We therefore investigated the effect of Endobarrier treatment on hepatic parameters in obese uncontrolled type 2 diabetes mellitus patients with NAFLD. The Endobarrier device was implanted for 12 months in the duodenum via an endo-scopic procedure in 44 uncontrolled diabetic, obese, NAFLD subjects (age 52.3±9.3y, 52.2% male, BMI 37.5±4.6 m2/kg). BMI, waist circumference, serum liver enzyme levels, glucose, HBA1c and lipid profile were performed as well as shear wave elastography (SWE) (Aixplorer SuperSonic Imagine, PD98059 purchase France) and Fibromax (FibroTest, ActiTest, SteatoTest, and NashTest) (BioPredictive, France) for the noninvasive evaluation of hepatic injury before, 3 and 6 months

during the implantation of the Endobarrier device and when removing the device (12 months). At 3 and 6 months after implantation of the Endo-barrier (interim results, n=29), the BMI, waist circumference, serum liver enzyme levels, glucose, HBA1c and lipid profile decreased significantly (from baseline and from 3 to 6 months). The fibrosis stage (evaluated by SWE) and the: SteatoTest (fat liver content),

and NashTest (steatohepatitis score) (evaluated by Fibromax) also improved significantly from baseline and from 3 to 6 months. In 9 subjects (20.4%) the Endobarrier was endoscopically explanted early. Conclusion: Endobarrier, a minimally invasive bariatric technique, achieved significant improvement Gefitinib purchase in hepatic injury, fat liver content, steatohepatitis score and fibrosis stage in advanced uncontrolled obese, diabetic, NAFLD patients.

This device may be suitable for the treatment of morbid obesity and its related comorbidities including NAFLD. Disclosures: The following people have nothing to disclose: Oranit Cohen-Ezra, Gabriella Segal-Lieberman, Alon Lang, Maor Lahav, Yeroham Kleinbaum, Sima Katshergin-sky, Keren Tsaraf, Ziv Ben Ari Background & Aims: Recent investigations demonstrated that circulating secreted factors, such as adiponectin, leptin, tumor necrosis factor-α (TNF-α), and fetuin-A significantly affect pathophysiological Protein tyrosine phosphatase progression in NAFLD. Fetuin-A (a2HS-gly-coprotein) is a liver glycoprotein secreted into the circulation at high concentrations. Fetuin-A is known as a transforming growth factor (TGF)-1 signaling inhibitor. Serum fetuin-A concentration is associated with nonalcoholic fatty liver disease (NAFLD) and cardiovascular disease. However, the usefulness of the serum fetuin-A level as a predictive fibrosis biomarker in NAFLD patients is unclear. In this study, we investigated the relationship between circulating fetuin-A levels and fibrosis related markers [platelet count, NAFLD fibrosis score, and carotid intima media thickness (IMT)] in subjects with NAFLD. We also investigated the effects of fetuin-A on hepatic stellate cells (HSCs), which play a pivotal role in the progression of hepatic fibrosis.

Matthew Picklo, University of North Dakota School of Medicine) complexes I (30 kD subunit), II

(30 kD subunit), III (core protein 1, Rieske iron sulfur), and IV (subunits I and IV) (Invitrogen, CA), phospho AMP-activated protein kinase (AMPK) and phospho ACC (Cell Signaling, MA), and detected using enhanced chemiluminescence (SuperSignal, West-Dura, Pierce, IL). All data represent the means ± standard error of the mean (SEM), n = 6 for control and ethanol groups and n = 5 for MitoQ-treated groups. Statistical significance was determined using Student’s t test, analysis of variance (ANOVA), and Newman-Keuls test as post-hoc test. P < 0.05 was taken as significantly different. Animals were pair-fed with either ethanol or control liquid diets containing MitoQ (0, 5, or 25 mg/kg/day) for 4 weeks. There was no SRT1720 concentration significant difference in body weight gain; however, the ethanol group had increased liver weight as compared to pair-fed controls which was prevented by MitoQ, although no effect was seen on liver to body weight ratios (Table 1). Consumption of ethanol did Pexidartinib not significantly increase serum alanine aminotransferase levels compared with controls. Ethanol consumption resulted in increased serum HDL levels as expected but was not changed by MitoQ.44 The serum

low-density lipoprotein (LDL) / very low-density lipoprotein (VLDL) also showed no significant changes with alcohol exposure or any treatment (Supporting Fig. 1). Chronic ethanol consumption is known to increase 4-HNE-protein adducts and iNOS-dependent protein nitration.7, 9, 20, 21 In agreement with these findings, liver tissues show intense staining for 4-HNE-protein adducts in chronic ethanol fed animals compared to pair-fed controls (Fig. 1A,B). HNE immunoreactivity was not uniform with hepatocytes around the central veins showing the most intense staining (zones 2, 3) and a gradual decline toward the periportal region (zone 1). MitoQ treatment completely abolished ethanol-induced 4-HNE staining

in all regions of the liver sections examined. Control experiments show no effect of MitoQ at either dose (Fig. 1A,B) www.selleck.co.jp/products/Staurosporine.html and omission of the primary antibody for HNE resulted in no detectable signal (result not shown). Consistent with previous studies, chronic ethanol feeding increased 3-NT and iNOS staining with highest in zone 3, with intermediate staining in zone 2 (Fig. 2A,B).9, 20, 45 MitoQ treatment significantly decreased 3-NT staining in the liver of ethanol fed rats; however, it did not have any effect on the induction of iNOS protein. Controls with excess free 3-NT or omission of the primary antibody for 3-NT resulted in no signal (result not shown). It has been shown that MitoQ inhibits mitochondrial ROS and the consequent activation of HIF1α.30, 31, 46 We first confirmed the activation of HIF1α in response to EtOH (Fig. 3A).

4A). An opposite effect was obtained when silencing the PLK2, PLK3, or PLK4 gene by siRNA in SNU-423 and HLE cell lines (expressing high levels of the PLK2, PLK3, and PLK4 genes). Indeed, suppression of PLK2, PLK3, or PLK4 was accompanied by a significant growth acceleration in the two cell lines (Fig. 3B-D) and resistance to apoptosis (Fig. 4B-D), suggesting that down-regulation of PLK2, PLK3, and PLK4 play

a protumorigenic role in human hepatocarcinogenesis. Next, we assessed the possible interplay between PLKs by determining the levels of PLK1-4 genes following siRNA-mediated silencing of the other members of the PLK family. Interestingly, suppression of both PLK2 and PLK3 led to up-regulation of PLK1 (Supporting Figs. 2 and 3), implying a modulatory role of PLK2 and PLK3 over PLK1 expression. No additional modifications in gene expression were detected following silencing of MAPK inhibitor PLK1 and PLK4 by siRNA (Supporting Figs. 2 and Epigenetics inhibitor 3). Thus, the present data suggest that PLK1 promotes the growth of human HCC cells, whereas the down-regulation of PLK2, PLK3, and PLK4 antagonizes the antiproliferative and

proapoptotic functions exerted by these proteins in nontumor cells. Because the most pronounced antitumorigenic effects on HCC cell growth were obtained by targeting PLK1, our following studies focused on the role of PLK1 in the regulation of cell cycle and apoptosis in HCC cells. Silencing of PLK1 expression by siRNA in Hep3B and HepG2 cells resulted in a block in G2/M phase (Fig. 5A) as well as in a strong increase of the sub-G1 fraction indicating apoptosis (data not shown), as confirmed by the detection of cleaved PARP protein

these (Fig. 5B). In addition, inhibition of PLK1 expression was followed by down-regulation of the antiapoptotic protein survivin (Fig. 5B), supporting the recent finding that PLK1 promotes cell survival through inhibition of survivin degradation in esophageal cancer cells.25 Previous evidence indicated that PLK1 can bind to p53 and abrogate its tumor suppressor functions,26 and recent reports have demonstrated that PLK1 is able to phosphorylate the tumor suppressor p73, with consequent inhibition of its transcriptional activity, thereby suppressing apoptosis.27, 28 Thus, we determined whether the activation of p53 and p73 proteins could be involved in the apoptotic response following PLK1 inhibition. In accordance with our hypothesis, up-regulation of p53 and p73 protein levels as well as activation of their target genes p21CIP1 and BAX was detected in HepG2 cells (p53 wild-type) following PLK1 inhibition (Fig. 6A). In Hep3B cells (p53 deletion), apoptosis induction was paralleled by a rise in p73 expression and the induction of p21CIP1 and BAX (Fig. 6A). Furthermore, siRNA-mediated silencing resulted in BAX activation in HepG2 and Hep3B cells, as demonstrated by its translocation to the mitochondria and subsequent release of cytochrome C into the cytoplasm (Fig. 6B).

16 The stress response in humans involves activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. The former is mediated by the release of corticotropin-releasing hormone, adrenocorticotropin hormone and cortisol while the latter is largely mediated by

the release of catecholamines.17 Both norepinephrine (noradrenaline) and cortisol levels have been shown to increase during unsedated upper endoscopy.18 In relation to stress and pancreatitis, stress responses could alter sphincter of Oddi motility and induce ductal hypertension or adversely affect the concentrations of cytoprotective molecules such Protein Tyrosine Kinase inhibitor as heat shock proteins.19 Although sympathetic blockade does not appear to influence sphincter motility in animal models,20 the effects of sympathetic

and parasympathetic activity on sphincter function in humans continues to be unclear. Of interest is an association between serum catecholamine levels, sphincter motility and anomalous responses to morphine in patients with biliary-type pain after cholecystectomy.21,22 There is also a report of beneficial effects from clonidine in five patients with persistent pancreatitis who had elevated levels of catecholamines and cortisol.23 Do the above observations have any clear messages? One is that myocardial ischemia during ERCP or other endoscopic procedures is probably more common than is currently recognized. A second message

is that the stress response prior to or during procedures such as ERCP may influence the Lorlatinib chemical structure Fenbendazole frequency of complications such as pancreatitis. This could be examined in a practical way by determining whether the frequency of ERCP pancreatitis is lower with unconscious sedation than with conscious sedation or whether ERCP pancreatitis can be minimized by sedation or sympathetic blockade prior to the procedure or even by the use of ampullary anesthesia prior to cannulation.24 “
“Alterations in DNA methylation frequently occur in hepatocellular cancer (HCC). We have previously demonstrated that hypermethylation in candidate genes can be detected in plasma DNA before HCC diagnosis. To identify, with a genome-wide approach, additional genes hypermethylated in HCC that could be used for more accurate analysis of plasma DNA for early diagnosis, we analyzed tumor and adjacent nontumor tissues from 62 Taiwanese HCC cases using Illumina methylation arrays (Illumina, Inc., San Diego, CA) that screen 26,486 autosomal CpG sites. After Bonferroni adjustment, a total of 2,324 CpG sites significantly differed in methylation level, with 684 CpG sites significantly hypermethylated and 1,640 hypomethylated in tumor, compared to nontumor tissues. Array data were validated with pyrosequencing in a subset of five of these genes; correlation coefficients ranged from 0.92 to 0.97.

Serum total bilirubin and cholestatic enzymes (ALP, GGT) are important

for assessing the activity and progression of PBC. Liver biochemical tests should be done every 3–6 months. In addition, thyroid hormone (every year) and bone mineral density (every 2–4 years) tests are recommended because PBC is likely to be complicated with other autoimmune diseases, such as Sjögren’s syndrome, chronic thyroiditis, and rheumatoid arthritis. Regular upper gastrointestinal endoscopy, depending on stage (1 or 2 times per year), is required because esophageal/gastric varices may develop even in patients without jaundice. Abdominal Daporinad manufacturer ultrasound (US) and serum AFP testing every 6–12 months are necessary in patients with definite or suspected liver cirrhosis. Liver cirrhosis, older age, and male sex are high risk factors for developing hepatocellular carcinoma (HCC). Therefore, testing for tumor markers and imaging studies [US and computed tomography (CT)] are required for early detection of HCC in patients with advanced PBC. Management

for other complicating autoimmune diseases should be done depending on each symptom. Finally, special attention should be paid to pregnancy in PBC and patients who have a desire to bear children. The chance for pregnancy could be the same in the early stage of aPBC as in the normal population; there is no evidence to recommend Midostaurin supplier avoidance of pregnancy in patients with aPBC. In sPBC, however, if worsening of icterus second or varices is reported, then avoidance of pregnancy could be justified. The impact of pregnancy on PBC is unclear because both exacerbation and improvement of cholestasis have been reported. Estrogen could potentially worsen cholestasis; pruritus may become severe in pregnancy and could be prolonged even after delivery. Conversely, it should be noted that cholestasis could be symptomatic after pregnancy. After a patient has become pregnant, monitoring for varices is necessary as in other

cirrhotic patients, especially after the second trimester, due to increase in circulating blood volume. The use of β blockers is considered to be safe. It is also advisable to shorten the second trimester of pregnancy, if possible. Recommendations: The blood and other clinical tests should be undertaken regularly to investigate complicating comorbidities, prevent complications, and detect portal hypertension and liver cancer as early as possible. (Table 13) (LE 3, GR B) It is advisable to consult with hepatologists when the diagnosis of PBC is made, or when patients with PBC become symptomatic. In patients with atypical forms of PBC such as PBC–AIH overlapping syndrome, earlier referral is recommended. (Table 14) (LE 6, GR A-B) For patients in the symptomatic stage, there is a likelihood of worsening of pruritus or icterus in the pregnancy, as well as an increased possibility of variceal rupture.

56, P < 0.0001; data not shown). In addition, another study has reported that BCAA-enriched supplements ameliorated IR in patients

with chronic liver disease.[26] Although serum BCAA levels were not significantly increased, the serum tyrosine levels decreased after the administration of BCAA-enriched supplements,[26] suggesting that changes in serum tyrosine levels reflect changes in IR. Although it remains unclear how BCAA caused a decrease in tyrosine levels, this result supports our finding that the serum tyrosine levels and IR are correlated. Therefore, the regulation of serum tyrosine concentrations may ameliorate IR in patients with HCV-related chronic liver disease. In addition, serum tyrosine may be associated with suppression of cytokine

signaling 3 (SOCS-3), which contributes to IR, because BCAA suppress Tanespimycin SOCS-3.[27] In addition to serum tyrosine, total cholesterol was a significant independent parameter contributing to IR in the present study. Total cholesterol may be associated with IR because HCV infection and chronic hyperinsulinemia cause disturbances in lipid metabolism.[28, 29] Our study has some limitations. First, we did not evaluate individual amino acids. Because BCAA and AAA have significant associations with future onset of diabetes mellitus,[15, 17] further investigation of the association between individual amino acids and IR is necessary. Second, we were unable to obtain liver specimens for all patients; therefore, we did not include histological findings in the analyses of clinical parameters contributing to IR. Similar studies that include histological findings for all patients should be Selleck SB203580 conducted. In conclusion, serum tyrosine levels may be associated with IR in patients with HCV-related chronic liver disease. Therefore, it may be important to regulate serum tyrosine to control IR in patients with HCV-related chronic liver disease.

We hope that our finding of an association between tyrosine and IR will lead to the discovery of new pathophysiological mechanisms underlying IR. “
“See article in J. Gastroenterol. Hepatol. 2012; 27: 1181–1186. “
“The incidence of liver disease progression among subjects with histologically advanced Carbohydrate but compensated chronic hepatitis C is incomplete. The Hepatitis C Antiviral Long-term Treatment against Cirrhosis Trial was a randomized study of 3.5 years of maintenance peginterferon treatment on liver disease progression among patients who had not cleared virus on peginterferon and ribavirin therapy. Patients were followed subsequently off therapy. Because maintenance peginterferon treatment did not alter liver disease progression, we analyzed treated and control patients together. Among 1,050 subjects (60% advanced fibrosis, 40% cirrhosis), we determined the rate of progression to cirrhosis over 4 years and of clinical outcomes over 8 years. Among patients with fibrosis, the incidence of cirrhosis was 9.9% per year.

3×10-9, odds ratio = 5.3). This variant has previously been associated in multiple large genome-wide studies with hepatic steatosis, fibrosis and related phenotypes. Further comparisons identified other promising candidates (Table 1) but these did not reach significance after multiple test correction. Conclusion: Identification

of the known PNPLA3 Selleckchem Opaganib risk variant despite a very small sample size suggests accurate phenotyping and supports the use of an extreme phenotype design in NAFLD. Future expansion of the sample size is likely to identify further key causal genetic variants contributing to advanced fibrosis from NAFLD using this approach. Disclosures: Thomas J. Urban – Patent Held/Filed: Schering Plough Manal F. Abdelmalek – Consulting: Islet Sciences; Grant/Research Support: Mochida Pharmaceuticals, Gilead

Sciences, NIH/NIDDK, Synageva, Genfit Pharmaceuticals David B. Goldstein – Advisory Committees or Review Panels: Astra Zeneca, NIH, Biogen, Gordon Research Conference; Board Membership: Knome; Consulting: glaxo smithkline, Severe Adverse Events Consortium, Roche, Gilead Sciences, Inc, Scienta Advisors; Employment: Duke University; Grant/Research Support: UCB, NIH, Biogen, Henry M Jackson Foundation, SAIC, Inc, Bill & Melinda Gates Foundation, Eisai, Inc; Patent Held/Filed: patent IL28B findings, patent ITPA findings, Merck & Company; GDC-0973 clinical trial Speaking and Teaching: Current Biology magazine, Illumina, Regeneron, Dermatology Society; Stock Shareholder: Pfizer Anna Mae Diehl – Consulting: Roche; Grant/Research Support: Gilead, Genfit The following people have nothing to disclose: Cynthia A. Moylan, Matthew Rein Background

& Aims: Fibroblast growth factor 21 EGFR inhibitor (FGF21) is a hepatokine that regulates glucose and lipid metabolism in the liver. Circulating FGF21 levels are closely correlated with hepatic fat content in multiple disease conditions. Hepatic fat accumulation is a hallmark of alcoholic liver disease (ALD). We sought to determine the role of FGF21 in hepatic ste-atosis in mice exposed to chronic alcohol treatment and to discern underlying mechanisms. Methods: Male FGF21 knockout (FGF21 KO) and control (WT) mice were divided into groups that were fed either the Lieber DeCarli diet containing 5% alcohol or an isocaloric (control) diet for 4 weeks. One group of WT mice exposed to alcohol received recom-binant human FGF21 for the last 5 days. Liver tissues were collected and examined for histologic alterations, liver fat and the corresponding gene and protein expression. Primary mouse hepatocytes and H4IIE cells were incubated with metformin or recombinant FGF21 protein. Genes and the products involved in in situ lipogenesis and fatty acid p-oxidation were analyzed. Results: Alcohol exposure increased circulating levels and hepatic expression of FGF21.

No perforation occurred during operation. Pathological examination confirmed leiomyoma in 24 cases, Selinexor cost lipomyoma in 8 cases, heterotopic pancreas in 3 cases, gastrointestinal stromal tumor (GIST) in 2 cases, xanthoma in 1 case and submucosal tissue hyperplasia in the rest 4. During a mean follow-up observation of 13.6 months (range: 2–26 months), no tumor recurrence was confirmed. Conclusion: ESE is a safe and effective treatment for gastroesophageal submucosal tumors. It is alternative to surgical therapy with its preservation of the integrity of the stomach and shorter hospital stay. Key Word(s): 1. ESE; 2. Submucosal Tumor; Presenting Author: XUEFENG LU Corresponding Author: XUEFENG

LU Affiliations: Qilu hospital of shandong university Objective: Transparent cap is becoming increasingly desirable for an attachment in endoscopic diagnosis and treatment, including EMR, ESD, assisting the colonoscope into the body, etc. But application in the treatment of duodenal lesions is not widely. In this study, we aimed to investigate its values in the relatively new field. Methods: A total of 135 patients who got duodenal bulb polyps or heterotopic gastric mucosa were retrospectively reviewed. All of them were treated with APC, during which 17 cases using transparent cap while 118 cases without using it. Then analysis the two groups from the following aspects: the exposure of operative areas, the complications and

residual lesions. Before this study, selleck we have developed the following criteria to define the vision clarity. Grade A: clear vision. Grade B: vision is affected. Results: In our transparent cap group, the exposure of operative areas were classified to grade A, B, were 70.6%(12/17), 29.4%(5/17), while in control group, the corresponding numbers belong to grade A, B, were 29.7%(35/118), 70.3% (83 /118), (P < 0.01). Thus transparent cap could reduce complications of perforation and bleeding, which came from eschar shedding because of the repeated endoscope comes and goes. We also find that the

rate of residues re-treatment was 5.9% (1/17), 10.2% (12/118), respectively (P < 0.05). Conclusion: Using transparent cap in the treatment of duodenal bulb lesions is valid, and we hope it can be utilized in wider areas. Key Word(s): 1. Transparent cap; 2. duodenal bulb; Fossariinae Presenting Author: YI-YI HU Additional Authors: YALI ZHANG Corresponding Author: YALI ZHANG Affiliations: Department of Gastroenterology, Nanfang Hospital, Southern Medical University Objective: This study is to evaluate the function of oddi sphincter and gall bladder after ERCP. Methods: We had a retrospective study of 58 patients who had ERCP from January 2006 to December 2012. Results: There are EST large incision group 21 cases (12 males, 9 females). EST medium and small incision group, 20 cases (8 males, 9 females), EBPD 17 cases (11 male and 9 females); Normal subjects group of 20 cases (12 males, 8 females).

00 hours on the day of the baseline (day −1). Subjects took each dose of revaprazan at 8.00 hours, after fasting overnight, and continued fasting until 4 h after administration of revaprazan on days 1 and 7. Each dose of revaprazan was wrapped in an opaque envelope and was given to the subject by a study coordinator who witnessed the emptying of the revaprazan into the subject’s mouth and the swallowing of the dose. On days 2–6, subjects received the dose once daily at the same time as on day 1, and continued fasting for 2 h after administration of revaprazan. A standardized meal buy Hydroxychloroquine was provided to the

subjects 4 h and 8 h after the 8.00 hours administration of revaprazan at baseline Fulvestrant ic50 and on days 1 and 7. Subjects were dismissed from the clinic after they had been observed eating the meal at baseline and on days 1 and 7. Each administration period was separated by a washout period of 7 days, during which no revaprazan was taken (Fig. 1). Drugs other than revaprazan were not allowed during the study period. Ambulatory 24-h intragastric pH monitoring was performed at baseline and on days 1 and 7 of each administration period (Fig. 1). After induction of anesthesia using a 1% lidocaine spray administered via the nose, a calibrated bipolar glass pH electrode catheter (Medtronic Synectics AB, Stockholm, Sweden) was inserted

into the stomach via the nose and positioned approximately 5 cm below the manometrically located lower esophageal sphincter.13 The catheter was connected to a portable digital data recorder (MicroDigitrapper 4 Mb, Medtronic Synectics AB), and intragastric pH was recorded every 8 s. Revaprazan was administrated after probe placement.

Data were analyzed after completion of the recording. Mean intragastric Digestive enzyme pH–time profile, 24-h median intragastric pH and mean percentage time of pH > 4 were calculated. Serum gastrin levels were measured under fasting conditions and 1 and 2 h postprandially (5 h and 6 h after administration of revaprazan) at baseline and on days 1 and 7 of each cross-over period (Fig. 1) using a commercial, validated radioimmunoassay (ALPCO, Salem, NH, USA). Blood samples for pharmacokinetic assessment of revaprazan were taken at set times on days 1 and 7 (Fig. 1). Blood samples (8 mL) were obtained via an indwelling cannula inserted into a forearm vein. Blood was sampled at baseline (pre-dose) and at 0.25, 0.5, 0.75, 1, 1.5, 2, 3, 4, 6, 8, 12 and 24 h after drug administration. The blood samples were centrifuged at 1200 × g for 10 min at 4°C, and the plasma was immediately stored in polypropylene tubes at −20°C or lower until required for analysis. The plasma concentration of revaprazan was determined by liquid chromatography/mass spectrometry.

01), and dominated by CD68+ macrophages and CD8+ lymphocytes, at all stages of disease. An increase NU7441 nmr in portal macrophages in NAFLD patients with steatosis alone (P < 0.01) was the earliest change detected, even before elevated expression of the proinflammatory cytokines, IL1B and TNF, in patients with early NASH (P < 0.05). Portal and periductal accumulation of all other cell types examined occurred in progressed NASH (all P < 0.05). Conclusion: Knowledge of the complex cellular composition of the portal inflammatory infiltrate and HPC/DR niche in NAFLD will shape future functional studies to elucidate the contribution of portal inflammation to HPC differentiation and

NAFLD pathogenesis. (Hepatology 2014;59:1393-1405) “
“Ulcerative colitis is a chronic relapsing inflammatory disease sharing many features with Crohn’s disease but differing in being confined to the colonic mucosa, without proximal involvement or penetration to the deeper layers of the bowel, in uncomplicated cases. Ulcerative colitis has changed

face over time; once considered rare, it is now a major gastroenterologic problem in the developed world with changing demographics. The first controlled clinical therapeutic trial of corticosteroids in ulcerative colitis half century ago highlighted gastroenterology as an early exponent of evidence-based medicine. More recently, the prognosis of patients with severe disease has improved with attention to detail, critical care and the advent of immunomodulatory agents.

However, despite remarkable advances, ulcerative colitis remains a significant burden on healthcare resources and a cause mafosfamide of much individual suffering. lambrolizumab “
“There are no data specifically correlating early intravenous volume infusion (IVI) with the length of hospitalization for postendoscopic retrograde cholangiopancreatography (ERCP) pancreatitis (PEP). We conducted a retrospective cohort study of patients admitted within 24 h after ERCP to our institute with PEP. IVI during the first 24 h after ERCP was assessed. Primary outcome was severity of PEP, defined by length of hospitalization according to consensus guidelines: mild ≤ 3, moderate 4–10, and severe > 10 days. Of 72 eligible patients, 41 (56.9%) had mild and 31 (43.1%) moderate/severe PEP. Both groups had comparable demographics, indications, and procedural factors except patients with moderate/severe PEP were older (median age 49 vs 36 years, P = 0.05) and more likely to be discharged and readmitted within the first 24 h (41.9% vs 14.6%, P < 0.01). Patients with mild PEP received significantly greater IVI during the first 24 h (2834 mL [2046, 3570] vs 2044 mL [1227, 2875], P < 0.02) and 50% more fluid post-ERCP (2270 mL [1435, 2961] vs 1515 [950–2350], P < 0.02) compared with those with at least moderate PEP. In patients with PEP, greater IVI during the first 24 h after ERCP is associated with reduced length of hospitalization.