Risk factors for HCC or ICC were selected using ICD-9-CM codes.31 Liver flukes: 121.3, 121.0; Biliary cirrhosis: 571.6; Cholangitis: 576.1; Cholelithiasis: 574; Choledochal cyst: 751.69; HBV infection: 070.2, 070.3, 070.42, 070.52, V02.61; HCV infection: 070.41,

070.44, 070.51, 070.54, 070.7, V02.62; Unspecified viral hepatitis: 070.9, 070.59, 070.49; Hemochromatosis: 275.0; Wilson’s disease: 275.1. Smoking: V15.82, 305.1, 989.84; Crohn’s disease: 555, 555.0, 555.1, 555.2, 555.9; Ulcerative colitis: 556, 556.0, 556.1, 556.2, 556.3, 556.5, 556.6, 556.9. Alcoholic liver disease was defined as alcoholic fatty liver disease (571.0), alcoholic hepatitis (571.1), alcoholic cirrhosis of the liver (571.2), alcoholic liver damage (571.3), or cirrhosis (571.5, 571.6) in the presence of alcoholism or other alcohol-related disorders (303, 305.0, V11.3, V79.1, 291). Nonspecific GSK-3 signaling pathway cirrhosis was defined as cirrhosis (571.5, 571.6) without HCV, HBV, or alcoholic liver disease. Age, race/ethnicity (white, black, Hispanic, Asian, other), geographic region (SEER-13 registry region), and state buy-in status were included as covariates. The state buy-in variable indicates whether a third-party pays a beneficiary’s Medicare premiums, and was thus used as an indicator of lower socioeconomic status. Demographic features and preexisting medical conditions were compared between cases and controls

using t tests for continuous variables and chi-square or Fisher’s exact tests for categorical variables. Logistic regression was used to calculate odds ratios (OR) and 95% confidence this website intervals (95% CI). Wald chi-square tests determined the significance of variables in the logistic regressions. Tests of statistical significance and CIs were two-sided. A P value < 0.05 was considered statistically significant. In addition to the main analyses, several sensitivity analyses were performed. The see more first sensitivity analysis excluded medical conditions diagnosed in the year preceding the cancer diagnosis, whereas the second excluded undifferentiated tumors. Statistical analyses were performed

using SAS, version 9.1 (SAS Institute, Cary, NC). During the study period, 16448 HCC cases and 3005 ICC cases were identified and 3649 HCC cases and 743 ICC cases met the inclusion criteria. Excluded were 6118 HCC and 1317 ICC cases without histopathological confirmation; 75 HCC and 11 ICC cases without known month of diagnosis; 286 HCC and 52 ICC cases with prior cancer diagnoses within the previous 5 years; 6286 HCC and 871 ICC cases who did not meet the age, enrollment interval, or enrollment type criteria; and 34 HCC and 11 ICC cases reported solely by autopsy or death certificate. Population controls included 195,953 persons without any prior cancer diagnosis who met the inclusion criteria as specified above. Table 1 shows the features and demographic characteristics of the study population. The HCC and ICC cases were younger (P < 0.

Previously rare and common

variants of NPC1L1 have been reported to influence sterol absorption.34, 35 Although NPC1L1 has never been regarded as a Lith gene, we cannot exclude the possibility that loss-of-function of this transport could contribute to GSD. Recently, several other LITH genes have also been detected.10 Although polymorphisms in these loci only moderately affect gallstone risk, we cannot exclude that they contribute to gallstone formation in the individuals included in our study. Interestingly, in the German cohort the association between cholesterol synthesis and transport with GSD was more pronounced Neratinib order in women than in men. This observation might be related to a lower number of men in the German cohort, which decreases the power of this analysis. Also, the Chilean cohort was predominantly female. Our findings suggest that

a distorted cholesterol homeostasis is more evident click here in women in whom GSD is in general more common. Cholesterol absorption and synthesis can also be affected by insulin sensitivity, which is, at least in part, determined genetically, but also associated with BMI and central obesity. Of note, both obesity and insulin resistance modulate cholesterol absorption and synthesis.36 Indeed, lean subjects with lower insulin sensitivity show higher cholesterol synthesis and lower sterol absorption. In our Hispanic and Amerindian cohorts, GSD and controls are similar in terms of BMI and insulin resistance, thus the specific sterol metabolic trait associated with GSD is not confounded by these variables. Cases and controls included in the follow-up study were matched for these variables at inclusion, and members of both subgroups developed obesity, insulin resistance and metabolic syndrome to similar extents. Although these changes might suggest that the metabolic variables selleck chemicals contributed to GSD, our refined analysis showed that only individuals

with lower sterol absorption at study entry were susceptible to gallstone development. Notably, we showed previously that this increment in metabolic syndrome traits in Chile during the period from 1992 to 2001 is higher than expected and related to changes of socioeconomic status.37 This study is notable because none of the subjects were under cholesterol reducing therapy with ezetimibe or statins. In fact, the cohorts were recruited before ezetimibe was introduced as a drug for hypercholesterolemia, and the use of statins was an exclusion criterion both in cases and controls. The results, therefore, provide novel and unique insights into cholesterol flux and its relation to gallstone formation (Fig. 5). Previous studies on the effect of drugs lowering cholesterol synthesis (i.e., statins) and absorption (i.e., ezetimibe) are controversial. Analyses performed in large human cohorts have documented lower prevalence of clinical relevant gallstone disease (i.e.

Results: In response to hypotonic stimulation (30%), control mouse BECs exhibited bulk ATP release and point-source release from confluent monolayers; and, in individual cells, an increase in the rate of exocytosis, trafficking and release of ATP-V as expected. In contrast, interruption of SNARE

complex formation by NEM blocked both Selleck MLN8237 bulk ATP release and point-source ATP bursts from monolayers, as well as decreased the rate of exocytosis and exocytosis of ATP-V in individual cells. Mouse BECs expressed STX -1A, -2, and -3A. STX -1B and -3B were not expressed. Immunostaining revealed strong STX-1A and -3A signal on the apical BEC membrane. In individual studies, transfection with specific siRNAs significantly decreased protein expression of each STX, though only the STX -1A and -3A knock-down was associated with inhibition of ATP release. Conclusion: Together, the findings

demonstrate that syntax- in-1A and -3A play an important role in ATP-V exocytosis and release of ATP by BECs. Targeting STXs may represent a novel therapeutic option to augment release of ATP into bile, increase biliary secretion, and promote bile formation for the http://www.selleckchem.com/products/OSI-906.html treatment of cholestatic liver diseases. Disclosures: The following people have nothing to disclose: Razan Bader, Qin Li, Charles Kresge, Abhijit Bugde, Matthew A. Lewis, Andrew P. Feranchak Introduction: Hepatobiliary excretion of bile acids is an essential liver function which is not accessible by conventional means of measurements. We examined

whether PET/CT using the radio-labeled conjugated bile acid analogue [N-methyl-11C]cholyl-sarcosine (11C-CSar) as tracer allowed quantitative assessment of this function in human subjects. Methods: Ten healthy subjects and ten patients with varying degrees of cholestasis each underwent two 60 minutes dynamic PET/CT recordings of the liver using intravenous bolus injection check details and continuous infusion of 11C-CSar. Blood concentrations of 11C-CSar were measured in samples collected from a radial artery and a hepatic vein. Concentrations of 11C-CSar in the liver tissue and common hepatic bile ducts were recorded by PET. Hepatic blood flow was measured using intravenous infusion of indocyanine green and Fick’s principle. Hepatic extraction fraction of 11C-CSar was calculated from the arterial and hepatic venous concentration measurements. Fractional biliary excretion at a given time point was calculated as the ratio between 11C-CSar excreted into bile and 11C-CSar supplied to the liver. Results: The 11C-CSar concentration in liver tissue showed an initial rapid rise, which was similar in patients and healthy subjects. The subsequent elimination of 11C-CSar from liver tissue to bile was significantly reduced in patients with cholestasis. In the common hepatic bile duct, the arrival of 11C-CSar was delayed and reached a lower peak concentration in the patients than in the healthy subjects.

Results: In response to hypotonic stimulation (30%), control mouse BECs exhibited bulk ATP release and point-source release from confluent monolayers; and, in individual cells, an increase in the rate of exocytosis, trafficking and release of ATP-V as expected. In contrast, interruption of SNARE

complex formation by NEM blocked both Selleckchem CH5424802 bulk ATP release and point-source ATP bursts from monolayers, as well as decreased the rate of exocytosis and exocytosis of ATP-V in individual cells. Mouse BECs expressed STX -1A, -2, and -3A. STX -1B and -3B were not expressed. Immunostaining revealed strong STX-1A and -3A signal on the apical BEC membrane. In individual studies, transfection with specific siRNAs significantly decreased protein expression of each STX, though only the STX -1A and -3A knock-down was associated with inhibition of ATP release. Conclusion: Together, the findings

demonstrate that syntax- in-1A and -3A play an important role in ATP-V exocytosis and release of ATP by BECs. Targeting STXs may represent a novel therapeutic option to augment release of ATP into bile, increase biliary secretion, and promote bile formation for the PLX3397 clinical trial treatment of cholestatic liver diseases. Disclosures: The following people have nothing to disclose: Razan Bader, Qin Li, Charles Kresge, Abhijit Bugde, Matthew A. Lewis, Andrew P. Feranchak Introduction: Hepatobiliary excretion of bile acids is an essential liver function which is not accessible by conventional means of measurements. We examined

whether PET/CT using the radio-labeled conjugated bile acid analogue [N-methyl-11C]cholyl-sarcosine (11C-CSar) as tracer allowed quantitative assessment of this function in human subjects. Methods: Ten healthy subjects and ten patients with varying degrees of cholestasis each underwent two 60 minutes dynamic PET/CT recordings of the liver using intravenous bolus injection learn more and continuous infusion of 11C-CSar. Blood concentrations of 11C-CSar were measured in samples collected from a radial artery and a hepatic vein. Concentrations of 11C-CSar in the liver tissue and common hepatic bile ducts were recorded by PET. Hepatic blood flow was measured using intravenous infusion of indocyanine green and Fick’s principle. Hepatic extraction fraction of 11C-CSar was calculated from the arterial and hepatic venous concentration measurements. Fractional biliary excretion at a given time point was calculated as the ratio between 11C-CSar excreted into bile and 11C-CSar supplied to the liver. Results: The 11C-CSar concentration in liver tissue showed an initial rapid rise, which was similar in patients and healthy subjects. The subsequent elimination of 11C-CSar from liver tissue to bile was significantly reduced in patients with cholestasis. In the common hepatic bile duct, the arrival of 11C-CSar was delayed and reached a lower peak concentration in the patients than in the healthy subjects.

8 cm adds specificity to the likelihood that the patient has neoplastic disease. Obviously,

recommendations are only meant to guide an “individualized” approach regarding management decisions that must take into account the variety of unique patient factors. We hope this clarifies our recommendations and check details places them in context vis-à-vis the EASL and AASLD guidelines and provides impetus for further investigations on the subject. Gregory Gores M.D., F.A.C.P.*, Keith D. Lindor M.D.*, Nataliya Razumilava M.D.*, * Division of Gastroenterology and Hepatology, Mayo Medical School, Rochester, MN. “
“ATP8B1 deficiency is a severe autosomal recessive liver disease due to mutations in the ATP8B1 gene characterized by a continuous phenotypical spectrum from intermittent (benign recurrent intrahepatic cholestasis; BRIC) to progressive familial intrahepatic cholestasis (PFIC). Current therapeutic options are insufficient and elucidating the molecular consequences of mutations could lead to personalized mutation-specific therapies. We investigated the effect on pre-messenger RNA splicing of 14 ATP8B1 mutations at exon-intron boundaries using an in vitro minigene system. Eleven mutations, mostly associated find more with a PFIC

phenotype, resulted in aberrant splicing and a complete absence of correctly spliced product. In contrast, three mutations led to partially correct splicing and were associated with a BRIC phenotype. These findings indicate an inverse correlation between the level of correctly spliced product and disease severity.

Expression of modified U1 small nuclear RNAs (snRNA) complementary to the splice donor sites strongly improved or completely rescued splicing for several ATP8B1 mutations located at donor, as well as acceptor, splice sites. In one case, we also evaluated exon-specific U1 snRNAs that, by targeting non-conserved intronic selleck kinase inhibitor sequences, might reduce possible off-target events. Although very effective in correcting exon skipping, they also induced retention of the short downstream intron. Conclusion: We systematically characterized the molecular consequences of 14 ATP8B1 mutations at exon-intron boundaries associated with ATP8B1 deficiency and found that the majority resulted in total exon skipping. The amount of correctly spliced product inversely correlated with disease severity. Compensatory modified U1 snRNAs, complementary to mutated donor splice sites, were able to improve exon definition very efficiently and could be a novel therapeutic strategy in ATP8B1 deficiency as well as other genetic diseases. This article is protected by copyright. All rights reserved. “
“The deregulation of microRNAs (miRNAs) plays an important role in human hepatocarcinogenesis. In this study, we highlight exosomes as mediators involved in modulating miRNA profiles in hepatocellular carcinoma (HCC) cells.

Further, sigmoidoscopy is easily performed, and appears to be a useful MAPK Inhibitor Library supplier way of making a judgement at 3 months as to which patients need more careful

follow up, and in whom further therapy to achieve mucosal healing might be warranted. Although this approach seems logical, it should be emphasized that while mucosal healing has been proven to be associated with good outcomes, to date, it has not yet been proven that striving harder to achieve mucosal healing benefits patients. It might simply be that we are “picking winners” early when we find those who heal promptly with whichever therapy we give. This conundrum of whether the benefits of treatment intensification outweigh its costs and adverse effects is one of the most important areas for future studies in inflammatory bowel disease. In conclusion, the time for studies fine tuning corticosteroid therapy in UC are probably past, with the Asian experience now shown to be similar to an extensive worldwide clinical experience, as to their efficacy.2,6,11,12 The bigger gains are to be made with identifying

non-responders early, prompt institution of 5-ASA maintenance therapy, stepping up early to thiopurines when indicated, and designing future studies to determine whether greater gains can be made by striving harder for mucosal healing without unacceptable cost or toxicities. “
“Diets high in saturated fat and fructose have been implicated in the development of obesity and nonalcoholic steatohepatitis (NASH) selleckchem in humans. We hypothesized that mice exposed to a similar diet would develop NASH with fibrosis associated with increased hepatic oxidative stress that would be further reflected by increased plasma levels of the respiratory chain component, oxidized coenzyme Q9 (oxCoQ9). Adult male C57Bl/6 mice were randomly assigned to chow, high-fat

(HF), or high-fat high-carbohydrate click here (HFHC) diets for 16 weeks. The chow and HF mice had free access to pure water, whereas the HFHC group received water with 55% fructose and 45% sucrose (wt/vol). The HFHC and HF groups had increased body weight, body fat mass, fasting glucose, and were insulin-resistant compared with chow mice. HF and HFHC consumed similar calories. Hepatic triglyceride content, plasma alanine aminotransferase, and liver weight were significantly increased in HF and HFHC mice compared with chow mice. Plasma cholesterol (P < 0.001), histological hepatic fibrosis, liver hydroxyproline content (P = 0.006), collagen 1 messenger RNA (P = 0.003), CD11b-F4/80+Gr1+ monocytes (P < 0.0001), transforming growth factor β1 mRNA (P = 0.04), and α-smooth muscle actin messenger RNA (P = 0.001) levels were significantly increased in HFHC mice. Hepatic oxidative stress, as indicated by liver superoxide expression (P = 0.002), 4-hydroxynonenal, and plasma oxCoQ9 (P < 0.001) levels, was highest in HFHC mice.

Delhem et al.[36] found that tumor-derived HCV core proteins, but not nontumor-derived ones, interact with and activate double-stranded RNA-dependent protein kinase (protein kinase R or PKR), which might modulate viral persistence and carcinogenesis. Gln70 was found in two of the three tumor-derived sequences, whereas Arg70 was found in two of the three nontumor-derived ones. As for the NS3 protein of HCV, the possible link between an N-terminal portion of NS3 encoding viral serine protease (aa 1027 to 1146) and hepatocarcinogenesis was reported.[21, 22] However, information about the

relationship between NS3 sequence diversity and HCC development is still limited. We previously reported a significant correlation between predicted secondary structure of an N-terminal portion of NS3 and HCC development.[34] In the present study, we demonstrated that HCV patients infected with HCV isolates Tamoxifen clinical trial with NS3-(Tyr1082/Gln1112) were at a higher risk Decitabine chemical structure to develop HCC than those infected with HCV isolates with non-Tyr1082/Gln1112 (Tables 2, 3; Fig. 2B). Computer-assisted secondary structure analysis of NS3 revealed that Tyr1082 was associated with the presence of a turn structure at around position

1083 while Phe1082 was associated with the absence of the turn structure.[34] Notably, the catalytic triad of NS3 serine protease consists of His1083, Asp1107, and Ser1165.[37] Since positions 1082 and 1112 are in close vicinity of the catalytic triad, sequences diversity at these positions might influence the serine protease activity and also pathogenicity of HCV. Large-scale,

multicenter this website clinical studies as well as more detailed experimental studies at the molecular and cellular levels are needed to clarify the importance of sequence diversity at positions 1082 and 1112 of NS3 in HCV-mediated hepatocarcinogenesis. HCV heterogeneity in NS5A-ISDR and NS5A-IRRDR are correlated with IFN-responsiveness.[17, 18, 25, 26] As IFN-based therapy reduces the risk of HCC development,[4, 28] we were interested to investigate whether there is a correlation between sequence heterogeneity in NS5A and development of HCC. Our present results revealed that a high degree of sequence heterogeneity in IRRDR (IRRDR≥6) was closely associated with HCC development (Table 2). We previously reported that IRRDR≥6 was significantly associated with good responses to PEG-IFN/RBV combination therapy.[26, 27] These results collectively suggest that oncogenic properties and PEG-IFN/RBV responsiveness are independent viral characteristics and that PEG-IFN/RBV therapy helps eliminate oncogenic HCV isolates, thus reducing the risk of HCC development. Position 2218 of NS5A, located within ISDR, appears to tolerate a wide range of aa substitutions as observed in different HCV-1b isolates.

Among those CM patients with CGRP levels below 72 pg/mL, 28% had low VIP levels and just 33.3% responded as compared with 77.4% responders in the remaining 72% who had high VIP levels. Therefore, the probability of being a responder in CM

patients with CGRP levels below the threshold was significantly higher in those patients with high VIP levels vs those with low VIP levels (OR: 6.857; 95% CI: 1.583-29.707; P = .012). Among CM patients with CGRP levels above the threshold, there was only one nonresponder who also had high VIP levels. As already reported by our group using in part subjects included here, this study first confirms that interictal CGRP and VIP levels measured in peripheral blood are increased in a large series of CM learn more patients this website vs healthy subjects with no headache history. In fact, both CGRP and VIP levels in CM were twice those of controls, which should be interpreted as distant signs of activation of the sensory and parasympathetic arms of the TVS, respectively. The levels of these two neuropeptides, and especially of CGRP due to its lower variability, measured in peripheral blood and outside migraine attacks have been proposed as the first biomarkers helpful for a more objective diagnosis of CM in the context of a patient with daily or almost daily headaches and a history of migraine, which could

be of value for a better selection of treatment for CM patients.[9, 10] The impact of CM in terms of quality of life and economic burden is very relevant.13-15 Treatment of CM is not easy.[14] Even selleckchem though in clinical practice we use oral preventatives with efficacy in EM, objective evidence of efficacy in CM is available only for topiramate16-18 and, to a lesser degree, for valproic acid.[19] It was not until

this decade that the efficacy of pericranial injections of 155-195 U of onabotA was shown in two large controlled phase III trials.[11] This efficacy has also been reported in several open studies20-23 and in this series in which three quarters of our patients showed an objective and subjective response to onabotA injections. The exact mechanism of action of pericranial injections of onabotA leading to migraine prevention is still unclear, and reliable potential predictors of response have not yet been identified. In the pooled analysis of the 2 phase III trials with onabotA in CM, there was no positive correlation between 85 possible clinical predictors and response to onabotA.[11] The main finding of the present work is that interictal CGRP, and to a lesser degree, VIP levels are potentially of great help on predicting response to onabotA. In fact, both CGRP and VIP levels were significantly higher in CM patients responding to onabotA as compared with nonresponders.

Therefore, we conducted a prospective cohort study in a clinical setting to assess bleeding risk attributable to gastric biopsy in patients taking antiplatelet agents and the validity of performing endoscopic biopsy with small cup biopsy forceps. Methods: The study was performed during

the 1-year for 5374 scheduled esophagogastroduodenoscopy performed. 1128 patients, PD 332991 including 65 patients taking antiplatelet agents underwent gastric biopsy with small cup biopsy forceps, and 2025 biopsy specimens were obtained from each part of the stomach. Clinical bleeding was investigated during and after endoscopy. Two pathologists assessed the presence of muscularis mucosae in biopsy specimens in addition to the suitability of specimens for histological diagnosis. Results: Ratio of appropriate

specimens obtained with small cup biopsy forceps was 99.3% (2010/2025) and muscularis mucosae was detected BTK inhibitor price in 27.8% (538/1394) of specimens. After endoscopy, 1 patient of 1049 patients who took no antithrombotic agents experienced major bleeding (0.095%); however, 65 patients receiving antiplatelet treatment experienced no bleeding. Conclusion: Endoscopic forceps with a small cup is useful and the absolute risk attributable to gastric biopsy in patients taking antiplatelet agents seems to be low. Key Word(s): 1. endoscopic biopsy; 2. antiplatelet agent; 3. bleeding; 4. biopsy forceps; 5. antithrombotic agent Presenting Author: KUNIO IWATSUKA Additional Authors: TAKUJI GOTODA, SHIN KONO, SHO SUZUKI, NAOKO YAGI, CHIKA KUSANO, MASAKATSU FUKUZAWA, TAKASHI KAWAI, FUMINORI MORIYASU Corresponding Author: KUNIO IWATSUKA Affiliations:

Tokyo Medical University, Tokyo Medical University, Tokyo Medical University, Tokyo Medical University, Tokyo Medical University, Tokyo Medical University, Tokyo Medical University Hospital, Tokyo Medical University Objective: Despite improvements in pharmacological click here and endoscopic hemostasis, gastrointestinal bleeding (GIB) remains fatal clinical event in the elderly patients. With increasing numbers of the elderly population, endoscopists might face such kind of serious cases. The aims of this study are to research treatment outcomes and clinical features of GIB in elderly patients. Methods: Medical records of 185 patients (mean age 68.2 years, range 10–99 years, male/female 123/62) with GIB who underwent esophagogastroduodenoscopy or colonoscopy from April 2012 to March 2014 were reviewed. Clinical outcomes and clinicopathological features including pre-existing co-morbidities, prescribed drugs (antiplatelet agent, anticoagulant, NSAIDs, corticosteroid) were compared between younger <70 years old) and elderly groups (≤70 years old). Results: Following features were specifically found in elderly patients (N = 100) compared to non-elderly patients (N = 85): presence of co-morbid diseases (90.0% vs. 62.4%: p < 0.001), low hemoglobin level (9.0 vs. 10.6 g/dl: p < 0.

Further investigation into the societal cost of cognitive dysfunction in cirrhosis is Bortezomib important to encourage routine diagnosis and therapy of MHE beyond the research setting. “
“See article in J. Gastroenterol. Hepatol. 2010; 25: 1416–1419. Drainage is needed for symptomatic or infected intraabdominal/pelvic fluid collections. The options are surgical, imaging-guided and endoscopic drainage. The surgical approach allows greater access, facilitates more thorough drainage and debridement,

and may address the predisposing condition at the same setting, but at the expense of being more invasive and associated with greater morbidity.1 An imaging-guided approach using computer tomography and ultrasound Everolimus price by the interventional radiologist is less invasive than surgical drainage. However, access for drainage may be limited by interposed organs, blood vessels, nerves and bony structures. There is also the possibility of inadvertent puncture of undetected interposed organs and vessels. Furthermore there is a need to insert an external indwelling drainage catheter for a prolonged period of time which can be uncomfortable for patients; the catheter may also be prone to slippage. Endoscopic transenteric drainage is less invasive than surgery, and may be able to access collections not possible with the imaging-guided approach. In addition, it does away with the need for an indwelling external drainage catheter because an internal

transenteric stent can be inserted, thus improving patient comfort. In the past, before the introduction of endoscopic ultrasound (EUS), endoscopic transenteric drainage was performed by puncturing the endoscopically visible intraluminal bulge caused by the fluid collection, after which guidewire and transenteric

stent insertion were performed under fluoroscopic guidance. Increasingly endoscopic drainage is being performed under real time EUS guidance.1 The difference between EUS and non-EUS guided endoscopic drainage is that during EUS-guided drainage, EUS is used to visualize the fluid collection and guide the initial puncture and guidewire insertion. All subsequent steps such as balloon dilatation of the puncture tract and stent insertion are similar between both approaches, and usually performed with fluoroscopic click here monitoring. EUS has made it possible for endoscopic drainage to be performed even in the absence of endoscopic bulging, because the collection can now be visualized directly, thus extending the spectrum of cases that are treatable endoscopically.2,3 With the use of colour Doppler ultrasound during EUS-guided drainage, EUS may potentially decrease the risk of puncturing interposed blood vessels.4 Most published data for EUS-guided drainage are in the context of pancreatic fluid collections, although drainage of liver and subphrenic abscesses has been reported.1,5 There are limited data concerning EUS-guided drainage of pelvic abscesses.