Circulatory and renal dysfunction and overactivity of the renin-angiotensin and sympathetic nervous systems are well-known risk factors of HRS development in patients with decompensated cirrhosis.[45] On the other hand, bacterial infections in cirrhosis are frequently associated IWR-1 molecular weight to the development of type-1 HRS.[45, 46] These factors could account for the higher risk of type-1 HRS observed in patients with RAI. Another interesting observation of our study was that patients with RAI and bacterial infection developed more frequently severe sepsis or shock. The more

severe impairment in circulatory function prior to infection and perhaps an exaggerated inflammatory response due to low circulating cortisol levels could account for this feature. The probability of death was significantly higher in noncritically ill patients with RAI than in those with normal adrenal function. The main cause of death was ACLF, a recently defined syndrome in patients with acute decompensation of cirrhosis characterized by one or more organ failures, intense systemic inflammatory response, and very high mortality.[31] The second cause of mortality in this series was septic shock. In the analysis of independent risk factors for the development of severe sepsis, type-1 HRS, and death, Selleckchem PD0325901 delta cortisol together with three important predictive variables (MELD, which estimates the degree

of liver and renal dysfunction, and plasma renin activity and norepinephrine concentration, which estimate the degree of circulatory dysfunction) were introduced in the models. Delta cortisol and MELD were found to be independent predictors of severe sepsis, type-1 HRS, and mortality. Plasma renin activity and plasma noradrenaline were also independent risk factors of severe sepsis and death, Acyl CoA dehydrogenase respectively. A potential

weakness of our study is the heterogeneity of patients included. The study was designed to evaluate the prevalence of RAI and its relationship to clinical course in noncritically ill cirrhosis patients with acute clinical decompensation, thereby including subjects with ascites, encephalopathy, bacterial infection, variceal bleeding, or HRS. Although the prevalence of RAI did not significantly differ among different patient groups (except for type-1 HRS), mechanisms of adrenal dysfunction and its association with clinical events may differ among different decompensations of cirrhosis. Further studies should clarify this point. In summary, our study shows that RAI is a relatively frequent event in noncritically ill cirrhosis patients with acute decompensation and appears to be associated with impairment in circulatory and renal function and higher risk of short-term development of bacterial infections, severe sepsis, type-1 HRS, and death. Additional Supporting Information may be found in the online version of this article.

Serum alpha-fetoprotein (AFP), normally highly expressed in the liver only during fetal development, is reactivated in 60% of

HCC tumors and associated with poor patient outcome. We hypothesize that AFP+ and AFP− tumors differ biologically. Multivariable analysis in 237 HCC cases demonstrates that AFP level predicts poor survival independent of tumor stage (P < 0.043). Using microarray-based global microRNA (miRNA) profiling, we found that miRNA-29 (miR-29) family members were the most significantly (P < 0.001) down-regulated miRNAs in AFP+ tumors. Consistent with miR-29's role in targeting DNA methyltransferase 3A (DNMT3A), a key enzyme regulating DNA methylation, we found a significant inverse correlation (P < 0.001) between this website miR-29 and DNMT3A gene expression, suggesting that they might be functionally antagonistic. Moreover, global DNA methylation profiling reveals that AFP+ and AFP−

HCC tumors have distinct global DNA methylation patterns and that increased DNA methylation is associated with AFP+ HCC. Experimentally, we found Midostaurin cost that AFP expression in AFP− HCC cells induces cell proliferation, migration, and invasion. Overexpression of AFP, or conditioned media from AFP+ cells, inhibits miR-29a expression and induces DNMT3A expression in AFP− HCC cells. AFP Y-27632 2HCl also inhibited transcription of the miR-29a/b-1 locus, and this effect is mediated through c-MYC binding to the transcript of miR-29a/b-1. Furthermore, AFP expression promotes tumor growth of AFP− HCC cells in nude mice. Conclusion: Tumor biology differs considerably between AFP+ HCC and AFP− HCC; AFP is a functional antagonist of miR-29, which may contribute to global epigenetic alterations and poor prognosis in HCC. (Hepatology 2014;60:872–883) “
“This chapter contains sections titled: Introduction

Induction of remission Treatment of therapy-resistant or steroid-dependent patients Maintenance of remission Summary References “
“Serum des-γ-carboxy prothrombin (DCP) is an established tumor marker in patients with hepatocellular carcinoma (HCC), which can be identified by using MU-3 antibody. The MU-3 antibody mainly reacts with the 9–10 glutamic acid residues of DCP (conventional DCP). Since other variants of DCP with fewer glutamic acid residues can be detected using P-11 and P-16 antibodies (code name: NX-PVKA), we examined the clinical characteristics associated with NX-PVKA, and whether NX-PVKA is a useful measure in HCC patients. Participants comprised 197 HCC patients admitted to our hospital between 2001 and 2010.

[51] Further, they have increased intestinal permeability and bacterial translocation, caused in part by portal hypertension and vascular congestion. Culture-independent techniques targeting the hypervariable 3 region of the bacterial 16S rRNA gene have shown a reduced microbial diversity and reduction

in Bacteroidetes, and an increase in Proteobacteria and Fusobacteria in patients with liver cirrhosis.[52] Although the exact reason for these changes remains unclear, reduced intestinal motility, decreased gastric acidity and pancreato-biliary secretions, and portal hypertensive enteropathy may all contribute. In an experimental EPZ015666 molecular weight mouse model of liver fibrosis, expression of profibrogenic genes (including transforming growth factor-β, matrix metalloproteinase-2, procollagen α-1, and tissue inhibitor of metalloproteinase-1), serum levels of pro-inflammatory cytokines (TNF-α and IL-6) and bacterial translocation showed progressive increase with increasing fibrosis.[53] Thus, the available data suggest a possible role for altered gut microbiota in liver fibrogenesis. However, majority of data that suggest

a pathogenetic relationship are based on animal studies. Human data on the association are limited to observational studies showing qualitative and quantitative alterations in gut microbiota in cirrhosis and are currently Montelukast Sodium SCH727965 research buy inadequate to prove a cause–effect relationship. The clinical course of liver cirrhosis is frequently complicated by development of GI bleed, HE, renal failure, or spontaneous bacterial peritonitis (SBP), leading to a detrimental effect on liver function and poorer clinical outcomes. Altered gut microbiome may also influence the risk of development and outcome of these complications. Patients with cirrhosis have an increased

risk of hospital-acquired infection than non-cirrhotic controls. Common bacterial infections in patients with liver cirrhosis include SBP, respiratory tract infections, urinary tract infection, and generalized sepsis. A large majority of these infections are caused by gram-negative enteric bacilli, suggesting an origin in the gut. Patients with chronic liver disease have an overgrowth and translocation of gut bacteria, as evidenced by an increased presence of bacterial DNA[54] as well as antibodies against microbes[55] in their circulation. Intestinal permeability is increased in cirrhotics with ascites, history of SBP, and higher Child–Pugh score.[56] In one study, the bacteria showing translocation from bowel to mesenteric lymph nodes belonged mostly to Enterobacteriaceae family, Enterococcus group and some Streptococcus species,[57] that is similar to those causing infections in patients with cirrhosis.

Reactions were repeated a minimum of three times. Mouse tissues were lysed in 2× total protein buffer containing 10 mM of Tris (pH 7.6),

1% NP40, protease inhibitors (Roche complete mini ethylene diamine tetraacetic acid [EDTA]-Free), and 2 mM of dithiothreitol. Then, cell lysates were sonicated and quantified using the Bio-Rad Protein Assay. Then, 40 μg of protein were loaded into each well and separated by 4%-15% sodium dodecyl sulfate Mini-Protean TGX gel (Bio-Rad). After transfer, the polyvinylidene fluoride membrane was blocked with 5% nonfat dried milk, then cut into two pieces. The upper panel was click here incubated with rabbit anti-β-galactosidase (CEDARLANE); the lower panel was incubated with mouse monoclonal anti-β-actin (Sigma-Aldrich) at 4°C overnight. After washing, the peroxidase-conjugated secondary antibodies were added for 1 hour at room temperature. Detection was achieved using SuperSignal West Dura Extended Duration Substrate (Pierce, Rockford, IL). Hepatocytes obtained from Sprague-Dawley GSK458 nmr rats were stained with PKH2 for cytoplasmic labeling, according to the manufacturer’s instructions (Sigma-Aldrich). After staining, hepatocytes were plated

on 24-well plates or T-150 culture flasks at a density of 1 x 104 cells/cm2. Fluorescence images of cells were obtained at predetermined time points on a Leica DMIL fluorescence microscope, using Leica application suite V3.1 software (Leica Microsystems, Buffalo Grove, IL). On days 1 and 14, the cells on flasks were collected and subjected to flow cytometry for quantitative analysis Demeclocycline of their fluorescence. For flow cytometric analysis, unlabeled cells were used as negative control. Mean fluorescent intensity was

determined for each sample, and total fluorescence was calculated by multiplying mean fluorescent intensity and the total number of cells. The value of total fluorescence on day 1 was given an arbitrary unit of 1. Total fluorescence on day 14 was calculated in an identical manner, then compared with that of day 1. Triplicates were used for statistical calculations. For flow cytometric analysis of hepatocyte purity, cells were fixed and permeabilized by 0.2% Triton X-100. After blocking with donkey IgG, cells were incubated with an anti-albumin/FITC (fluorescein isothiocyanate) antibody (1:20; CEDARLANE) for 30 minutes at room temperature. The negative control was FITC/rabbbit IgG. Fluorescence-activated cell-sorting acquisition was performed, using a FACSCalibur flow cytometer (BD Biosciences), and data were analyzed using FlowJo 6.4. A statistical analysis was done by the Student’s t test to identify significant differences. A P value less than 0.05 was considered significant. Flow cytometric analysis of LDPC purity was performed in an identical fashion, except for the antibody, which was PE-conjugated rabbit anti-CD45 antibody (BD Biosciences).

2 G6Pase-α and G6PT, both embedded in the endoplasmic reticulum (ER) membrane, form a functional complex that maintains glucose homeostasis between meals: G6PT translocates glucose-6-phosphate (G6P) from the cytoplasm into the lumen of the ER, and G6Pase-α hydrolyzes G6P into glucose and phosphate. A deficiency in G6Pase-α causes GSD-Ia, and a deficiency in G6PT causes GSD-Ib and both are autosomal recessive disorders with an overall incidence XL765 price of approximately 1 in 100,000.3 Both GSD-Ia and GSD-Ib patients fail to hydrolyze G6P to glucose and thus share symptoms, including life-threatening hypoglycemia, hepatomegaly, and seizures, within the first year

of life. Long-term complications include growth failure, pulmonary hypertension, formation of hepatic adenomas, and, occasionally, hepatocellular carcinoma (HCC) and renal failure. Therapies are aimed at controlling glycemia by dietary supplementation or continuous parenteral or intragastric infusion of carbohydrates. In contrast to most other inborn errors of metabolism, enzyme-replacement therapy is not possible selleck chemicals llc for von Gierke’s disease because the deficient enzyme is a hydrophobic ER-associated transmembrane protein that cannot be expressed in a soluble form. Gene therapy, which utilizes a vector to deliver the therapeutic gene to

the target tissues, provides an attractive alternative therapy. A vector based on adeno-associated virus (AAV) has been chosen as the main vector platform for GSD-Ia gene therapy because of its safety profiles, high in vivo transduction efficiency, stable transgene expression, and modest immunogenicity. The availability of both small-4 and large-animal5 models that closely mimic severe GSD-Ia in humans makes a preclinical evaluation

of the efficacy of gene therapy feasible. The main target tissue is the liver, Olopatadine based on the success with human patients after liver transplantation (LT). The kidney is also a target organ to prevent renal failure, which frequently presents as a late complication in GSD-Ia patients with or without LT. Initial studies using AAV serotype 2–based vectors expressing G6Pase-α to treat infant GSD-Ia in dogs or mice showed suboptimal improvement.6, 7 In subsequent years, several new advances in the AAV field, such as novel AAV serotypes from nonhuman primate or human tissues8 and the discovery of self-complementary (sc)AAV,9 enabled researchers to further improve the efficacy of gene therapy for GSD-Ia. AAV serotype 8 (AAV8), a highly liver-tropic and efficient vector with low preexisting immunity in human populations, has become one of the preferred vector serotypes, especially for liver-directed gene therapy. Using AAV8 or AAV1 vectors prolonged survival, and partial biochemical correction was demonstrated in G6pc−/− mice.

6%. The value of MELD score above 15 on these dates only detected in 15.6% of patients. Stable condition is ascertained in 21 patients (65.6%) and in 3 cases observed moderate activity cirrhotic process. Progressive liver failure with a high degree of activity in the period after 3 and 6 months after surgery was detected in 2 (6.3%) patients. In the 2 cases of observation there has been Selleckchem Cisplatin a bleeding, in one case from EGV when shunt thrombosis occurred, in another case of the stomach erosions in portal gastropathy. Ascites observed in 4 (12.5%) patients. By hepatic failure after 6 months of PSSh died 1 (3.1%) patient. Conclusion: Thus, the high incidence

of bleeding from EGV, in the compensatory reserve of the liver, leaving PSSh method of choice to reduce the need for liver transplantation or to delay its implementation. Key Word(s): 1. MELD SCORE; 2. PORTOSYSTEMIC SHUNT; Presenting

Author: ABDUL MATIN Additional Authors: PRAVEEN SHARMA, ABDUL RAUF, PANKAJ TYAGI, VIKAS SINGLA, NARESH IWR-1 clinical trial BANSAL, ASHISH KUMAR, ANIL ARORA Corresponding Author: ABDUL MATIN, PRAVEEN SHARMA, ABDUL RAUF, PANKAJ TYAGI, VIKAS SINGLA, NARESH BANSAL, ASHISH KUMAR, ANIL ARORA Affiliations: Sir Ganga Ram Hospital; India Objective: Transient elastography (FibroScan) is a new, non-invasive, rapid, and reproducible method allowing evaluation of liver fibrosis by measurement of liver stiffness. The aim of this study was to evaluate the sensitivity filipin of liver stiffness measurement (LSM) for the detection of complications of cirrhosis Methods: All consecutive patients with cirrhosis were studied. Cirrhosis was diagnosed either on liver biopsy or on clinical, biochemical and radiological

basis. Patient’s Child-Pugh score (CTP), model for end stage liver disease (MELD) and complications due to portal hypertension were recorded. Liver stiffness measurement (LSM) by Fibroscan was done at the time of admission Results: Patients (n = 210) (age 51 ± 12 yr, M : F 164 : 46) were enrolled. Their baseline CTP score (8.8 ± 2.2), MELD score (17.1 ± 7.8) and LSM was 54.9 ± 18.9 kPa. Etiology of cirrhosis was due to alcohol, n = 63, cryptogenic, n = 89, HBV, n = 25, HCV, n = 20, autoimmine, n = 10 and Wilson, n = 3. LSM was significantly correlated with CTP score (0.415, p = 0.001), MELD score (0.28, p = 0.001), total bilirubin (0.169, p = 0.01), albumin (−0.213, p = 0.002) and platelet count (−0.156, p = 0.02). The cut off values for the presence of oesophageal varices (49.3 kPa sensitivity 74%, specificity 77%), cirrhosis Child-Pugh B or C (54.1 kPa, sensitivity 76%, specificity 66%), past history of ascites (52.6 kPa, sensitivity 84%, specificity 70%), hepatocellular carcinoma (62.

Fifty consecutive patients with ALI/ALF were recruited prospectively from admissions at VCU Medical Center. ALI was defined as liver injury in a patient with no known previous liver disease, an admission INR of ≥1.5, and a duration of illness of ≤26 weeks. ALF was defined as ALI in the presence of HE. Some patients in the current study population also participated in two previous studies exploring hemostasis in ALI/ALF.6, 8 For the present study, 13 healthy volunteer controls were also recruited for the collection of 5 mL of whole blood for plasma. Controls were of similar age (39 years) and gender distribution

(54% female) as the study population (P = 0.6 and 0.2, respectively). SIRS components were determined at time of admission to the study by standard criteria, and the presence of the SIRS was defined as two to four positive EPZ-6438 supplier SIRS components.24 Complications

of ALI/ALF, including bleeding, thrombosis, and infection, were defined previously6 and occurred late after admission (on or after day 3). Bleeding sites included gastric mucosal erosions (N = 6) and cutaneous (N = 3), none of which lead to the need for blood transfusion. Thrombotic events MI-503 clinical trial included occlusion of renal replacement therapy (RRT) catheters (N = 6), portal venous thrombosis (N = 2), and limb vessel thrombosis (N = 1). Sites of infection included lung (N = 5), urine (N = 4), blood (N = 3), and ascites (N = 1) and were identified relatively late after admission (>3 days after admission). As per ALFSG protocol, outcomes (death, LT, or transplant-free survival [TFS]) were determined at day 21 after admission. Standard laboratories were collected

on admission to the hospital (day 1) and daily for 7 days. For the analyses herein, laboratories drawn on days 1 and 3 after admission were analyzed. Whole blood from days 1 and 3 was also collected for PPP in 5-mL citrated Vacutainer tubes. Because enrolled patients were purposely chosen to represent a wide range of liver injury severity, blood was drawn by in-dwelling venous catheters, radial artery catheters, and butterfly needle catheters, depending upon whether patients were in a floor bed Silibinin or intensive care unit, and the availability of vascular access. Blood was centrifuged at 1,500×g for 20 minutes at room temperature, aliquotted, and PPP was frozen at −80°C within 2 hours of drawing. MPs were analyzed by Invitrox Sizing, Antigen Detection, and Enumeration (ISADE; Invitrox, Inc., Research Triangle Park, NC).23 Batches of 10-20 PPP samples, randomly selected, were injected into the detection chamber using a fixed volume of 200 μL/sample. Testing time for sizing and enumeration was 6 minutes/sample. To eliminate any contribution from buffer/diluent, background counts were subtracted from each sample result.

Fifty consecutive patients with ALI/ALF were recruited prospectively from admissions at VCU Medical Center. ALI was defined as liver injury in a patient with no known previous liver disease, an admission INR of ≥1.5, and a duration of illness of ≤26 weeks. ALF was defined as ALI in the presence of HE. Some patients in the current study population also participated in two previous studies exploring hemostasis in ALI/ALF.6, 8 For the present study, 13 healthy volunteer controls were also recruited for the collection of 5 mL of whole blood for plasma. Controls were of similar age (39 years) and gender distribution

(54% female) as the study population (P = 0.6 and 0.2, respectively). SIRS components were determined at time of admission to the study by standard criteria, and the presence of the SIRS was defined as two to four positive learn more SIRS components.24 Complications

of ALI/ALF, including bleeding, thrombosis, and infection, were defined previously6 and occurred late after admission (on or after day 3). Bleeding sites included gastric mucosal erosions (N = 6) and cutaneous (N = 3), none of which lead to the need for blood transfusion. Thrombotic events VX-765 cost included occlusion of renal replacement therapy (RRT) catheters (N = 6), portal venous thrombosis (N = 2), and limb vessel thrombosis (N = 1). Sites of infection included lung (N = 5), urine (N = 4), blood (N = 3), and ascites (N = 1) and were identified relatively late after admission (>3 days after admission). As per ALFSG protocol, outcomes (death, LT, or transplant-free survival [TFS]) were determined at day 21 after admission. Standard laboratories were collected

on admission to the hospital (day 1) and daily for 7 days. For the analyses herein, laboratories drawn on days 1 and 3 after admission were analyzed. Whole blood from days 1 and 3 was also collected for PPP in 5-mL citrated Vacutainer tubes. Because enrolled patients were purposely chosen to represent a wide range of liver injury severity, blood was drawn by in-dwelling venous catheters, radial artery catheters, and butterfly needle catheters, depending upon whether patients were in a floor bed Florfenicol or intensive care unit, and the availability of vascular access. Blood was centrifuged at 1,500×g for 20 minutes at room temperature, aliquotted, and PPP was frozen at −80°C within 2 hours of drawing. MPs were analyzed by Invitrox Sizing, Antigen Detection, and Enumeration (ISADE; Invitrox, Inc., Research Triangle Park, NC).23 Batches of 10-20 PPP samples, randomly selected, were injected into the detection chamber using a fixed volume of 200 μL/sample. Testing time for sizing and enumeration was 6 minutes/sample. To eliminate any contribution from buffer/diluent, background counts were subtracted from each sample result.

In other chronic biliary diseases such as extrahepatic biliary atresia (EHBA), PSC, and primary biliary cirrhosis (PBC), the morphology

and severity of DRs depend on disease stage.12 All three will have foci of DRs with dense fibrous stroma similar to those in chronic obstruction. This is the only pattern seen in PBC, because only smaller bile ducts are involved. In EHBA and PSC, with involvement of larger ducts, there is a mix of this chronic form as well as superimposed obstructive-type DR. As disease progresses, the DR can become more variable, and may be sparse in the end stages of disease. In liver diseases of nonbiliary origin, even more variable DR phenotypes are seen. The most profound DRs can be encountered in fulminant hepatic failure.14 The severe loss of hepatic parenchyma is accompanied by massive DRs with sparse fibrosis or inflammation.5 The hepatobiliary Cabozantinib nmr cells in these reactions are more “hepatocyte-like” than those that predominate in biliary tract disease. In fibrosing cholestatic variants Selleck Roxadustat of hepatitis B and C in the setting of a compromised immune system,

DRs are still more dramatically expanded, floridly extending into the hepatic parenchyma in a “starburst” pattern and accompanied by more prominent stroma.15 In chronic viral hepatitis, DRs predominantly appear later in the disease process, years or even decades after infection, although they may be subtly present earlier. These DRs are more tightly compacted at the stromal–parenchymal interface.4,16 In autoimmune hepatitis (AIH), DRs may be variable: similar to fulminant hepatitis during severe flares or more like viral hepatitis when fibrosis is advanced or activity less marked. Hepatocytic rosettes are often a prominent feature of AIH-DRs containing a range of hepatocyte to cholangiocyte-like phenotypes,

best highlighted not by immunostains. The prominence of the DR varies with etiology. A greater magnitude of DRs is present in AIH compared with hepatitis C virus (HCV) infection, whereas the latter can show more DRs than prefibrotic alpha-1-antitrypsin deficiency.17 In fatty livers without steatohepatitis, DRs are inconspicuous, although increased periportal, K7-positive cells occur.18 The DRs become more prominent with steatohepatitis, particularly in those with portal or septal fibrosis.18 A slightly different DR occurs in ischemic diseases such as hepatic vein outflow obstruction, where the reaction is typically centrilobular.12 Focal liver lesions such as focal nodular hyperplasia and the inflammatory type hepatocellular adenoma also contain DRs.19 In summary, DR are encountered in virtually all liver diseases in which there is organ wide liver damage and cell loss, but are also present in focal lesions such as focal nodular hyperplasia and hepatocellular adenoma. Moreover, diverse DR phenotypes can be present within one disease entity, shaped by the etiology and the evolution of the disease.

0 vs.17.5 IU/L), alkaline phosphatase (165.0 vs.146.8 IU/L), total-cholesterol (200.0 vs.186.2 mg/dL), and LDL-cholesterol (155.3 vs.80.5 mg/dL) were significantly different (P<0.05). However, baseline glucose level and diabetes were not statistically significant for tamoxifen-induced steatosis (P>0.05). BMI was the only independent risk factor of tamoxifen-induced steatosis (Hazard ratio: 1.227, 95% confidence interval: 1.039-1.448; P=0.016).

Furthermore, of excluded 36 patients with NASH at baseline, the levels of aminotransferase of 19 patients were normalized after tamoxifen therapy (52.8%). The normalization of aminotransferases took 108.6±66.8 days after administration of tamoxifen. SRT1720 cell line Conclusions: Our study showed that tamoxifeninduced hepatotoxicity might be associated with BMI, and tamoxifen could cause hepatoprotective effect as well as liver injury. Disclosures: The following people have nothing to disclose: Myung Jin Oh, Heon Ju Lee, Si Hyung Lee, Sung Bum

Kim, Yeoun Su Jung, Jung Woo Lee BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a common cause of hepatic steatosis in patients with inflammatory bowel disease (IBD). Both metabolic syndrome (MetS) and intestinal inflammation are implicated in NAFLD pathogenesis. In our see more hospital population of patients with dual diagnosis of NAFLD and IBD, the prevalence of MetS parallels national trends. We examined whether MetS and IBD severity increase the risk of NAFLD severity in patients with NAFLD and IBD. METHODS: A retrospective medical record review was performed for all patients entered into the electronic medical record of a tertiary care university hospital from January 1997December 2011. Patients with a dual diagnosis ID-8 of

IBD and NAFLD were included. We excluded patients with viral, alcoholic, autoimmune or genetic etiology of hepatic steatosis. Patients were grouped according to “MetS” (>3 of the following: hypertension, hyperlipidemia, BMI>30, and diabetes/insulin resistance) or “non-MetS. ” BARD score or liver pathology was used to grade NAFLD severity. Physician global assessment and Montreal classification were used to determine IBD severity/pattern. Patient demographics, medications, and serology were analyzed. Statistical analysis was performed using Fisher Exact test or Mann-Whitney U test. RESULTS: 84 pts were included in our analysis (25 UC, 59 Crohn’s). Pts were predominantly female (57%) and Caucasian (85%). The majority of UC pts had ulcerative proctitis; most Crohn’s pts had ileocolonic disease. Pts were diagnosed with NAFLD a mean of 12 years after the time of IBD diagnosis.25% of pts had MetS. Pts with IBD and MetS were diagnosed with NAFLD at older age than IBD and non-MetS pts (54.8 vs 45.8, p=0.015). Mean BMI at NAFLD diagnosis was 34.4 and 28.8 kg/m2 in MetS and non-MetS pts (p<0.001).30% of pts were referred to hepatology independent of MetS diagnosis. Compared with nonMetS, MetS pts had higher ALT (57 vs 38, p=0.007); AST (56 vs 36, p=0.