7, 8 Epidemiological investigation reveals a high risk association with anal-receptive sexual activity including “fisting”, selleck chemicals suggesting that anal mucosal trauma is a key element of HCV transmission. The reason that the increase in acute HCV among gay men is being seen now remains contentious. Some investigators believe that widespread use of HAART has created a permissive atmosphere reminiscent of 1980s bathhouse behavior, with multiple sexual

exposures in a short window of time. Others do not believe that behaviors have changed, and the perception of increased incidence represents an ascertainment bias. It was suggested that HIV spread in the 1980s was divided into two distinct epidemics: one in MSMs and the other in injection drug users. The MSM spread predominated in the 1980s, and these patients did not have high concomitant rates of HCV infection. Over the years, the risk behaviors of high-risk sexual

activity and injection drug use merged, leading to higher prevalence of HCV in the MSM population and contributing to the current acute HCV outbreaks. Additionally, there is evidence that noninjection methamphetamine use may be associated with cases of acute HCV transmission.9 This hypothesis will need to be studied in more detail and represents an important area of epidemiologic research. The natural history of HCV is altered when HIV is present. We have known for some time that low CD4 counts (<200 cells/mm3) are associated with more rapid progression of hepatic fibrosis, development of cirrhosis, and time to appearance of decompensated these EPZ-6438 chemical structure liver disease.10–13 Recent data suggests that HIV viral load may be an important and independent factor in accelerated disease progression as well. These data are primarily derived from large treatment or observational cohort studies (e.g., SMART, EUROSIDA, GESIDA) which show decreased progression to ESLD when HIV viral loads are low or undetectable.14, 15 Clearly, it is difficult to separate the effect of CD4 from HIV viral load because these are highly related covariates, but study of large cohorts does permit some insight into the

independent effects of these variables. Furthermore, there are biological data regarding the effect of HIV on cells residing in the liver that support the epidemiologic associations. These data are described more fully in the section on Pathogenesis below. Unpublished data presented by Dr. Tuma demonstrated that rates of progression to cirrhosis in a HAART-treated Spanish cohort did not differ significantly from those with HCV alone. Similarly, Dr. Rimland provided data from a cohort in Atlanta, Georgia, indicating that liver-related deaths among HCV/HIV-coinfected patients are decreasing. Taken together, these data suggest a role for effective HIV treatment in HCV/HIV-coinfected patients, but additional supporting data is clearly needed.

‘Declined’ is at least one endoscopist decided NBI is inferior. ‘Unchanged’ is other than above evaluations. Results: Concordance rate of diagnosis by BLI and NBI with microvascular classification was 91.7 %. The preoperative diagnostic rate of depth of invasion was in eight of ten lesions (accuracy rate 80.0%). 50% was improved and 40% was unchanged

in visibility. Only one case was declined by BLI. Conclusion: This study suggested that BLI is equivalent with NBI in the diagnosis of early esophageal cancer. In addition, BLI may have superior visibility compared with NBI. Key Word(s): 1. IEE; 2. BLI; 3. esophageal cancer; Presenting Author: LIANG ZHAO Additional Authors: YI-JUAN DING, HONG-GANG YU, TAO DENG, JUN LIU, HE-SHENG LUO Corresponding Author: LIANG ZHAO Affiliations: Department of Gastroenterology, Renmin Hospital of Wuhan University Objective: To investigate the safety, diagnostic value and clinical impact of double balloon Rapamycin solubility dmso Poziotinib manufacturer enteroscope (DBE) on advanced aged patients and analysis etiological characteristics. Methods: The

clinical data of advanced aged patients underwent DBE in the Department of Gastroenterology in Remin Hospital of Wuhan University from January 2008 to June 2012 were retrospectively analyzed. Results: DBE presents a diagnostic yield of 83.7 %(72/86) and a complication rate of 1.2% (1/86) in 42 advanced aged patients, with clinical impact on 76.2%(32/42) of all patients. The leading causes of OGIB were tumor (53.3%, 11/30) and ulcer (16.7%, 5/30) while angioectasis (6.7%, 2/30) was uncommon. Conclusion: DBE is an ADAM7 effective and safe method for diagnosis of small bowel disease on advanced aged patients. Tumor and ulcer were common causes of OGIB while angioectasis was uncommon. Diagnosis and therapeutic strategy based on those characteristics is worthy of further investigation. Key Word(s): 1. DBE; 2. Aged patient; 3. Small bowel disease; Presenting Author: SHANYU QIN Additional Authors: HAIXING JIANG Corresponding Author: HAIXING JIANG Affiliations: The First Affiliated Hospital of Guangxi Medical University Objective: Cytological smear is widely employed to analyse specimens

obtained from endosonography-guided fine-needle aspiration (EUS-FNA), but false-negative or inconclusive results may occur. A better diagnostic yield can be obtained from processing cell blocks. We compared the effectiveness of the conventional smear cytology, liquid-based cytology (LBC) and the cell block in the diagnosis of pancreatic neoplasms. Methods: From December 2010 to March 2013, 53 patients with pancreatic tumors were evaluated by EUS-FNA. Surgery was performed in 43 cases, and the other 8 patients were followed clinically for an average of 9 months. In total, all patients were evaluated with cytological smears and cell blocks. The EUS-FNA samples of all patients were processed by conventional smear cytology, liquid-based cytology (LBC) and the cell block. Results: Malignant disease was detected in 39 (73.

10% in the control group, P>0. 01) and apoptotic cell death (free drugs 34. 5% vs. MNP-coated drugs 53. 5%, P=0. 001). Conclusions: TMZ and ABT888 can be incorporated simultaneously into MNPs and thus released to an extended degree and gradually, over time. ABT-263 mouse The nanocarriers were able to enter the tumor cells and release both drugs inside them. The apoptotic effect thus induced was greater than that

produced by non-vehiculized drugs. Disclosures: The following people have nothing to disclose: Jose Antonio Munoz-Gamez, Laura Sanjuan, Rosa Quiles, Andrés Barrientos, Julian Lopez-Viota, Josefa León, Angel Carazo, Jorge Casado, Esther-José

Pavón-Castillero, Ana Belen Martin, Angeles Ruiz-Extremera, Javier Salmeron Aim: To describe the clinical features of trimethoprim/sulfamethoxazole (TMP/SMZ) drug-induced liver injury (DILI) among patients enrolled in the Drug-Induced Liver Injury Network (DILIN). Methods: 67 suspected cases of DILI due to TMP/SMZ were identified within 1, 257 patients enrolled in DILIN between 2004 and April 2013. 31 cases were adjudicated and scored as definite (> 95%), highly likely (75% – 95%) or probable (50%-74%). Results: Table 1 depicts clinical features. Patients commonly presented with immuno-allergic signs/symptoms (fever, rash). Jaundice and abnormal liver enzymes were identified soon thereafter and usually peaked early during the Talazoparib ic50 course of the liver injury with mean peak ALT of 685 U/L, AST 579 U/L, alkaline phosphatase 493 U/L and total bilirubin 13. 7 mg/dL occurring at days

3, 3, 18 and 16, respectively after onset. The pattern of liver injury varied from hepatocellular (11/30, 37%), cholestatic (11/30, 37%) and mixed (8/30, 27%) types. Eight patients (26%) had a history of other drug allergies; 5/30 (17%) had a positive ANA, 7/28 (25%) a positive ASMA, and 5/30 eosinophilia. Injury was typically moderate many to severe and required hospitalization in 77% of cases. Resolution was slow, with most patients remaining symptomatic for more than 4 weeks. Normalization of liver tests took up to 6 months. Of the 27 patients with follow-up available, 7 (26%) still had abnormal serum enzymes or clinical, findings of liver disease beyond 6 months. There was 1 liver-related death; no patient required transplantation. Conclusion: TMP/SMZ hepatotoxicity has a distinct phenotype with a short latency and immuno-allergic features. The pattern of biochemical injury varies but is typically moderate to severe and slow in resolving. Thus, TMP/SMZ remains a common cause of DILI but is rarely fatal.

Results: Gallbladder was enlarged in 35 patients (89 [86-106] mL) and within normal

range in 42 (41 [35-47] mL). Patients with enlarged gallbladders did not significantly differ from others regarding gender (65% vs. 66% males), median age (43 vs. 42 years), time from diagnosis (5 vs. 5.5 years), body mass index (21.6 vs. 23.7), associated inflammatory bowel disease (71% vs. 50%), UDCA treatment (89% vs. 90%), other MRI features including cystic abnormalities (8.5% vs. 12%), clinical or histological parameters of liver disease (Mayo risk score of −0.18 [−0.45-0.27] vs. −0.005 [−0.63-0.56]). Notably, malignancy was less frequent in the group with enlarged gallbladder, occurring in 2 (5.7%) vs. 11 (26.2%) patients with normal gallbladder size (P=0.029). Colorectal cancer in particular was 6.7-fold less frequent, occurring in 1 (2.8%) selleck chemicals vs. 8 (19%) patients (P=0.037, OR=6.7 [0.9- 354])). In patients with enlarged gallbladder, the serum concentrations of secondary bile acids were lower than in other patients (1.6 [1.3-1.9] vs. 2.5 [2-3.1]

μmol/L, P=0.0004). This was true for deoxycholic acid (0.7 [0.5-1] vs. 2.2 [1-6-3] μmol/L, P=0.0001), a secondary bile acid known to promote colon carcinogenesis. Patients in this group also had higher concentrations of primary bile acids (10.5 [6.6-16.7] vs. 4.3 [3.5-5.3] μmol/L, P=0.0001) STI571 molecular weight and of UDCA (44.0 [29.4-52] vs. 27.2 [14.6-31.1] μmol/L, P=0.001). Furthermore, they had higher serum concentrations of the gallbladder-relaxing hormone FGF19 (211.6 [168.6-234.6] vs. 88.6 [72.7-121.6] pg/mL, P=0.0001), NADPH-cytochrome-c2 reductase which concentration was correlated with gallbladder volume (R2=0.46, P=0.001) Conclusion: Gallbladder is enlarged in approximately half of PSC patients, which can be caused by increased FGF19 levels, and which is associated with a lack of secondary bile acids, enhanced UDCA enrichment and a lower prevalence of colorectal cancer, consistent with protective properties of gallbladder enlargement in PSC. Disclosures: Olivier Chazouillères – Consulting: APTALIS, MAYOLY-SPINDLER The following

people have nothing to disclose: Mourad Aissou, Lionel Arrivé, Dominique Rainteau, Sara Lemoinne, Astrid Donald D. Kemgang Fankem, Delphine Firrincieli, Nicolas Chignard, Christophe Corpechot, Chantal Housset [Background and Aims] Although it is well established that treatment with ursodeoxycholic acid (UDCA) improves long-term outcome in patients with primary biliary cirrhosis (PBC), it is still uncertain whether “early” PBC, with normal or low ALP levels and at early histological stages, would benefit from UDCA treatment. In Japan nationwide surveys for PBC have been performed every three year since 1980, and so far clinical data of 7,376 cases have been accumulated. In the current study we examined the long-term outcome of asymptomatic PBC patients with normal or low ALP and at early histological stages in whom UDCA treatment was not initiated.

Because cancer-related genes associated with cellular proliferation steadily increased, those associated with cell-cycle checkpoint control and cell-type specification were down-regulated. This indicates that patients with progressive liver disease experience a loss of differentiation and checkpoint cell-cycle arrest, consistent with the concordant gradual increase in proliferative capacity. This also suggests a mechanism by which chronic HCV infection contributes to tumorigenesis of hepatocellular

carcinoma (HCC). The SVD-MDS method used in the analysis presented in Fig. 2G-J and Supporting Fig. 1G-J allows the computation of two additional parameters aside from Kruskal stress (i.e., information loss during dimensionality reduction): external isolation (i.e., the arithmetic average intergroup Staurosporine price distance) Ensartinib nmr and internal cohesiveness (i.e., the intragroup distance). Both parameters determined for the analyses peak 3-6 months post-OLT (Fig. 4A), indicating that the signatures derived from these time categories generate the relative maximal resolution. Hence, the early stages

of HCV reinfection best characterize overall clinical outcome. We then used the time-specific analysis to define a gene-expression pattern-based distance measure between any of the individual groups and with combined G2345 and G345, as well as G45 longitudinal analysis. To investigate severe liver disease progression according to time and patient outcome, these measures were then subjected to k-means clustering13 using intergroup distances as additional constraints. This analysis indicates the existence of a common precursor

state (G345) for all progressor groups (Fig. 4B, red), from which all three adverse outcomes split individually. This precursor state is comprised of 35 DEGs (Table 2), which distinguish the transformation to a progressive disease outcome long before histological or clinical evidence of severe disease. In the Palmatine absence of time-resolved samples from healthy, non-HCV patients, we were not able to determine whether a common G2345 (Fig. 4B, black) state exists or how this hypothetical intermediate state would relate to G2 and G345. More important, the predicted common G345 precursor state confirmed our observation that eventual severe liver disease is programmed early post-OLT, and in combination with the time-specific analyses described above, identified DEGs distinguishing progressors and nonprogressors within 6 months of transplantation. Using IPA, we generated a network of directly interacting molecules based on the network analysis of the transitional signature and the G345e time-specific gene sets (Fig. 4C and Supporting Fig. 2). We confirmed that repression of genes involved in cell-cycle regulation and stress responses (e.g., cyclin D1 and X-box-binding protein), innate immunity (e.g.

44, P < 0.0001). Worsening adipose tissue IR was not Protein Tyrosine Kinase inhibitor associated with worsening hepatic steatosis (Q1: 2.1 ± 0.2; Q2: 1.8 ± 0.2; Q3: 2.1 ± 0.1; Q4: 2.1 ± 0.1; all nonsignificant), consistent with the nonsignificant increase in liver fat by MRS (Table 2). Similarly, necroinflammation was also present, but not different, between Q1 versus Q4, even as patients had more dysfunctional fat (Q1: 2.4 ± 0.2; Q2: 2.8 ± 0.2; Q3: 2.8 ± 0.1; Q4: 2.8 ± 0.1; all nonsignificant). The NAFLD activity score (NAS) was similar across Q1-Q4 groups (Fig. 6A). In contrast, adipose tissue IR played an important role on the severity of liver fibrosis, as suggested when comparing Q3 and Q4 versus Q1 and Q2 (Fig. 6B; P < 0.05). A fibrosis stage 2 or 3 was

present in 18% of subjects in Q1 (3 of 17) and Q2 (5 of 29), compared to stages 2-4 occurring in 30% of Q3 and Q4 patients (P < 0.05). The aim of the present study was to understand the role of dysfunctional adipose tissue on metabolic and histological parameters of obese patients with NAFLD. To this end, we performed in each patient an in-depth metabolic assessment coupled with a liver biopsy. This approach allowed an integrated metabolic and histological evaluation of the liver in relation to adipose tissue in NAFLD and led to the following important clinical findings: (1) MHO subjects with Selleck Daporinad normal insulin-sensitive adipose tissue

do not usually develop hepatic steatosis and have a near-normal metabolic profile; (2) there is a low threshold for the metabolic effects of dysfunctional adipose tissue. Even modest adipose tissue IR rapidly leads to an elevation of liver aminotransferases, dyslipidemia (i.e., high TG/low HDL-C), reduction in plasma adiponectin, marked liver and muscle IR, hepatic steatosis and NASH; and (3) from an histological perspective, adipose tissue IR triggers the development of hepatic lipotoxicity in NASH (also with a rather low threshold), but appears to play less of a role in determining the severity of necroinflammation. In contrast, fibrosis is susceptible to the severity of adipose tissue

IR. Taken together, these observations have significant clinical implications PAK5 to the prevention and treatment of patients with NAFLD. There were major differences in the severity of adipose tissue dysfunction in obese subjects with and without NAFLD for similar degrees of adiposity (i.e., similar BMI and whole body fat). Plasma FFA levels were much higher in patients with NAFLD, despite higher insulin levels, which is indicative of a severe defect in the suppression of plasma FFA by insulin (Table 1; Fig. 1). This observation should shift our focus about the metabolic effect of obesity in NAFLD from the severity of adiposity to the magnitude of adipose tissue dysfunction (i.e., from quantity to quality), a concept explored previously in the fields of cardiovascular risk assessment21-23 and type 2 diabetes mellitus (T2DM),24 but never carefully examined in NASH.

24 Hyperinsulinemia induces hepatic SREBP-1c expression while hyperglycemia stimulates ChREBP activity. These events lead to transcriptional activation of all lipogenic genes including adenosine triphosphate MK-2206 citrate lyase, acetyl-CoA carboxylase, and FAS,25 effectively increasing FAS flux. Because citrate formed in the TCA cycle and shuttled to the cytosol is the primary metabolite required in the production of fatty acids, there is inevitably an increase in demand for this intermediate. Therefore, it is unsurprising that a recent 13C isotopomer

study found a 2-fold increase of hepatic TCA cycle flux in patients with nonalcoholic fatty liver disease.26 Because only pyruvate that enters the TCA cycle through PC produces a net increase in cycle intermediates, whereas pyruvate entering through PDH is restricted to energy production only,27 the elevated PC flux and OAA pool observed in diabetic mice must have also catered

to the increased FAS demand. This agrees with our recent observation in the hypertrophied heart, in which a larger 13C-citrate signal (from increased pyruvate anaplerosis) was recorded.28 Moreover, detection of citrate pool with hyperpolarized [2-13C]pyruvate substrate selleck inhibitor has recently been demonstrated to be feasible in the study of myocardial TCA flux29; therefore, similar measurements in the insulin-resistant liver will undoubtedly aid in validating the hypothesis that an enlarged citrate pool supports FAS. Metformin is used clinically to counter elevated FAS and gluconeogenesis in diabetes, primarily through its activation of adenosine-monophosphate–activated protein kinase.30 In this study, we demonstrated that metformin treatment

leads to reduced HGP by, at least IMP dehydrogenase in part, decreasing PC activity, as well as production of malate and aspartate from pyruvate. The advent of hyperpolarized 13C MRS has enabled visualization of real-time metabolism in the in vivo mouse liver, in particular, the anaplerosis of pyruvate into the TCA cycle. The distinct patterns in downstream metabolite progression suggest that hyperpolarized 13C MRS is sensitive to subtle differences in metabolic conversions. It is worth noting that LDH-, ALT-, MDH-, and AST-mediated conversions are reversible. Therefore, the appearance of lactate, alanine, malate, aspartate, and OAA peaks resulted from the enzyme-mediated exchange of the hyperpolarized 13C label, in which equilibrium is dependent on the concentrations of both substrate and product, as well as the redox potential. Hence, these metabolite signals reflect the concentration of each metabolite that already exists within the cellular environment and in the plasma, rather than net metabolite production.

1A) [15]. Helicobacter canis strains NCTC 12740 (human-origin) [1], NCTC 12739 (dog-origin) [2], MIT 98-0152 (cat-origin) [4], and MIT 99-7633 (rhesus macaque-origin) were analyzed simultaneously ALK inhibitor review for comparison. Sheep-origin H. canis isolates shared the same banding pattern by REP-PCR, indicating clonality, but were distinct from the control strains tested (Fig. 1B). All sheep-origin isolates were catalase, urease, and γ-glutamyl transpeptidase-negative, oxidase-positive, and did not reduce nitrate

to nitrite. Strains from other species shared the same biochemical profile, except that non-sheep strains were γ-glutamyl transpeptidase-positive. Because a previously reported H. canis strain was shown to produce cytolethal distending toxin, all isolates were evaluated for in vitro cytotoxicity. The sheep-origin Selleck Ulixertinib isolates did not induce cellular changes consistent with cytotoxicity. 16S rRNA sequencing and BLASTn analysis confirmed that the three sheep-origin isolates tested shared 99% identity with H. canis. A neighbor joining phylogenetic tree

was constructed based on sequence similarity (Fig. 1C). Sheep-origin H. canis isolates clustered with H. canis strains from other species, but were distinct from other enterohepatic Helicobacter species (EHS) previously isolated from sheep. In addition to H. canis, sheep have been shown to harbor EHS, namely, H. bilis (Flexispira taxon 2) and H. trogontum (Flexispira taxa 4 and 5) [19-21]. Two of these sheep-origin strains were associated with fetal hepatic necrosis and late-term abortion, a phenomenon that was later experimentally reproduced [21-23]. Helicobacter canis has Meloxicam not been associated with a specific ovine disease syndrome, though

interestingly it has been isolated from a dog’s liver with active hepatitis [3]. As no definitive connection has been established, the flock studied here has had several mummified and late-term dead fetuses born to ewes delivering multiple lambs. Also, the flock has historic exposure to dogs and cats. This study identifies sheep as a new and potentially important H. canis reservoir host that could promote direct zoonotic transmission or transmission via dogs or cats. Interestingly, a similar dynamic has been proposed to explain the high H. pylori prevalence in individuals with direct or indirect sheep or sheep dog exposure. Several prior reports showed 98% H. pylori prevalence in Sardinian [24] and Polish [25] shepherds by CagA ELISA and 13C urea breath test. Sheep contact also disproportionately increased H. pylori prevalence odds in Columbian children when measured by 13C urea breath test [26]. These prior studies established sheep as a potential H. pylori reservoir and have fueled speculation that sheep may be a natural H. pylori host species.

Procedures were performed essentially as described.15 Briefly, CD8+ PBMC or peptide-specific this website T-cell lines (0.2 × 106 per well, 96-well plate) were stimulated with peptides in the concentrations indicated in the figure panels in the presence of 50 U/mL human rIL-2 and 1 μL/mL brefeldin A (BD PharMingen). After 5 hours incubation (37°C, 5% CO2), cells from each well were blocked with immunoglobulin G1 (IgG1) antibodies and stained with antibodies against CD8. After permeabilization with Cytofix/cytoperm

(BD PharMingen), cells were stained with antibodies against IFN-γ and fixed in 100 μL CellFIX (BD PharMingen) per well before FACS analysis. When indicated in the figure legends, cells were not directly restimulated with Doxorubicin manufacturer peptide, but with autologous or partially HLA-matched Epstein-Barr virus

(EBV) immortalized B-cell lines that had been loaded with peptide overnight and extensively washed (6×) prior to the 5-hour coculture with the target cells.16 Additional experimental procedures can be found in the Supporting Materials. First, we performed a database analysis and compared the consensus sequence of the NS5B2841-2849 epitope region between the different HCV genotypes. Although the consensus sequences from subtypes 1a and 1b were identical to the described HLA-B27-restricted CD8+ T-cell epitope, the consensus sequences of genotypes other than 1 differed by one, two, or three amino acid residues within the nine amino acid-long epitope

region (Fig. 1A). In Fig. 1B, available sequence data are shown for genotypes 1a (178 sequences), 1b (242 sequences), and 3a (163 sequences), which are the most frequent subtypes world-wide and for which not sufficient sequence data are currently available. Although the epitope region was conserved within a given genotype, genotype 3a sequences differed by three amino acids from the genotype 1 consensus sequence. Interestingly, the consensus sequence of genotype 3a reflects the possible escape variants observed in genotype 1. The HLA-binding positions are identical in both genotypes; however, different combinations of the A284lV, I2844V, and L2845M substitutions are frequently observed in sequences from HLA-B27-positive genotype 1-infected subjects.6, 13, 17 The above results raised the possibility that sequences from genotype 3a (and probably also the remaining HCV genotypes other than 1) may not be recognized by CD8+ T cells specific for the genotype 1 epitope region. To address this issue, we generated cytotoxic T lymphocyte (CTL) lines from nine HLA-B27+ patients infected with HCV genotype 1 (two patients with acute-resolving infection, two patients with spontaneously resolved infection, and five patients with chronic infection) through two rounds of peptide stimulation with the genotype 1 consensus NS5B2841-2849 peptide (ARMILMTHF).

If biliary complications develop at a younger age, they are less likely to be successfully treated by non-surgical approaches. Disclosures: The following people have nothing to

disclose: Nicholas Fidelman, Andrew Lee, Robert Kerlan, John P. Roberts Purpose: Although the Milan criteria have been accepted as standard selection criteria for liver PD0325901 transplantation (LT) candidates with hepatocellular carcinoma (HCC), many transplant centers have accepted some extended criteria and focus on the patient selection. The purpose of this study is to evaluate whether neurtophil-lymhocyte ratio (NLR) and C-reactive protein (CRP) predict survival of patients with HCC who undergo LT. Methods: From October 2000 to November 2011, 224 patients underwent living donor liver transplantation (LDLT) for HCC at our institution. Results: Akt inhibitor 37 patients (16.5%) experienced HCC recurrence during the study period. The 5 yrs disease free survival (DFS) and overall survival (OS) were 81.6% and 76.6% respectively. In multivariate analysis, DFS and OS were significantly related to AFP > 100 (P=0.017, P=0.048), maximal tumor size > 5cm (P<0.001, P=0.001), NLR >6 (P=0.049, P=0.003),

CRP >1.0 (P=0.010, P<0.001). The patients with NLR <6 or CRP <1.0 were significantly better DFS and OS than the patients with NLR >6 or CRP >1.0, especially in beyond Milan criteria group. The scoring system with NRL and CRP were correlated with prediction of DFS and OS. Conclusion: Preoperative NLR and CRP are useful biomarkers for predicting DFS and OS, especially in beyond Milan criteria. Combined with the Milan criteria, NLR and CRP may be new selection criteria for LDLT candidates with HCC. Disclosures: The following people have nothing to disclose: Dong Goo Kim Background. There are no studies measuring the impact of tumor morphological staging, microvascular

invasion (mVI), and model-for-end-stage-liver-disease (MELD) score on the benefit of liver transplantation (LT) over hepatic resection (HR) for hepatocellular carcinoma (HCC). Methods. Exclusion criteria: very large (>10 cm) tumours, macrovascular invasion and extra-hepatic metastases. Study population: 1106 HCC cir-rhotic ALOX15 patients undergoing HR from one Eastern (n=424) and two Western (n=682) surgical units. We identified 3 tumor stages: I (within Milan, n=806), II (beyond Milan within Up-to-7, n=123), III (beyond Milan and Up-to-7, n=177). Patient survival observed after HR by proportional hazard regression model was compared to that predicted after LT by the Metroticket calculator. The benefit obtainable from LT compared to resection was analyzed in relationship with staging, mVI, and MELD using Monte Carlo simulation. Results. MELD score had the most important effect on transplant benefit independently form tumor characteristics: mean 5-year LT benefit was −2.22 months (95% CI, −2.45 – −1.98) for patients with MELD score < 10, and 6.32 months (95% CI, 6.08–6.