It is frequently associated with the metabolic syndrome (MS). Nonalcoholic fatty liver disease can progress to cirrhosis and/or carcinoma hepatocellular (HCC). The objectives of this study are to compare the presentation, treatments, evolution

of HCC regardless of the underlying liver disease, whether viral, alcohol-related or related to metabolic syndrome as the only factor risk. Methods: From 01/2005 to selleck chemical 12/2012, 452 patients meeting these criteria were admitted to our unit for the management of HCC (Virus n = 196, Alcohol n = 173, metabolic syndrome n = 83). Results: Cirrhosis click here was more frequently associated with viral or alcoholic etiology (p 50 mm (p p = 0.27) probably due to the size of resected tumors in the metabolic syndrome group. Conclusion: HCC associated with metabolic syndrome as the only risk factor are the third cause of primary malignant liver tumors in this series. They have distinct characteristics with a non-cirrhotic liver development and more unique macronodule, which allow more frequently surgical resection. But comorbidities related to the MS and

the large size of lesions involved in relapse, should be taken into account. Response and tolerance

to non-surgical treatments (TACE or Sorafenib) appears similar to other etiologies. Given the frequency of metabolic syndrome in our population, patients at risk should be clearly better defined. Key Word(s): 1. hepatocellular carcinoma nonalcoholic fatty liver disease liver cirrhosis surgical resection TACE Presenting Author: XAVIER ADHOUTE Additional Authors: GUILLAUME PENARANDA, PAUL CASTELLANI, HERVE PERRIER, GAELLE LEFOLGOC, GUILLAUME CONROY, JEAN PIERRE BRONOWICKI, MARC BOURLIERE, JEAN LUC RAOUL Corresponding Author: XAVIER ADHOUTE Affiliations: Alphabio Laboratory, Hôpital Saint-Joseph, Hôpital Saint-Joseph, Hôpital Saint-Joseph, Hôpital De Brabois Cytidine deaminase Chu Nancy, Hôpital De Brabois Chu Nancy, Hôpital Saint-Joseph, Oncology Objective: HKLC is new staging system with treatment guidelines determined from a large cohort of B virus-related HCC (80%), treated or not, aimed to improve the prognostic classification for HCC, using surgery in subsets of intermediate and advanced HCC (Yau T and al. Gastroenterology 2014; 146). This score includes the following prognostic factors: tumor size, number, vascular invasion, distant metastases, patient performance score (ECOG PS) and liver function.

Pharmacies situated in Gothenburg, Sweden, were selected based on a list from the Medical Products Agency. A request for participation was made to the regional managers of the six largest pharmacy companies in Gothenburg. One of the regional managers did not respond, which resulted in 53 eligible pharmacies from 5 pharmacy companies. Every pharmacy manager was asked for permission

to distribute the questionnaire to their staff, through an e-mail giving information learn more about the study. Two declined participation, 5 were excluded because of no response at all from the pharmacy manager, and an additional 2 were excluded because of too few, ie, 1 or 2, employees. After approval, all pharmacy managers were e-mailed regarding a contact person at the pharmacy and a suitable date for distribution of the questionnaire. The study subjects included all pharmacy staff with permission to give advice to customers on OTC medication (pharmacists, dispensing pharmacists, pharmacy technicians, and other counseling staff). Pharmacists

have a master of science degree (5 years of university education), and dispensing pharmacists have 2–3 years of university education. Pharmacy technicians have 1–2 years of vocational training. Other counseling staff have a few weeks’ internal counseling training, conducted through educational CP-868596 in vitro programs implemented by the different pharmacy companies. Responsibilities differ among the different professional categories, where pharmacists and dispensing pharmacists are the only ones who have permission to dispense prescription medications.

Data were collected during the fall of 2012. A total of 326 questionnaires were distributed. The questionnaires were distributed together with response envelopes and participant information, 1 per counseling staff member at each pharmacy. The questionnaires were placed in each staff member’s personal compartment at the pharmacy or given to the contact person at the pharmacy. In addition, a box for anonymous collection of completed questionnaires was left at every pharmacy in a suitable place. After 2 weeks, new questionnaires were distributed to each pharmacy as a reminder for those who had not yet responded. The questionnaires were anonymous, selleck chemicals llc and no single response could be identified, nor could the pharmacy company be identified. Hence, no information was collected for non-responders. The study protocol was approved by the Regional Ethical Review Board in Gothenburg (registration number 531-11). The questionnaire included background questions on sex, age, and professional category, number of years since graduation/completed education, and number of years working in a pharmacy. Pharmacy technicians and other counseling staff were merged into one group called “counseling staff.

Median APRI at entry were similar (0.53 vs 0.49 vs 0.50) in those who reported no THC use,

log HCV RNA [HR 1.3 (1.10-1.54) p=0.002] and log HIV RNA [HR 1.14 (1.02-1.29) p=0.03] at entry were associated with progression to severe fibrosis; higher Kinase Inhibitor Library nmr CD4+ count [per 50 cells HR 0.96 (0.93-0.98) p<0.0004] was associated with lower fibrosis; whereas cumulative alcohol use [risk per 1 drink increase per week [HR 1.03 (1.02-1.04) p<0.001] was associated with greater risk of progression at follow-up. In multivariate analysis, entry APRI, HCV RNA, CD4+ count and cumulative alcohol use remained significant. Cumulative THC use was not independently associated with a greater risk of fibrosis progression [HR 1.00 (95% CI 0.996-1.003)] even in those with moderate fibrosis at entry [HR 1.00 (95% CI 0.995-1.005)]. CONCLUSION In this large cohort of HCV/HIV co-infected women, THC use was not associated with liver fibrosis progression. Prospective collection of cumulative alcohol and THC use provided granular data to associate with predictors of liver fibrosis. Interestingly, alcohol https://www.selleckchem.com/products/CP-690550.html use was strongly associated with

THC use and independently associated with liver fibrosis, and may better predict fibrosis progression in HCV/HIV co-infected women. Disclosures: Phyllis Tien – Advisory Committees or Review Panels: BMS; Consulting: Genentech Marion G. Peters – Advisory Committees or Review Panels: Janssen; Consulting: Merck; Employment: Hoffman La Roche -Spouse The following people have nothing to disclose: Erin Kelly, Jennifer L. Dodge, Monika Sarkar, Audrey Tau-protein kinase French, Marshall Glesby, Elizabeth T. Golub, Michael Augenbraun, Michael Plankey Introduction: On-treatment HCV RNA measurements are crucial for the prediction of a sustained virological response (SVR) and

to determine treatment futility during several direct antiviral-based HCV triple therapies. In patients with advanced liver disease an accurate risk/benefit calculation based on reliable HCV RNA results can reduce the number of serious adverse events as well as save costs. However, currently recommended treatment algorithms are based on a single HCV RNA assay that is rarely used in clinical practice. The different available HCV RNA assays vary in their diagnostic performances, which may have important clinical implications. Aim: To investigate the clinical relevance of concordant and discordant HCV RNA results of the two most widely used HCV RNA assays during triple therapy with boceprevir and telaprevir in patients with advanced liver fibrosis/cirrhosis.

We retrieved all published case reports of cancer-associated FVIII auto-antibodies from PubMed for the period 1950–2010. The search Kinase Inhibitor Library cell assay in the literature revealed 13 patients in whom

a FVIII inhibitor developed after uncomplicated surgery for cancer and a bleeding-free time interval of up to 6 months; 11/15 patients had abdominal cancers (five colon cancer, four pancreatic cancer, gastric cancer and choledochus carcinoma one each). The median time period between surgery and antibody detection was 3 months (1 week–6 months). In most cases, the antibody titre was low (median: 14 BU mL−1, range: 1.7–64 BU mL−1). Immunosuppressive treatment was successful in most of the cases – nine of the treated patients reached a sustained CR of the antibody after a median time of 3 months. Postoperative paraneoplastic FVIII inhibitors may be regarded as a special, not yet recognized subgroup of acquired FVIII antibodies. They share some characteristics with postpartum FVIII inhibitors with regard to the latency period between the triggering event and the appearance of the antibody, and between the usually low antibody titres

and their GPCR Compound Library good response to immunosuppressive treatment. “
“Summary.  Inhibitory antibodies to exogenous FVIII/FIX are a major complication of haemophilia treatment. Up to 30% of previously untreated patients (PUPs) with severe haemophilia A develop inhibitors, most likely during the initial 50 exposure days to concentrate. In addition to classical cohort studies, a European monitoring system (EUHASS) has been set up to evaluate inhibitor development in PUPs. The present study addresses the reliability of estimating the cumulative incidence of inhibitor development in this registry. Data from the retrospective CANAL cohort study, including 288 PUPs with severe haemophilia A and complete

treatment records until the 50th exposure to FVIII, were used to simulate the consequences of several cross-sectional sampling techniques Tau-protein kinase on the estimated incidence of inhibitors. Both mathematical calculus and computer modelling were applied to study the effects of sample size and the introduction of a new product. For existing concentrates, both longitudinal cohort study methods and the EUHASS method yielded similar estimates of the cumulative incidence of inhibitor cases over a 5-year time period: 27.9% (95% CI: 21–36) vs. 29.4% (22–38). For a newly introduced concentrate, a reliable estimate of inhibitor incidence with the EUHASS method could only be made after 3–4 years, even in large datasets. The results from EUHASS in inhibitor incidence in PUPs are expected to be valid. After introduction of a new concentrate, the inhibitor incidence on this concentrate can only be reliably determined after an observation period of several years. “
“Inhibitors are a rare but serious complication of treatment of patients with haemophilia.

rhKD/APP

has activity of the Kunitz of serine protease inhibitors. It is known to inhibit proteolysis of kallikrein, plasmin and trypsin. The role of rhKD/APP has always been considered to be due to the inhibition of the exocrine pancreatic secretion in order to reduce pancreatic autodigestion and was deeply investigated. In the meanwhile rhKD/APP can inhibit cytokines and inflammation, it play a therapeutic and preventive role in AP. Methods: We use the model of ANP which is induced by injection of sodium deoxycholeaye solution into the main pancreatic duct of rats. Amylase and lipase activity were assayed and histopathological LY2606368 ic50 changes were observed after treatment with rhKD/APP. We observe the therapeutic and prevent effect of rhKD/APP on acute pancreatitis in rats. Results: Compared with the model group, RhKD/APP markedly inhibited Amylase and Lipase avtivity and ameliorated histopathological changes of on acute necrosis pancreatitis. Conclusion: Whereas the role of rhKD/APP in the pathogenesis of AP still need discussion. Key Word(s): 1. FDA approved Drug Library ic50 rhKD/APP; 2. pancreatitis; 3. rat; 4. pathophysiology; Presenting Author: JUNFENG XIE Additional Authors: PING XU Corresponding Author: JUNFENG XIE Affiliations: THE PEOPLE’S HOSPITAL OF GANZHOU CITY; Songjiang Branch of Affiliated First people’s Hospital of shanghai jiaotong University Objective: To study the role of NF-κB and Caspase-3 in the pathogenesis of acute pancreatitis-associated

lung injury (APALI) in rats, and the effect of pioglitazone, a ligand of peroxisome proliferator-activated receptor gamma, on these factors. Methods: A total of 54 Sprague Dawley rats were randomly and averagely divided into 3 groups, named group A, C and T. Group A and C served as SAP model and sham operation group, respectively. The rats in group T were treated with pioglitazone, an agonist of peroxisome proliferator activated receptor. The modified Li Qing-hua’s method was used to

reproduce serve acute pancreatitis (SAP) models, The histopathological changes of pulmonary tissues were examined by microscopy. The activity of myeloperoxidase (MPO) in pulmonary tissues were measured. The expression of pulmonary NF-κBp65 and Cleaved-Caspase 3 were determined by immunohistochemical staining (ABC). Results: The histological Meloxicam examination revealed intensively inflammatory response in pulmonary tissues after SAP model was induced, but inflammatory response was alleviated in group T. The activity of MPO in group T were significantly decreased compared with group A. The activity of NF-κBp65 in group A was markedly upgraded compared with group C at all pionts (P < 0.01), which was decreased significantly in group T compared with group A at 6 h (P < 0.05). The lung expression of Cleaved-Caspase 3: The activity of Cleaved-Caspase 3 in group A and group T was markedly upgraded compared with group C at all pionts (P < 0.

2 It is therefore evident that the presence of a risk factor is not a sufficient determinant of disease. Most researchers would deduce that fatal or drastic diseases based on genetic variation, in addition to those based on lethal mutations, are eliminated by natural selection on the long road of human evolution. Therefore, for the discovery of genetic variations showing a strong association with phenotype, the most effective research objective is directed GSK3235025 at patients treated with curative medicines that target that host factor. These drugs can be made with small molecular weight chemicals, human antibodies, or they can be obtained from natural products, modified to bring out the positive

effect against disease. Because human beings have not been under selective pressure of these medicines since recorded history, their contemporary pressure will reveal the fine results associated with clinical response to drug treatment. Based on this theory, we have started to discover genetic variations associated with response to chronic hepatitis C treatment using pegylated interferon and ribavirin. The SNPs obtained from whole genome analysis were reported by a number of research groups simultaneously in 2009

and many related studies have been uploaded to September 2011. The aim of Ruxolitinib this review is to summarize the relationship between genetic variation and hepatitis C infection. Since 2001, the standard of care for patients with chronic hepatitis C has been the combination of pegylated interferon (PEG-IFN) and ribavirin (RBV).3,4 This combination has produced sustained virologic response (SVR) rates of 50% to 60% in patients infected with hepatitis C virus (HCV) genotype 1 who adhere to the recommended therapeutic regimen, and 40% in intention-to-treat populations, as defined by an HCV RNA negative after 6 months of completing therapy (SVR). Transient viral response (TVR) is defined as re-appearance either of HCV RNA in serum after treatment has been discontinued in a patient who had undetectable HCV RNA during the

therapy or on completion of the therapy (Fig. 1).3,4 In all, only about 65% of patients become HCV RNA-undetectable when treated with this regimen;3–5 the remaining one-third of all treated patients are classified as nonresponders (NR). Some of these patients have relatively mild liver disease but may have symptoms of HCV viremia, while others have advanced fibrosis and are at risk for developing liver complications, including decompensated cirrhosis and hepatocellular carcinoma, and the requirement for liver transplantation. Current therapies are limited by expense, ineffectiveness in a relatively high proportion of patients, numerous side effects, some of which are severe or which cause dose reduction and/or premature termination of treatment.

3A). Ethanol-fed HIF1dPA mice had the highest LW/BW ratios (P < 0.05 versus HIF1dPA pair-fed mice). Examination of liver triglycerides in whole-liver extracts revealed that alcohol caused an up-regulation of triglyceride in hepatic extracts in

control mice at 4 weeks (Fig. 3B). Triglyceride levels were higher in pair-fed HIF1dPA mice versus pair-fed control mice (P < 0.05, VX-770 research buy HIF1dPA pair-fed versus Alb-Cre pair-fed) indicating an effect of constitutive HIF-1α on lipid accumulation in the absence of any other stimulus. Alcohol-fed HIF1dPA mice had the highest average hepatic triglyceride content (P < 0.05 versus all other groups). The presence of HIF1dPA transgene also led to serum ALT levels comparable to Alb-Cre ethanol-fed mice (Fig. 3C). Histopathology analysis also confirmed that ethanol-fed HIF1dPA mice had more lipid vacuolization than ethanol-fed Alb-Cre mice (Fig. 3D). These results suggested that constitutive HIF1 activation in hepatocytes (HIF1dPA CFTR modulator mice) results in liver abnormalities reminiscent of ALD and that alcohol feeding and constitutive HIF-1 activation cooperatively up-regulated

hepatic steatosis. Because our findings suggested an effect of hepatocyte-specific HIF-1α expression on lipid accumulation, we sought to test whether elimination of HIF-1α activity in hepatocytes could ameliorate the pathology associated with chronic ethanol feeding. We used a mouse engineered by Johnson and coworkers11 where native HIF-1α is flanked by LoxP sites, and coexpression of Cre recombinase results in tissue-specific deletion of HIF-1α. Analysis of mice with hepatocyte-specific deletion of HIF-1α and controls maintained on the ethanol diet revealed increased LW/BW ratios in WT ethanol-fed mice versus control mice at 4 weeks. In contrast, HIF-1α(Hep−/−) mice showed no significant difference in LW/BW ratio between pair-fed and ethanol-fed groups (Fig. 4A). Consistent with the role of HIF-1α in hepatocyte steatosis, HIF-1α(Hep−/−) mice were old protected from the increase in liver triglyceride content observed in WT mice after

alcohol feeding (Fig. 4B). WT mice showed a robust cooperative up-regulation of serum ALT with chronic ethanol and LPS challenge (P < 0.02, WT ethanol/LPS versus WT pair-fed). In contrast, HIF1α(Hep−/−) mice were protected against serum ALT increase, even in the presence of chronic ethanol and LPS (Fig. 4C). Next, we performed immunoblotting on nuclear extracts from WT and HIF-1α(Hep−/−) mice. Ethanol feeding resulted in a significant increase in HIF-1α expression in nuclear extracts prepared from WT mice (Fig. 4D). In contrast, nuclear extracts from HIF-1α(Hep−/−) mice had very low levels of HIF-1α expression, and no further up-regulation with ethanol feeding was observed, confirming suppression of HIF-1α signaling in our mouse model (Fig. 4D,E).

Additional details are provided in the Supporting Information. HEK293T, Chinese hamster ovary, Buffalo rat liver, Huh7, Huh7.5-GFP, and Huh7.5.1 cells were cultured as described.18, 23-25 Primary human hepatocytes were isolated as described.18 Chinese hamster ovary and Buffalo rat liver cells expressing SR-BI were produced as described.11, 15, 23 Polyclonal15 and monoclonal antibodies (mAbs) directed against the extracellular loop of SR-BI were raised by genetic immunization of Wistar rats and

Balb/c mice as described15 according to proprietary technology (Aldevron GmbH, Freiburg, Germany). Anti–SR-BI mAbs were purified using protein G affinity columns and selected via flow cytometry for their ability to bind to human SR-BI.15 To determine the affinity of the anti–SR-BI mAbs for human SR-BI, Huh7.5.1 cells were incubated

with increasing concentrations of mAbs, and binding was assessed using Selleck Dasatinib flow Doxorubicin cost cytometry. Kd values were determined as half-saturating concentrations of the mAbs.26, 27 Antibodies will be provided on request using a material transfer agreement (MTA). Anti-CD81 (JS-81), anti–SR-BI (CLA-1), and phycoerythrin-conjugated anti-mouse antibodies were from BD Biosciences. Anti-His and fluorescein isothiocyanate–conjugated anti-His antibodies were obtained from Qiagen, rabbit anti-actin (AA20-30) antibodies were obtained from Sigma-Aldrich, and mouse anti-NS5A antibodies were obtained from Virostat. Anti-E1 (IGH520, IGH526, Innogenetics), anti-E2 (IGH461, Innogenetics; AP33, Genentech; CBH23, a kind gift from S.K.H. Foung), and patient-derived

anti-HCV immunoglobulin G (IgG) have been described.16, next 25, 27 Luciferase reporter cell culture-derived HCV (HCVcc), HCV pseudoparticles (HCVpp), murine leukemia virus pseudoparticles, and vesicular stomatitis virus glycoprotein pseudoparticles (VSV-Gpp), infection and kinetic experiments have been described.15, 18, 25, 27, 28 Unless otherwise stated, HCVcc experiments were performed using Luc-Jc1, and infection was analyzed in cell lysates via quantification of luciferase activity.29 For combination experiments, each antibody was tested individually or in combination with a second antibody. Huh7.5.1 cells were preincubated with anti–SR-BI or control mAb for 1 hour and then incubated for 4 hours at 37°C with HCVcc (Luc-Jc1) or HCVpp (P02VJ) (preincubated for 1 hour with or without anti-envelope antibodies). Synergy was assessed using the combination index and the method of Prichard and Shipman.30-32 Cell viability was assessed using a MTT test.2 Recombinant His-tagged soluble E2 (sE2) was produced as described.23 Huh7.5.1 cells were preincubated with control or anti–SR-BI serum (1:50), anti–SR-BI or control mAbs (20 μg/mL) for 1 hour at room temperature, and then incubated with sE2 for 1 hour at room temperature. Binding of sE2 was revealed using flow cytometry as described.18, 23 Huh7.5.

As shown in Fig. 4B, knocking down AR with siRNA in the AR+/y primary cultured HCC cells enhanced cell migration, and addition of AR in L-AR−/y primary cultured HCC cells AZD6738 order reduced cell migration. As knockdown of AR also increased migration, but not cell mobility, in SKAR+ human HCC cells (Fig. 4C; Supporting Fig. 2C), we further examined MMP9 messenger RNA (mRNA)/protein expression in the SKAR+ cells and found that the addition of DHT reduced MMP9 mRNA and protein expression (Fig. 4D). As an early study suggested that prostate epithelial AR could suppress MMP9 expression by way of modulation of NF-κB activity,29 we examined NF-κB expression in the mice HCC.

Indeed, our data showed loss of hepatic AR led to higher expression/activation of NF-κB in 60-week-old livers (Fig. 4E). Mechanistic INK 128 in vitro dissection revealed that AR could suppress the tumor necrosis factor alpha (TNF-α)-induced NF-κBRE-luciferase activity29, 30 and MMP9 promoter-luciferase activity in SKAR+ human HCC cells (Fig. 4F). Together, the results from Fig. 4, Supporting Fig. 2B,C suggest that hepatic AR could also function through the NF-κB-MMP9 pathway to modulate cell migration ability to suppress HCC metastasis. With the contradictory AR functions (tumor initiation versus migration/anoikis) taken into

consideration in HCC therapy, we hypothesized that applying current molecular targeting agents (suppressing cell growth and migration) combined with the addition of AR (suppressing cell migration and anoikis) might benefit the current

PI-1840 therapeutic paradigm. As the above results demonstrated that AR could play negative roles on HCC metastasis, we were encouraged to determine if we could enhance the therapeutic efficacy of HCC survival by targeting hepatic AR. Sorafenib (Bayer), a molecular target agent that has passed phase III clinical trials by way of targeting multiple kinases, yet has higher median inhibitory concentration (IC50) on p38,31 has been applied to treat advanced HCC patients with some benefits and fewer complications.32 We first titrated the sorafenib dose in human SKhep1 HCC cells and found 5 μM of sorafenib had a moderate cytotoxicity effect during 2 days treatment (Fig. 5A). Using this dose, we found sorafenib reduced ERK phosphorylation (pERK) significantly, yet had little influence on p-p38 (Fig. 5B, lane 3 versus 1). However, adding AR with 5 μM of sorafenib resulted in abolished p-p38 (Fig. 5B, lane 4 versus 2). Furthermore, we found that sorafenib treatment alone could enhance cell anoikis and reduce cell migration in the SKhep1 cells (Fig. 5C,D, lane 2 versus 1), and addition of AR alone could also enhance SKhep1 cell anoikis and suppress SKhep1 cell migration (Fig. 5C,D, lane 3 versus 1). As expected, the combination treatment of adding AR plus sorafenib resulted in additive enhancement of cell anoikis and suppression of migration (Fig. 5C,D, lanes 4 versus 3).

This polymorphism is also associated with more severe disease as determined by MELD score on the day of admission. Disclosures: The following people have nothing to disclose: Alison Jazwinski,

Amit Raina, Charles Gabbert, Shahid M. Malik, Michael O’Connell, David C. Whitcomb, Jaideep Behari Aim: to compare efficacy and safety of Budesonide and Pred-nisolone in treatment of acute alcoholic hepatitis (AAH). To determine predictors of non-response, predictors of short-time mortality. Methods: 35 patients with AAH were enrolled 3-deazaneplanocin A nmr in the prospective trial and randomised in 2 groups. Group 1: 15 patients (7 men, 8 women), average age 46,53±11,01. Median alcohol daily intake – 77 g., lower and upper quartiles – 55 and 96 g. Duration of alcohol intake – 13,41+8,55 years. Discriminant function (DF) average value was 65,22 (from 37,2 to 145,4). Group 2: 20 patients (16 men, 4 women), average age 46,5±11,89. Median alcohol daily intake – 70,55 g., lower and upper quartiles – 37 and 88 g. Duration of alcohol intake – 16,85+13,32 years. The average value of DF – 58,11 (from 32,1 to 121,7). Groups were comparable in key features. In group 1 Budesonide was prescribed 9 mg/daily per os. In group 2 – Prednisolone 40

mg/daily per os. Treatment duration was 28 Daporinad days. Response criteria – Lille model. Statistical analysis was performed using SPSS 17.0 statistical package (chi-squared, Mann-Whitney and Wilcoxon tests, Kaplan-Meier method and Cox regression model).

Results: Efficacy (p = 0,810) and short-term survival (p = 0,857) in budesonide group are equal to prednisolone group. In group 2 adverse events (infections, hepatorenal syndrome, hyper-glycemia, upper gastrointestinal bleeding and Cushing’s syndrome) were statistically more frequently than in group 1: 70% vs. 26,7% (p = 0,011). Hepatorenal syndrome occurred more frequently in group 2 (p = 0,033). Predictors of non-response are MELD score (p=0,009), ABIC score (p=0,011), hepatic encephalopathy level (p=0,035), total bilirubin level (p=0,016). Predictors of mortality are Lille score (p=0,018), serum glucose level (p=0,017), total bilirubin level at the 7th day of the therapy (p=0,030). There is a positive PD184352 (CI-1040) correlation between BMI and absence of therapy response (correlation coefficient 0,519 ) and short-time mortality (correlation coefficient 0,630). Conclusions: Short-time survival in budesonide group is equal to prednisolone group, so budesonide can be used in treatment of this disease. According to the data resulting from the study budesonide is the drug of choice in patients with concomitant infections, hepatorenal syndrome and glucose intolerance. Disclosures: The following people have nothing to disclose: Inna Komkova, Marina V. Maevskaya, Vladimir T.