drug, sorafenib, which targets several kinases that may control VEGF-mediated angiogenesis, prolongs survival of patients with advanced HCC, likely reflecting HCC dependence on angiogenesis.10 Of note, several preclinical studies have shown that both CEPs and MDSCs (or subsets of these cells) contribute to tumor angiogenesis in mouse models of cancer.7,12 Therefore, increased CEP and MDSC numbers in the blood of HCC patients4,5,8 Fenbendazole may also have the potential to foster HCC angiogenesis and progression to increased malignancy. TEMs are another BMDC type with proangiogenic activity in mouse models of cancer.13 In humans, TIE2 expression is higher in nonclassical (CD14lowCD16+) than classical (CD14+CD16–) monocytes14–16 and identifies a subset of circulating monocytes endowed with proangiogenic activity.14 Infiltrating TEMs

are also detected in a variety of human cancers.14,17 Matsubara et al.3 report on the frequency of circulating TEMs in a cohort of 168 HCV-infected patients, of which 89 were with HCC. The investigators found that the frequency of TEMs was significantly higher in patients with HCC than HCV-infected patients without HCC or healthy subjects, thus establishing TEMs as a stage-independent, diagnostic biomarker for HCC. Although TEM frequency did not correlate with tumor stage, HCC patients with higher TEM levels in their blood had a worse recurrence-free survival after HCC resection or radiofrequency ablation (RFA) therapy than patients with lower TEM levels, suggesting that TEMs may also represent a prognostic biomarker for this tumor type.

2A) and motor time (Fig. 2B). Whereas 30 subjects (12.4%) have a moderate improvement in their reaction time at Tmax, most subjects show a delay in their reaction time

with a maximum of 386 milliseconds (183% compared with the average basal value). Interestingly, the distribution of the effects of alcohol in reaction time is bimodal. Regarding motor time, a bimodal distribution also can be observed (Fig. 2B). Improvement in the motor times at peak ethanol concentrations was observed in 78 individuals (31.2%), but most subjects have a delay, with a maximum Doxorubicin datasheet of 170 milliseconds (over 200% compared with basal values). No sex-related differences were observed in the bimodal distribution for reaction or motor times. Ethanol drinking habits

did not influence reaction or motor times. The extent of delays in the reaction and motor times were not related to the peak ethanol concentration (Pearson’s correlation coefficient = 0.373 and 0.170, respectively) or to any other pharmacokinetic parameters analyzed in this study, indicating that factors other than ethanol concentration or pharmacokinetics see more contribute to the interindividual variability in ethanol effect. Table 4 summarizes the polymorphism for ethanol-metabolizing enzymes analyzed in the current study. Regarding the ADH1B gene, two of the four SNPs analyzed, namely Asn57Lys and Arg370Cys, were monomorphic in the population study. Because major ADH1B alleles are defined by the presence or absence of the SNPs in positions 48 and 370, and because the SNP in 370 was monomorphic ROS1 in the population study, the variant alleles ADH1B*1 (Arg48, Arg370) and ADH1B*2 (His48, Arg370), but not ADH1B*3 (Arg48, Cys370), were identified in the population study. In addition, the SNP Thr60Ser proved to be polymorphic

in the population study; eight individuals were heterozygous for this SNP, and all of them had the haplotype His48+Ser60. The observed frequency for the Arg48His SNPs is in concordance with that reported for white subjects.18, 19 No previous studies analyzed the SNP Thr60Ser, but the allele frequencies observed in the current study are consistent with those reported in public databases for white individuals (see the website http://www.ncbi.nlm.nih.gov/SNP/snp_ref.cgi?rs=6413413). Regarding the ADH1C gene, three of the six SNPs analyzed, namely Arg48His, Pro166Ser, and Pro352Thr, were monomorphic in the population study (Table 4). Although no published studies have analyzed the occurrence of these SNPs in white subjects, these findings are in agreement with the absence or extremely rare occurrence of these SNPs in public databases for white subjects (http://www.ncbi.nlm.nih.gov/projects/SNP/snp_ref.cgi?chooseRs=coding&go=Go&locusId=126).

45 μM and 10 μM, respectively. Furthermore, the IC90 value of pitavastatin, AR, and interferon alfa was 0.25 μM, 10 μM, and 1.0 IU/mL, respectively. These data demonstrated 90% inhibition of HCV RNA replication. Moreover, the combination of pitavastatin, AR, and interferon alfa was overwhelmingly more effective, compared with the previous results for the combination treatment of interferon alfa with ribavirin3 or the combination treatment of interferon alfa plus

fluvastatin.4 In particular, we could decrease the doses of interferon alfa and statin in order to get an IC90 value by the combination of pitavastatin, AR, and interferon alfa, that is comparable with the results Erismodegib of the combination treatment of interferon alfa plus fluvastatin.4 For example, in the former combination, pitavastatin and interferon alfa was 0.25 μM and 1.0 IU/mL, respectively. On the other hand, in the latter combination, selleck chemicals llc interferon alfa and fluvastatin was 4.0 IU/mL and 6.7

μmol/L, respectively.4 This would be meaningful in order to avoid the adverse effects of drugs. Next, we also generated human hepatocyte-like cells from human induced pluripotent stem cells (iPSCs),5 and we tried to investigate the hepatotoxicities for the combination of pitavastatin (0.25 μM), AR (10 μM), and interferon alfa (1.0 IU/mL) by using the normal human hepatocyte-like cells.5 As a result, we found the activities of glutamic oxaloacetic transaminase and lactate

dehydrogenase (LDH) in the culture medium of the normal human hepatocyte-like cells were not significantly different between the combination of pitavastatin (0.25 μM), AR (10 μM), and interferon alfa (1.0 IU/mL) and the combination of interferon alfa (4.0 IU/mL) plus ribavirin (25 μM). Therefore, considering the abovementioned observations, the antiviral effects and safeties for the combination therapy of pitavastatin (0.25 μM), AR (10 μM), and interferon alfa (1.0 IU/mL) could be confirmed. However, by using the patient-specific hepatocyte-like Dynein cells differentiated from human iPSCs of patients with hepatitis C virus 1b (HCV-1b) infection, the efficacies and toxicities of the abovementioned combination therapy for the individual patients with HCV-1b infection should be more precisely evaluated in the near future. In conclusion, we found a novel combination therapy for HCV-1b infection by using our replicon system2 and human iPSCs. We are grateful to members of our laboratories for technical support. Furthermore, we are also grateful to Ms. Satoko Iioka for helpful discussions. Hisashi Moriguchi* † ‡, Raymond T.

The chi-square test or Fisher’s exact test was used to compare categorical variables, and nonparametric Mann-Whitney tests were used to compare continuous variables. P values below the level of 0.05 were considered significant. As described previously, four different sets of pathologic criteria were used to establish the diagnosis of NASH. After the agreement between these different pathologic

criteria for NASH was assessed with κ statistics20 (Table 1), each diagnostic criterion for NASH was tested separately for its ability to independently predict LRM (after adjustments for relevant demographic and clinical confounders). Cox proportional Staurosporine hazards models were used to calculate adjusted hazard ratios (aHRs) and to identify independent predictors of LRM, and aHRs with P values ≤ 0.05 were considered potentially significant. Furthermore, two different schemes for grading fibrosis (NAS and the current study’s

criteria) were tested for agreement with Spearman’s correlation coefficient. Next, the individual pathologic features that constituted each of the four pathologic protocols were tested individually for their ability to independently predict LRM. Because in the original criteria for NAFLD these features were described in the form of ordinal variables, series of tests were performed to identify the thresholds for transforming each pathologic feature into a binary classifier. The threshold for each pathologic feature was selected find more so that the log-rank test for LRM associated with a transformed binary pathologic feature returned the highest P value in comparison with other possible thresholds for that feature. The transformation of ordinal features into binary features was supposed to eliminate nonequidistant distributions

of the degrees of pathologic processes described by the respective pathologic features. The transformed binary pathologic features were further used for building a multivariate survival model for LRM with the aims of (1) identifying those features independently predicting LRM and (2) establishing potential ways of improving existing pathologic protocols. All analyses were performed with SAS 9.1 (SAS Institute, Inc., Cary, NC). Liver biopsy slides and clinical data were available for 257 NAFLD patients (67% with NASH and 33% with non-NASH NAFLD); 142 of these patients 3-mercaptopyruvate sulfurtransferase were from the Armed Forces Institute of Pathology, 72 were from our previously reported NAFLD cohort, and 43 were from Inova Fairfax Hospital. For 209 patients (81%), both liver biopsy slides and mortality data were available, and they were used to calculate pathologic predictors of LRM. Demographic and laboratory data for the studied cohort are summarized in Table 2. The median follow-up length was 146 months (maximum = 342 months, interquartile range = 59-186 months); during follow-up, 31% of the subjects died. Of those deceased at the time of follow-up, 28% died of liver-related causes.

Differently from TACE, radioembolization does not depend on embolic induced hypoxia as the Yttrium-90 microspheres endure within the microvascular bed of HCCs and allow a pure radio-therapeutic effect also in patients with PVT. Despite a wide range of studies and applications of radioembolization (e.g., downstaging/bridging to transplantation or resection, macrovascular-invading tumors, advanced and even metastatic disease), the lack of prospective phase 2 investigations have impeded a precise identification of a specific

population of patients with HCC who may benefit from Y90RE as a first-line treatment. Long before its current use, Y90RE relied on individual basis and local expertise, but in the last few years the standardization of practice and indications yielded a progressive improvement of results. According to the most recent studies, a median Selleckchem AZD6244 survival of about 17 months (range, 16.9-17.2 months) in intermediate HCC and 11 months (range, 10-13.8 months) in find more advanced HCC are expected after Y90RE, with a disease control rate of 37%-60%, a severe (bilirubin) toxicity of 6%-20%, and a mortality rate of 3-6.8% at 30-90 days, respectively.6, 7, 15, 18 The acceptable safety profile and the efficacy of Y90RE in controlling

tumor progression has been acknowledged in several guidelines,2, 3 and the device is approved for treatment of HCC with or without PVT both in

Europe and America. This is the first phase 2 trial sought to determine efficacy and safety of Y90RE in intermediate and advanced HCC. To a large extent, the study captured HCCs with precluded access to curative options (such as transplantation) because of tumor-related portal invasion in patients with good performance. The consistent median follow-up (36 months) allowed the collection of reliable data across well-established prognostic groups of HCC, especially in the presence of PVT. The observed outcomes, which accounted for 9.6% of complete responses, revealed a high degree of concordance with previous investigations. The obtained results (i.e., rate of tumor STK38 progression at 2 years, 62%; median TTP, 11 months; disease control rate, 79%; median OS, 15 months—with the lower limit of the CI interval being higher than the 10-month survival estimated for these patients—with no difference between non-PVT versus PVT patients) demonstrated the competitive potentials of Y90RE with respect to conventional therapeutic options for HCC at similar stages and support further studies focused within each tumor category treated with radioembolization. At first glance, the results of Y90RE compare quite favorably with sorafenib in PVT patients (BCLC-C) and seem to achieve similar outcomes in intermediate stage HCC (BCLC-B) if compared with TACE (median survival, 14-16.5 months).

This study aimed to assess the influence of these factors on treatment initiation, decompensation, hepatocellular carcinoma

(HCC) and death. Methods: Consecutive patients with CHC were referred at our hospital through the network REVHEPAT or claissic hepatology consultation between January 1st 2000 and December 31st 2010 were followed-up until death, transplantation or study closure in 31st December 2013. Gender, age, Metavir score, diabetes, alcohol BYL719 manufacturer abuse, HCV genotype, HIV coinfections were collected at inclusion. Decompensation of cirrhosis, HCC and death were recorded at inclusion and during follow-up. The association between baseline factors and liver-related outcomes at inclusion and during follow-up were tested using logistic regression and Cox model, respectively. Results: A total of 3167 naïve patients with CHC (61% men, median age 47 years, time between testing and presentation median of 14 months) were included. At baseline, 29% of the patients had late testing, 6% alcohol abuse and 4% HIV coinfection. Time between testing and presentation ≥14 month (p < 0.001), delay presentation (p = 0.03) and Metavir score (p = 0.02) were independently associated with death related all cause. Late presentation was independently associated with rapid treatment initiation (p = 0.04), cirrhosis (p = 0.001) and HCC (p < 0.001) at inclusion. However delay presentation was

independently associated with progression to cirrhosis (p = 0.05), decompensation (p = 0.008) and Everolimus hepato-cellular carcinoma (p = 0.043) during the follow-up (median of 6 years). Conclusion: In patients with CHC, delay presentation to care is an independent prognostic factor. Different strategies should be developed to optimize early access to care and after testing, that may improve clinical outcomes. Disclosures: Patrick Marcellin – Consulting: Roche, Gilead,

BMS, Vertex, Novartis, Janssen, MSD, Abbvie, Alios Chorioepithelioma BioPharma, Idenix, Akron; Grant/Research Support: Roche, Gilead, BMS, Novartis, Janssen, MSD, Alios BioPharma; Speaking and Teaching: Roche, Gilead, BMS, Vertex, Novartis, Janssen, MSD, Boehringer, Pfizer, Abbvie Nathalie Boyer – Board Membership: MSD, JANSSEN, Gilead, Abbvie; Speaking and Teaching: BMS The following people have nothing to disclose: Blaise K. Kutala, Laurent Cattan, Christine Aurière, Alexandrine Di Pumpo, Beatrice Monnier, Nathalie Giuily, Kevin Appourchaux, Corinne Castelnau Background: Identifying patients at risk with increased mortality is crucial in the management of patients with liver cirrhosis. MELD-score and Child-Pugh-Score (CPS) offer adequate prediction of mortality. vWF-Ag shows adequate performance in predicting CSPH and mortality in cirrhotic patients. VITRO-score shows adequate performance in predicting cirrhosis in chronic HCV patients. We hypothesized that VITRO-score can predict mortality in a cohort of HCV cirrhotic patients. Methods: Data of 130 patients with chronic hepatitis C cirrhosis were analysed.

V BULL, P HA, L SAHHAR, S SPRING, S LE, A DEV Monash Health Introduction: An estimated 160,000 individuals in Australia have chronic hepatitis B (CHB). The chronicity of this disease and in many cases indefinite monitoring and treatment require adherence to management protocols. Disease specific knowledge, health perception and expectations

are important factors to consider in the education and management of CHB patients. Our aim was to identify the level of disease specific knowledge in CHB patients newly referred to a tertiary hospital outpatient clinic. Methods: We conducted a qualitative study that included 6 participants with CHB. These participants were enrolled prior to their first appointment with a Hepatologist at Monash Health between January 2014 and May 2014. Participants were invited to respond anonymously to a questionnaire that included questions on transmission, treatment and complications of CHB, perception and RNA Synthesis inhibitor attitude towards CHB and preferred methods of knowledge acquisition. The questionnaire also extracted demographic data. Four weeks after the first consultation, the same questionnaire was administered to measure longitudinal changes in knowledge of CHB. Results: The study included 6 males with CHB who were naive to anti viral treatment. All participants were fluent in English NVP-LDE225 concentration and the mean

age was 46 ± 9.1 years. 60% of participants were permanent residents and 50% had completed tertiary education. The mean age of HBV diagnosis was 38.2 ± 5.2 years. The longitudinal change in knowledge improved in questions examining modes of transmission and antiviral treatment. There was no significant change in knowledge in the domains of disease prevention or long-term complications. Only 40% of participants were aware of HBV vaccination and believed treatment Rho was only warranted in the setting of symptoms. There were also no longitudinal

changes in perception and health expectations. Conclusions: Our study has identified important shortfalls in disease specific knowledge including the natural history of CHB infection screening and transmission. We are currently expanding this study to assess additional ways to improve knowledge before first presentation and during the period of engagement in the liver clinic. N HANNAH,1 B HOCKEY,2 D MOORE,2 J LIN,1 D NJOKU,3 A DOYLE,1 F AMICO,1 A GORELIK,4 D LIEW,4 J HALLIDAY,1 AJ NICOLL1 1Departments of Gastroenterology and Hepatology, 2Anaesthetics and Pain Management, 4Melbourne EpiCentre, Royal Melbourne Hospital, Melbourne, Australia, 3John Hopkins Medical Centre, Baltimore, USA Introduction: Volatile anesthetic agents (VA) have a long history of association with liver injury. Modern VA have not been studied and actual incidence is unknown. Retrospective audit suggested an incidence of post-operative transaminitis of 3% due to modern VA. Our aim was to prospectively determine the incidence and risk factors for volatile anesthetic drug induced liver injury (VA-DILI).