Saffron also blocked the depletion in the number of cells positive for TUNEL (terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling) and M30 CytoDeath in liver tissues of DEN-treated rats. In vitro experiments carried out using HepG2 cells also confirmed these findings and showed inhibition of

nuclear factor-kappa B activation, increased cleavage of caspase-3, www.selleckchem.com/products/XL184.html as well as DNA damage and cell cycle arrest upon saffron treatment. Conclusion: This study provides evidence that saffron exerts a significant chemopreventive effect against liver cancer through inhibition of cell proliferation and induction of apoptosis. This report also shows some evidence that saffron protects rat liver from cancer via modulating oxidative damage and suppressing inflammatory response. (HEPATOLOGY 2011;) Hepatocellular carcinoma (HCC) is the fifth most common cancer and the third leading cause of cancer mortality in the world. Chronic infection with hepatitis B Doxorubicin order and C are the major risk factors for HCC worldwide. Other factors that contribute to the formation of HCC include exposure to environmental carcinogens, iron overload, fatty liver disease, and alcohol abuse.1 Diethylnitrosamine (DEN) is one of the most important environmental carcinogens and is present in tobacco smoke, cosmetics,

gasoline, and various processed foods such as milk and meat products.1 DEN is also commonly used to induce lesions in rats that mimic different types of benign and malignant tumors in humans.2 Given the limited treatments available, preventive control approaches have been considered among the best strategies to protect against cancer. Cancer chemoprotection is based on the use of exogenous phytochemicals to enhance endogenous mechanisms against various stages of cancer development.3 Lately, there has been a lot of

interest in exploring the chemopreventive properties of natural herbs and plants. Saffron is a naturally derived plant product from the click here dried stigma of the Crocus sativus flower (family Iridaceae) that may have biologically useful properties. In fact, saffron extract and its biologically active compounds, including crocin, crocetin, carotene, and safranal, have been shown both in vitro and in vivo to possess antioxidant, anticancer, anti-inflammatory, and memory-improving properties.4-6 Saffron is also used in folk medicine as an antispasmodic, antidepressant, and aphrodisiac.4 Furthermore, it is one of the most commonly used species around the world for flavoring and coloring foods.4 Saffron has recently gained considerable interest for its capacity to interfere with cancer at initiation and promotion stages as well as for cancer treatment.

[23] Long-term follow-up studies are currently ongoing to assess whether these variants will be replaced by wild-type sequence. Apparent decay of a daclatasvir-resistant variant was observed in Patient 7,

who relapsed during dual treatment. Clonal analysis revealed that emergent NS5A-Q30E was no longer detected at posttreatment Week LY2157299 chemical structure 48. Interestingly, another resistance variant (NS5A-Y93N) outgrew the original NS5A resistance variant even though it was only first detected at posttreatment Week 36. Since Q30 substitutions linked with Y93N were no longer detected at posttreatment Week 48, NS5A-Y93N may offer a fitness advantage. In conclusion, treatment of prior null responder patients with quadruple therapy (daclatasvir, asunaprevir, and peginterferon alfa-2a and ribavirin)

resulted in all HCV GT1 patients being cured in this sentinel study. Treatment with dual therapy (daclatasvir and asunaprevir) also resulted in all of the GT1b patients being cured, while response rates were significantly lower in GT1a patients. When viral breakthrough occurred in patients infected with HCV GT1a receiving dual therapy, daclatasvir-resistant and asunaprevir-resistant substitutions emerged together. These substitutions were similar to those reported previously. Treatment intensification in patients who experienced virologic breakthrough was capable of providing SVR in a minority of patients despite prior null response to peginterferon alfa-2a and ribavirin. Finally, signature NS5A resistance-associated variants persisted throughout the study, while Neratinib NS3 resistance-associated variants decayed, suggestive of a lower relative fitness cost of NS5A variants. Additional studies will enhance understanding

of HCV treatment with daclatasvir and asunaprevir. We thank the patients for their participation and commitment during the study. We also thank the investigators and contributors learn more from each study site. The authors thank Bing He for involvement in the pharmacokinetic analysis. Professional medical writing and editorial assistance was provided by Carolyn Carroll, PhD, an employee of Bristol-Myers Squibb. Parts of this study were presented at 46th EASL Congress, Berlin, Germany, March 30-April 3, 2011, Oral Abstract 63, and HepDART 2011, Koloa, Hawaii, December 4-8, 2011. Additional Supporting Information may be found in the online version of this article. “
“With the advent of potent antiviral compounds against hepatitis B virus (HBV) with low susceptibility to resistant mutation, the choice of first-line treatment has become quite clear. However, selection of treatment candidates remains less straightforward. As with any clinical circumstance, individual patient management decisions must be based on risks and benefits of treatment.

SVR12 data will be available for all patients on 12 week treatments and EOT data will be available for all patients on 24 week treatments at the meeting. Disclosures: Steven L. Flamm – Advisory Committees or Review Panels: Gilead, Bristol Myers Squibb, AbbVie, Janssen, Salix; Consulting: Merck, Janseen, Bristol Myers Squibb, AbbVie, Salix, Gilead; Grant/Research ABC294640 manufacturer Support: Janssen, Bristol Myers Squibb, Merck, Vertex, Gilead, AbbVie, Boehringer Ingelheim; Speaking and Teaching: Salix Bruce R. Bacon – Advisory Committees or Review Panels: Bristol-Myers Squibb, Kadmon, Janssen; Consulting: Merck, ISIS; Grant/Research Support: Merck, Bristol-Myers Squibb, Kadmon, AbbVie; Speaking and Teaching: Merck, Kadmon,

LGK-974 molecular weight AbbVie, Salix, Janssen Douglas Dieterich – Advisory Committees

or Review Panels: merck, Idenix, Jans-sen ; Consulting: Gilead, BMS Kris V. Kowdley – Advisory Committees or Review Panels: AbbVie, Gilead, Merck, Novartis, Trio Health, Boeringer Ingelheim, Ikaria, Janssen; Grant/Research Support: AbbVie, Beckman, Boeringer Ingelheim, BMS, Gilead Sciences, Ikaria, Janssen, Merck, Mochida, Vertex Eric Lawitz – Advisory Committees or Review Panels: AbbVie, Achillion Pharmaceuticals, BioCryst, Biotica, Enanta, Idenix Pharmaceuticals, Janssen, Merck & Co, Novartis, Santaris Pharmaceuticals, Theravance, Vertex Pharmaceuticals; Grant/Research Support: AbbVie, Achillion Pharmaceuticals, Boehringer Ingel-heim, Bristol-Myers Squibb, Gilead Sciences, GlaxoSmithKline, Idenix Pharmaceuticals, Intercept Pharmaceuticals, Janssen, Merck & Co, Novartis, Presidio, Roche, Santaris Pharmaceuticals, Vertex Pharmaceuticals ; Speaking and Teaching: Gilead, Kadmon, Merck, Vertex Scott Milligan -

Grant/Research Support: Gilead Naoky Tsai – Advisory Committees or Review Panels: Gilead, Vertex; Consulting: BMS, Gilead, Merck; Grant/Research Support: BMS, Gilead, Genentech, Vertex, Novartis, GSK, Bayer, Abbvie, Janssen, beckman; Speaking and Teaching: BMS, Gilead, Genentech, Vertex, Merck, Salix, Bayer, Janssen The following people have nothing to disclose: Zobair Younossi BACKGROUND: The optimal antiviral therapy for HCV infection in HD patients remains to be established. There are no data on the use of new direct-acting antiviral agents in patients with end-stage this website renal disease on HD but studies are ongoing. Safety and efficacy data of IBT in KT recipients with non functional grafts on HD are scarce but case reports have shown a high risk of graft intolerance syndrome of the failed kidney allograft in HD patients treated with IBT. AIMS: 1) To evaluate the efficacy and safety of IBT in KT recipients with failed kidney allograft on HD. 2) To compare the risk of GIS between KT recipients with failed kidney allograft on HD undergoing antiviral therapy and untreated patients. METHODS: Retrospective analysis of KT recipients who started HD between January 1999 and December 2013 at Hospital Clinic Barcelona.

Conclusion: Our study suggests that 7.6% of children with IBD also Selleckchem Pexidartinib have either PSC, ASC or AIH in this cohort. Recently, there has been increasing recognition of this association in the paediatric population. We suggest that in children with IBD who have abnormal liver biochemistry, further liver specific investigations including liver biopsy and MRCP to be considered since the additional diagnosis of PSC, ASC or AIH will have therapeutic and prognostic implications.

A JACOB,1 R BHATIA2 1Department of Gastroenterology, Western Health, Victoria, Australia., 2Department of Gastroenterology, Royal Hobart Hospital, Hobart, Tasmania, Australia Context: Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease in Western populations. Currently, liver biopsy is the gold standard method for definitive diagnosis and differentiation of simple-steatosis (SS) from non-alcoholic steatohepatitis (NASH). Objective: Visfatin/nicotinamide phosphoribosyl transferase (NAMPT) is a recently discovered novel adipokine which is elevated in obesity and various other conditions. Based on its pro-inflammatory CB-839 properties and its role in fat and glucose metabolism, we hypothesised that visfatin might be involved in the pathogenesis of NAFLD and its measurement in serum may help in differentiating SS from NASH. Design and setting: We conducted clinical

studies at a referral medical centre on 75 morbidly obese patients presenting for lap-banding surgery, 50 with well-characterized NAFLD (SS/NASH). Main outcome measures: We examined the serum NAMPT/visfatin in patients learn more with NAFLD, and compared it in the study population (SS and NASH). Results: Visfatin was significantly elevated in NASH compared to SS in univariate analysis and in models adjusted for BMI, age, and sex. In univariate analysis mean serum visfatin was 7.05 (95%CI: 6.27–7.83) ng/ml for SS and 9.79

(95%CI: 7.95–11.62) ng/ml for NASH (p value 0.003). In BMI, age and sex adjusted models, visfatin was 7.02 (95%CI: 6.26–7.79) ng/ml and 10.12 (95%CI: 8.25–12.00) ng/ml for SS and NASH respectively (p value 0.001). Conclusion: Serum visfatin is elevated in NASH and may be useful as a predictive tool and prognostic marker in NAFLD. Visfatin may be involved in the pathogenesis and progression of NAFLD. AS RAJ,1,2 GA MACDONALD,1,2 P BHAT,1,2 LM FLETCHER,1 C TRAN,3 M BLACK,1 G HOLTMANN1,2 1Princess Alexandra Hospital, Brisbane, Australia, 2School of Medicine, University of Queensland, Brisbane, Australia, 3Womens and Children’s Hospital, Adelaide, South Australia, Australia Background: Increased small intestinal mucosal permeability may drive progression of chronic liver disease. Clinical assessment of intestinal permeability is limited by lack of standardisation of methods and assessment of liver fibrosis by liver biopsy is not without risk.

International collaborative efforts are required to design and conduct the studies necessary to answer this question. As an initial step, the World Federation of Hemophilia (WFH) is presently carrying out a project to review and catalogue the existing bleeding questionnaires including plans to highlight the strengths and weaknesses of these tools. Ophira Salomon, Institute of Thrombosis and Hemostasis, Chaim Sheba Medical Center, Tel Hashomer and Sackler Faculty of Medicine, Tel Aviv

University, Tel Aviv, Israel. FXI BMN 673 molecular weight deficiency is a rare bleeding disorder which is distinct from other coagulation factor deficiencies as bleeding usually occurs following surgery or trauma, and sometimes only after scar tissues have detached. Severity of bleeding does not

correlate with FXI levels, and replacement therapy may be associated with a risk of thrombosis [10, 17]. The main concern when treating patients with severe FXI deficiency is the excessive administration of prophylactic treatment to non-bleeding patients, and perhaps inadequate therapy for bleeding patients. Unfortunately, to date, there is no bleeding score available to estimate the quantity or extent of bleeding and their correlation with bleeding risk in upcoming find more procedures, for FXI deficient patients. Furthermore, the current approach is not applicable to patients with no prior surgeries. The roles of thrombophilia; levels of VWF, FVIII, fibrinogen and thrombomodulin; as well as platelet counts as “bleeding modifiers” in the context of FXI deficiency are still unknown. However, gene-environment interactions act as a phenotype modifier of FXI deficiency under conditions such as pregnancy [18, 19] and sepsis. The thrombin generation test (TGT), one of the global assays used to assess overall haemostasis in a given patient, seems to distinguish between bleeders and non-bleeders through peak height [20, 21], however, this data needs further

investigation and standardization. In addition, it was recently shown that patients with a selleckchem history of bleeding exhibited reduced fibrin network density, in comparison with non-bleeders when assessed by laser scanning confocal microscopy [22]. In the meantime, in the absence of a sensitive and standardized laboratory method for assessment of bleeding risk in patients with severe FXI deficiency, prophylactic treatment for invasive procedures is required prior to surgery regardless of bleeding history. Currently, the treatment most commonly offered to patients with severe FXI deficiency is fresh frozen plasma (FFP) at a dose of 15 mL kg−1, targeting 40% FXI activity, for approximately a week [17]. The treatment is associated with potential complications such as volume overload in patients with congestive heart failure and renal failure.

Our previous meta-analysis showed that serum CagA seropositivity was associated with gastric cancer even in East Asian countries. However, it remains unclear why serum CagA-positive status is associated with gastric cancer. In this study, we aimed to examine the relationship between anti-CagA antibody titer and the levels of pepsinogen (PG), and histological score. Eighty-eight H. pylori-positive Japanese patients with gastritis were included. Serum CagA antibody titer, PG I, and PG II were evaluated click here by ELISA. Histological scores were

evaluated according to Update Sydney System. CagA expression was examined by immunoblot. Seroprevalence of CagA antibody was found in 75.0%. Interestingly, serum CagA antibody titer was significantly MI-503 nmr correlated with PG I and PG II levels (P = 0.003 and 0.004, respectively). Serum CagA antibody titer was also significantly correlated with mucosal inflammation in the

corpus (P = 0.04). On the other hand, bacterial density was not related with CagA antibody titer. CagA expression level of the strains was irrespective of the status of PG and serum CagA antibody. Subjects with higher serum CagA antibody titer can be considered as high-risk population for the development of gastric cancer from the point of strong gastric inflammatory response even in Japan. Host recognition rather than bacterial colonization might be associated with the difference of serum CagA antibody titer. Helicobacter pylori is a spiral Gram-negative bacterium that infects more than half of the world’s population.[1] H. pylori infection is now accepted to be linked to severe gastritis-associated diseases, including peptic ulcer and gastric cancer.[1] The infection remains latent in the majority of infected patients, only a minority of individuals with H. pylori infection ever develop it.[2] Uemura et al. reported that gastric cancer developed in approximately 3% of H. pylori-infected patients compared with none of the uninfected patients.[3] In addition to host, environmental,

selleck products and dietary factors, the differences in the virulence of H. pylori strains are related with the varying outcomes of H. pylori infection. The best-studied virulence factor of H. pylori is the CagA protein. CagA-producing strains are reported to be associated with severe clinical outcomes, especially in Western countries.[4-7] CagA is a highly immunogenic protein with a molecular weight between 120 and 140 kDa.[8, 9] In 2003, Huang et al. performed meta-analysis of the association between CagA seropositivity and gastric cancer.[10] They concluded that the infection of CagA-positive strains increase the risk of gastric cancer. However, because they included studies from both Western and Asian countries, it was not clear whether an association between CagA seropositivity and gastric cancer really exists in East Asian countries. In East Asian countries, it is difficult to prove the importance of the cagA gene in clinical outcomes because almost all H.

Genotypic and phenotypic analyses20, 21 were also performed on isolates from all patients experiencing virologic breakthrough (≥1 log10 increase from nadir) at the time breakthrough occurred. All data analyses are descriptive.

Tabulations by treatment group are presented for each of the efficacy and safety variables. Continuous variables are summarized using the mean, median, minimum, and maximum values. Binary variables are summarized by counts and percentages. Efficacy endpoints were assessed among patients with available samples. An additional sensitivity analysis using the last observation carried forward method (LOCF) was conducted for the endpoint of HBV DNA <300 copies/mL at Week 240 (Year 5). In this analysis, Dabrafenib chemical structure the last observed HBV DNA levels MAPK Inhibitor Library cost were carried forward for those patients without Year 5 measurements, i.e., patients who had either discontinued prior to Year 5 or who were still on study but had a missing HBV DNA measurement

at Year 5. Safety analyses for the cohort include all adverse events that occurred on-treatment in study ETV-901 and all deaths that occurred on-study (during treatment in ETV-901 or during off-treatment follow-up). Serum HBV DNA was quantified by a central laboratory using the Roche COBAS Amplicor PCR assay (v. 2.0; lower limit of quantification 300 copies/mL [57 IU/mL]; Pleasanton, CA). In study ETV-022, HBV serologies (HBsAg, anti-HBs, HBeAg, anti-HBe) were assessed

in a central laboratory using the Abbott AxSYM microparticle enzyme immunoassay (Abbott Laboratories, North Chicago, IL) and DiaSorin enzyme immunoassay. In study ETV-901, HBV serologies were assessed in local laboratories using available methodologies. ALT was assessed by local laboratories in studies ETV-022 and ETV-901. Genotyping of HBV DNA involved PCR amplification of the HBV reverse transcriptase domain, followed by nucleotide sequence analysis. selleck compound In phenotypic analyses, substitutions that emerged on-treatment were cloned into HBV expression vectors, which were transfected into HepG2 hepatoma cells in the presence of entecavir. The amounts of replicated, encapsulated HBV DNA was immunocaptured from the culture media and quantified to determine the susceptibility to entecavir.20–22 The study was designed by the sponsor in collaboration with expert hepatologists. The sponsor collected the data, carried out the statistical analyses, and coordinated the writing of the article with all authors. Of the 354 patients who were randomized to treatment with entecavir 0.

Results: 102 adults, [41% male, 47% with diabetes, mean (SD) age of 51 (12) years] were reviewed. The prevalence of significant fibrosis (F2-4), advanced fibrosis (F3,4) and cirrhosis

was 28%, 18% and 5% respectively. The median (inter-quartile range) stiffness measurement for the cohort was 10.7 (7.1-14.1) kPa. The area under the ROC curve for predicting significant fibrosis, advanced fibrosis and cirrhosis using Fibroscan was 0.801, 0.855 and 0.977 respectively. selleck products Hepatic steatosis quantified by image morphometry was highly correlated with steatosis grade scored by the histopathologist (Spearman r=0.74, p<0.001). Similarly, liver stiffness was highly correlated with histopathologist scored fibrosis stage (Spearman r=0.55, p<0.001). Hepatic steatosis determined by liver pathologist grade or image morphometry, was

not significantly associated with liver stiffness (beta= −0.09, p=0.4 and beta=−0.68, p=0.5, respectively). Liver stiffness was positively associated with serum ALT (p=0.057), lobular inflammation (p=0.002), hepatocyte ballooning (p=0.003) and the NAFLD Activity Score (p=0.02), but these all became non-significant after adjusting for fibrosis. Notably, among the 74 individuals with no/minimal fibrosis (F0/1), liver stiffness was higher in the presence of NASH (n=23) versus those without NASH (n=51) [10.2 (8.6-14.8) kPa vs. 8.6 http://www.selleckchem.com/products/chir-99021-ct99021-hcl.html (5.8-11.7) kPa, p=0.04]. Furthermore, in subjects with no/minimal fibrosis on histology, “cirrhosis” defined by Fibroscan (cut-off 16.0 kPa) was present in 9/74 individuals and tended to be more common in subjects with

NASH (22% find more vs. 8%, p=0.1). Conclusion: NASH but not steatosis or ALT may confound liver stiffness interpretation in subjects with NAFLD and cause a false positive diagnosis of cirrhosis. Disclosures: Michael J. House – Consulting: Resonance Health; Patent Held/Filed: Resonance Health Stuart K. Roberts – Board Membership: Jannsen, Roche, Gilead, BMS Matthew T. Kitson – Consulting: MSD, Roche; Grant/Research Support: MSD; Speaking and Teaching: Janssen-Cilag Gary P. Jeffrey – Advisory Committees or Review Panels: MSD, Novartis The following people have nothing to disclose: Ranesh Palan, William W. Kemp, Bastiaan DeBoer, Jeffrey M. Hamdorf, Gerry C. MacQuillan, George Garas, Helena Ching, Ross Mac Nicholas, Leon Adams Background: Nonalcoholic fatty liver disease (NAFLD) is a broad spectrum of disease entity ranging from nonalcoholic fatty liver (NAFL) to nonalcoholic steatohepatitis (NASH) and NASH-related cirrhosis. Patients with NAFLD, especially NASH, are at risk for cardiovascular disease (CVD). Lectin-like oxidized LDL receptor−1 (LOX-1), which was identified as an endothelial cell surface major receptor for oxidative modification of LDL cholesterol, has been shown to relate with CVD disease, diabetes and metabolic syndrome.

Results: 102 adults, [41% male, 47% with diabetes, mean (SD) age of 51 (12) years] were reviewed. The prevalence of significant fibrosis (F2-4), advanced fibrosis (F3,4) and cirrhosis

was 28%, 18% and 5% respectively. The median (inter-quartile range) stiffness measurement for the cohort was 10.7 (7.1-14.1) kPa. The area under the ROC curve for predicting significant fibrosis, advanced fibrosis and cirrhosis using Fibroscan was 0.801, 0.855 and 0.977 respectively. Ibrutinib purchase Hepatic steatosis quantified by image morphometry was highly correlated with steatosis grade scored by the histopathologist (Spearman r=0.74, p<0.001). Similarly, liver stiffness was highly correlated with histopathologist scored fibrosis stage (Spearman r=0.55, p<0.001). Hepatic steatosis determined by liver pathologist grade or image morphometry, was

not significantly associated with liver stiffness (beta= −0.09, p=0.4 and beta=−0.68, p=0.5, respectively). Liver stiffness was positively associated with serum ALT (p=0.057), lobular inflammation (p=0.002), hepatocyte ballooning (p=0.003) and the NAFLD Activity Score (p=0.02), but these all became non-significant after adjusting for fibrosis. Notably, among the 74 individuals with no/minimal fibrosis (F0/1), liver stiffness was higher in the presence of NASH (n=23) versus those without NASH (n=51) [10.2 (8.6-14.8) kPa vs. 8.6 DNA Damage inhibitor (5.8-11.7) kPa, p=0.04]. Furthermore, in subjects with no/minimal fibrosis on histology, “cirrhosis” defined by Fibroscan (cut-off 16.0 kPa) was present in 9/74 individuals and tended to be more common in subjects with

NASH (22% selleck chemicals vs. 8%, p=0.1). Conclusion: NASH but not steatosis or ALT may confound liver stiffness interpretation in subjects with NAFLD and cause a false positive diagnosis of cirrhosis. Disclosures: Michael J. House – Consulting: Resonance Health; Patent Held/Filed: Resonance Health Stuart K. Roberts – Board Membership: Jannsen, Roche, Gilead, BMS Matthew T. Kitson – Consulting: MSD, Roche; Grant/Research Support: MSD; Speaking and Teaching: Janssen-Cilag Gary P. Jeffrey – Advisory Committees or Review Panels: MSD, Novartis The following people have nothing to disclose: Ranesh Palan, William W. Kemp, Bastiaan DeBoer, Jeffrey M. Hamdorf, Gerry C. MacQuillan, George Garas, Helena Ching, Ross Mac Nicholas, Leon Adams Background: Nonalcoholic fatty liver disease (NAFLD) is a broad spectrum of disease entity ranging from nonalcoholic fatty liver (NAFL) to nonalcoholic steatohepatitis (NASH) and NASH-related cirrhosis. Patients with NAFLD, especially NASH, are at risk for cardiovascular disease (CVD). Lectin-like oxidized LDL receptor−1 (LOX-1), which was identified as an endothelial cell surface major receptor for oxidative modification of LDL cholesterol, has been shown to relate with CVD disease, diabetes and metabolic syndrome.

There is

limited evidence to guide albumin dosing in this clinical scenario. Current recommendations are to give 1gm/kg/day of albumin up to 100gm/day. Our goal in performing this retrospective chart review is to identify differences in outcomes among patients with cirrhosis who present with AKI and who receive differing daily doses of albumin. Using Vanderbilt University Hospitals EMR, 1,124 charts were reviewed from all patients admitted to the Hepatology service from 2010–2013 with 149 subjects identified. Patients with an admission diagnosis of AKI were included if their admission serum creatinine was >2.0mg/dL and had increased from their prior baseline by ≥0.3mg/dL, or find more their admission serum creatinine was 1.5 times their baseline value. Subjects who met these criteria were excluded if they were diagnosed learn more with spontaneous bacterial peritonitis during their

hospital stay. We then looked at the admission creatinine, and creatinine after a 48hour albumin challenge to assess for improvement in renal function. Our results show no evidence that increasing doses of albumin are associated with increasing degree of change in creatinine from pre-to-post intervention (p=0.49). In a multivariable model including MELD scores, PRBC administration and urine sodium; there is no evidence that MELD scores, PRBCs, urine sodium or albumin are associated with changes in creatinine. For subjects receiving less than or equal to 0.5 g/kg of albumin BID, creatinine decreased by 0.44 units from pre to post check details intervention; in subjects receiving more than 0.5 g/kg of albumin,

creatinine decrease by 0.42 units. This is a difference of 0.02 units (95% CI: [−0.24 to 0.28]) due to albumin dosing. While we were unable to show that increasing albumin dose had a greater effect on improving renal function, in general there was an improvement. This study shows no association between albumin dose and effect on improving kidney function, glomerular filtration rate or hospital length of stay in patients with known cirrhosis. These results allowed us to develop a hypothesis that larger doses of albumin are no more effective than low dose albumin regimens in effecting change in overall kidney function. Moving forward it is our goal to create a prospective study with the aim of more effectively using albumin as a hospital resource given Vanderbilt University Hospital as a whole spent 4.6 million dollars on albumin from 2010–2013. Disclosures: The following people have nothing to disclose: Derek J. Feussner, Amy P. Myers, James C. Slaughter, Andrew Scanga Introduction: Hospital-acquired infections in cirrhosis patients are associated with significant morbidity and mortality.