Although NA tend to provide lower variability than BA [7-10], how laboratories perform NA varies almost as much as how laboratories perform BA; thus, variability still remains high. The percentage of falsely positive and falsely negative results in FVIII-inhibitor-negative samples is also unacceptably high (up to 32% for false positives; up to 5% for false negatives) [7-10]. To improve reproducibility, ECAT performed a quality improvement cycle including these steps: (i) an external survey among

51 laboratories that participated on a regular basis in the ECAT FVIII-inhibitor programme; (ii) selection from these of 15 representative laboratories for a centralized

workshop; (iii) during the workshop, a zero ITF2357 ic50 point measurement using participants’ own methods and reagents and (iv) separate measurements with a fully standardized and universal method Forskolin (NA) and reagents; (v) an external survey among 13 workshop participants 3 months after the initial workshop and (vi) an external survey among 22 of the original 51 laboratories with standardized methods (BNPP with FVIII activity ranging from 0.95 to 1.05 IU mL−1, FVIII-deficient plasma as reference sample, standardized sample dilution with FVIII-deficient plasma). In each step of the cycle, an identical set of seven samples was used (one negative and six positive). The means and CVs of results using the six inhibitor-positive samples at the various steps (Table 1) clearly show that very low inter-laboratory variations can be achieved using a centralized setting with uniform methods and reagents (step 4), and acceptable inter-laboratory variations are possible in EQA surveys by significant standardization of the methods (step 6). The inhibitor activity of the negative sample was also below the cut-off value in all participants

Resminostat bar one in steps 4 and 6. Additional pitfalls as well as strategies for improvements in this area of testing are extensively covered in a recent review [10]. In brief, pitfalls occur at any stage of the diagnostic process, including pre-analytical issues (doctors test request, sample collection), analytical (methodology as detailed above), and post-analytical (laboratory interpretation and reporting, doctors’ interpretation and action). Main strategies comprise: (a) pre-analytical: (i) check test orders for accuracy and relevance (to ensure performance of the correct tests); (ii) check and be aware of blood sampling issues (correct anticoagulant, proper fill, etc.

The number of autophagic vesicles in hepatocytes was counted by using transmission electron microscopy. Expression of cathepsin B, D, L and p62

in the liver section was analyzed by immunohistochemical staining. The histological severity of NAFLD is assessed by NAFLD activity score (NAS). The Maraviroc purchase number of autophagic vesicles in hepatocytes was significantly increased in both CHC and NAFLD groups, but not CHB and PBC, more than control. Although hepatocytes with aggregation of p62 were observed in less than 15% of CHC, p62 aggregation was detected in approximately 65% of NAFLD. Cathepsin B, D and L expression was significantly suppressed Adriamycin cell line in the liver from NAFLD patients. Suppression of cathepsin B, D and L expression was not observed in CHB, CHC and PBC. In NAFLD patients, p62 aggregation was correlated with serum alanine aminotransferase value and inflammatory activity by NAS. These results indicate that a decrease in hepatic cathepsin expression in NAFLD is associated with autophagic

dysfunction. Hepatic inflammation correlates with autophagic dysfunction in NAFLD. These findings indicate that the suppression of autophagic proteolysis by hepatic steatosis is involved in the pathogenesis of NAFLD. “
“Gastrointestinal diseases characterized by inflammation, including the inflammatory bowel diseases, chemotherapy-induced mucositis and non-steroidal anti-inflammatory drug-induced enteropathy, currently have variably effective treatment options, highlighting the need for novel therapeutic approaches. Recently, naturally-sourced PIK3C2G agents including prebiotics, probiotics, plant-extracts and marine-derived oils known to possess anti-inflammatory and anti-oxidant properties have been investigated in vitro and in vivo. However, animal-derived oils are yet to be extensively tested. Emu Oil is extracted from the subcutaneous and retroperitoneal fat of the Emu, a flightless

bird native to Australia, and predominantly comprises fatty acids. Despite the limited rigorous scientific studies conducted to date, with largely anecdotal claims, Emu Oil, when administered topically and orally, has been shown to possess significant anti-inflammatory properties in vivo. These include a CD-1 mouse model of croton oil-induced auricular inflammation, experimentally-induced polyarthritis and dextran sulfate sodium-induced colitis. Recently, Emu Oil has been demonstrated to endow partial protection against chemotherapy-induced mucositis, with early indications of improved intestinal repair. Emu Oil could therefore form the basis of an adjunct to conventional treatment approaches for inflammatory disorders affecting the gastrointestinal system.

RANTES can also directly target HSCs to promote their proliferation and migration, and mice deficient for RANTES or its receptors chemokine (C-C) motif GSK-3 beta pathway receptor 1 (CCR1) and CCR5 display substantially reduced fibrosis.30 Here, we show that deficiency of c-Rel is associated with substantially reduced baseline and injury-induced expression of RANTES, which may therefore help explain the reduced numbers of recruited neutrophils, lower numbers of α-SMA+ HSCs, and the attenuated

fibrogenic response. However, using the culture model of HSC transdifferentiation, we also discovered inherent defects in c-rel−/− HSCs, specifically reduced expression of collagen I and α-SMA transcripts. NF-κB is a regulator of HSC survival and their expression of inflammatory regulators intercellular cell adhesion molecule-1 and interleukin-6.31 Pharmacological blockade of NF-κB can promote HSC apoptosis and regression of liver fibrosis.32, 33 However, the precise contribution of the individual NF-κB subunits toward the fate and function of HSCs has not been investigated. Our previous report that the p50 subunit is a suppressor of the inflammatory properties of HSC-derived myofibroblasts,13 taken together with the potential for c-Rel

to regulate expression of collagen I, α-SMA, and RANTES suggests the need for detailed studies of the functions of the NF-κB subunits in HSCs and fibrosis. Nonparenchymal cells, including HSCs, can influence liver regeneration through paracrine stimulation of hepatocyte proliferation.34 Defective function of the inflammatory and BMS-777607 supplier fibrogenic compartments may therefore contribute to the attenuated DNA synthesis and mitosis of hepatocytes observed Acetophenone in injured and PHx livers of c-rel−/− mice. However, we propose that c-Rel also plays a more direct role as a regulator of hepatocyte DNA replication. B cells deficient in c-Rel display deficiencies in cyclin

D3 and cyclin E expression, cyclin-dependent kinase activity, Rb phosphorylation, and E2F activity and fail to progress through the cell cycle in response to B cell receptor stimulation.35 Because ChIP analysis confirmed recruitment of c-Rel to the FoxM1 promoter following PHx, we suggest that c-Rel regulates hepatocyte proliferation via transcriptional control of the cell cycle regulator FoxM1, which following PHx, was not induced at the appropriate time or level of expression in c-Rel–deficient livers. FoxM1 regulates proliferation of many cell types and in the developing liver and heart is essential for normal mitosis.36 Expression profiling identified a cluster of FoxM1-regulated genes including G2/M-specific genes such as cyclin B1 and CENP-F (centromere protein F).37 In particular, transcriptional activation of cyclin B1 by FoxM1 is crucial for timely mitosis.37 Induction of cyclin B1 was delayed in the regenerating c-Rel–deficient liver.

Conclusion: When colonizes in esophagus, H. pylori increases the severity of esophageal inflammation and the incidence of BE and EA. The process may involve in the activation of NF-kB signaling pathway. Key Word(s): 1. esophagus; 2. NF-kB; 3. Helicobacter pylori; Presenting Author: SHU-JUN WANG Additional Authors: WEI-HONG WANG, YUN-XIANG CHU, GUI-GEN TENG Corresponding Author: WEI-HONG WANG

Affiliations: Peking University First Hospital Objective: To compare the efficacy of concomitant therapy for 7 days with standard triple therapy for 7 or 10 days in H. pylori eradication in China. Methods: 246 patients who were diagnosed as H. pylori infection by rapid urease test or 13C-urea breath test were included. All patients had never received PD0325901 datasheet eradication therapy. Patients were randomly divided into concomitant therapy for 7 days and standard triple therapy for 7 or 10 days. Concomitant therapy composed of esomeprazole (20 mg),

amoxicillin (1000 mg), clarithromycin (500 mg) and tinidazole (500 mg); all drugs were given twice a day. Standard triple therapy consisted of esomeprazole (20 mg), amoxicillin (1000 mg) and clarithromycin (500 mg); the drugs were given twice a day. The eradication rates were determined 4 weeks after the end of the treatment by 13C-urea Tipifarnib cost breath test. The incidence of adverse reaction were recorded. Results: 242 of the 246 patients completed the follow-up. The intention-to-treat analyse (ITT) and the per-protocol analysis (PP) indicated that the concomitant therapy (91.4% and 92.5%) was superior to standard triple therapy for 7 days (79.3% and 81.2%) and 10 days (79.5% and 80.5%) (P < 0.05). The difference for the eradication rate between the standard triple therapy for 7 days and 10 days was not

significant (P > 0.05). There were no significant difference for the adverse reactions between the concomitant therapy (8.8%), standard triple therapy for 7 days (7.5%) and 10 days (9.8%) (P > 0.05). Conclusion: Concomitant therapy for 7 days is an effective and a safe strategy for H. pylori eradication and deserves consideration for the Montelukast Sodium initial eradication treatment in China. Key Word(s): 1. Helicobacter pylori; 2. eradication; 3. Concomitant therapy; Presenting Author: MARA BARBOSA Additional Authors: CARLA MARINHO, JOSE COTTER Corresponding Author: MARA BARBOSA Affiliations: Centro Hospitalar Do Alto Ave Objective: BACKGROUND: Subclinical hepatic encephalopathy (SHE) is characterized by a mild cognitive impairment. It is controversial if Helicobacter pylori infection has a role in SHE by contributing to the hyperammonemia that exists in cirrhosis. AIM: To assess the relationship between H. pylori infection, hyperammonemia and the presence of SHE in cirrhotic patients. Methods: METHODS: A prospective study was conducted. One-hundred and two cirrhotic outpatients were evaluated.

Supporting experiments indicated that ectopic expression of miR-148a-5p or miR-363-3p induced a consistent G0/G1 arrest in HepG2 and BEL-7402 cells, but not HL7702 cells (Fig. 2D). Ectopic expression of miR-148a-5p and miR-363-3p also inhibited the migration in HepG2 and BEL-7402 cells (Supporting

Fig. 7). To determine whether mir-148a-5p or mir-363-3p could inhibit tumor growth, HepG2 cells ectopically expressing mir-148a-5p or mir-363-3p were injected into the flanks of nude mice. This resulted in a significant decrease of tumor growth compared with the tumors expressing empty vector (Fig. 2E). Taken together, these data suggest that miRNAs induce cell cycle arrest and inhibit tumor growth in HCC cells. To elucidate JNK pathway inhibitor the molecular mechanism by which both miRNAs induce CX-5461 purchase cell cycle arrest and inhibit tumorigenicity, we performed miRDB, miRanda, miRwalk, and RNAhybrid analyses to identify functional targets of miR-148a-5p and miR-363-3p. These analyses revealed the 3′-UTR of Myc to contain one highly conserved miR-148a-5p binding site from human to Canis familiaris

(Fig. 3A), whereas the 3′-UTR of USP28 mRNA, the ubiquitin protease of Myc, contains one highly conserved from human to Equus caballus and the other nonconserved miR-363-3p binding sites (Fig. 4A). We tested whether Myc or USP28 are direct targets of miR-148a-5p Linifanib (ABT-869) or miR-363-3p, respectively. For this, a GFP reporter assay was employed to detect the potential interaction of each miRNA with the 3′-UTR of targets. The results showed that miR-148a-5p inhibited the GFP expression of a vector containing the predicted miR-148a-5p binding site but not the GFP vector only (Fig. 3B). We also found that miR-363-3p repressed the GFP expression of a vector containing either one or both of the predicted miR-363-3p binding sites, but not the nonconserved

binding site (Fig. 4B). These data supported direct inhibition of Myc by miR-148a-5p and USP28 by miR-363-3p. As expected, ectopic expression miR-148a-5p in HepG2 and BEL-7402 HCC cells resulted in a marked decrease of Myc mRNA and protein and an increase in mir-363-3p. This was further associated with decrease in USP28 mRNA and protein (Fig. 3C,D); ectopic expression miR-363-3p in HepG2 and BEL-7402 cells resulted in a marked decrease of USP28 at both mRNA and protein levels, while in a marked decrease of Myc at protein level but not mRNA level (Fig. 4C,D). Although the 3′-UTR of Myc does not contain predicted binding sites for miR-363-3p, ectopic expression miR-363-3p also led to a marked decrease of Myc protein but not mRNA (Fig. 4C,D). The reduction in Myc protein could be prevented, however, if the cells were exposed to MG132, a proteasome inhibitor (Fig. 5A).

pylori infection. When comparing H. pylori-infected children to adults, a clear pattern emerged whereby the children had a weaker PS-341 research buy Th1 response. Although the density of H. pylori organisms was the same in children as compared to adults, the mean gastric concentration of IL-1 and TNF was significantly

higher in children. However, IL-2, IL-12, and IFN were significantly lower in children. In addition, the Th1 cytokines were noted to increase to adult levels by 18 years of age. As we continue to study and evaluate various vaccine strategies, a number of laboratories continue to focus on the mechanisms of protection following successful immunization. A study published in 2000 by Shirai et al. [47] suggested that salivary antibodies are a critical factor in successfully preventing H. pylori infection by vaccination. Ng et al. followed up and tried to confirm this observation by determining whether immune mediated Paclitaxel cell line changes and/or mucin production were key factors in protection following immunization [5, 48]. Although they were able to confirm increased levels of salivary IgA as a result of immunizations, there was no increase

in mucin production or cytokine levels. Based on this study, the protection mechanism against H. pylori following immunization does not appear to be mediated by the cytokines within the salivary glands. There is much evidence confirming that chronic H. pylori infection results in the production of T-regulatory cells which play a role in its chronicity. Winter et al. [49] also recently demonstrated that the VacA and γ-glutamyl transferase found in membrane vesicles may also inhibit T cells from clearing this infection. The final study regarding the protection mechanism following H. pylori immunization contributes to a collection of reports demonstrating that promoting either Th1 or Th17 immunity is sufficient to protect mice from H. pylori. To the extent that the host

response to H. pylori infection is generally limited due to the induction of regulatory T cells, there is now considerable evidence that the key to inducing protection is to pre-empt or override regulatory T-cell activity by promoting Th1 and/or Th17 mediated immunity. Indeed, Ding et al. [50] demonstrated that it was possible to induce sterilizing immunity in infected mice through cytokine therapy with IL-12, even in the absence of immunization. Avelestat (AZD9668) A previous study by Velin et al. [51] achieved a reduction in bacterial load using a short-term IL-17 therapy. These findings may be particularly relevant in the continuing efforts to improve an H. pylori vaccine for use in humans. While the success achieved in murine models has not translated well in clinical trials, the results of Ding et al. indicate that a significant improvement may be achieved by the addition of cytokine adjuvants, or the development of pharmacologic agents able to specifically induce Th1 or Th17 cells in the absence of toxicity. H.

Kandathil, Johnanathan Wood, Fuat Kurbanov, Jeffrey Quinn, Justin Richer, Yvonne M. Higgins, Lois Eldred, Zhiping Li Background: Sustained virological response (SVR) rates with pegylated interferon (pIFN) + ribavirin (RBV) in HIV-infected men are significantly higher in acute HCV (∼65%) than in chronic HCV (∼35%), but treatment is lengthy (24-48 wks) and SVR rates

are suboptimal. We hypothesized that adding telaprevir (TVR) to pIFN+RBV would both shorten treatment and increase the SVR rates in acute HCV in HIV-infected men. Methods: This is an IRB-approved, open-label, consecutive enrollment pilot study of TVR 750 mg/8 hr + pIFN-α 180 μg/wk + weight-based RBV for 12 wks in HIV-infected men with acute gt 1 HCV infection. Stopping rule was HCV VL > 1,000 IU/mL at wk 4.Allowed ARVs were tenofovir+emtricitabine, efavirenz check details (with TVR dose adjustment), rilpivirine, atazanavir/ritonavir, and raltegravir. HCV MK-1775 price VL was measured by transcription-mediated amplification (TMA, LLOD 5 IU/mL). The comparator group was HIV-infected men with acute gt 1 HCV treated during the 3 yrs prior to the FDA approval of TVR and those ineligible for TVR. The primary endpoint, SVR 12,

is reported without statistical analysis due to the small sample sizes. Results: In the TVR-based triple therapy group, 84% (16/19) achieved the primary endpoint, SVR 12, compared to 63% (31/49) in the comparator group. Among men with SVR, the median time to VL < 5 was wk 2 in the TVR group vs wk 4 in the comparator group, and 94% vs 55% had VL < 5 by wk 4.In the TVR group there were no relapses after ETR, and 13 men (81% of SVR 12) have achieved SVR 24 so far. Two of the 3 patients in the TVR group who failed therapy had non-response

(gt 1b, white, CT; gt 1a, black, TT), and one had rebound at wk 12 (gt 1a, Hispanic, CT). Most (81%) in the TVR group received ≤ 12 weeks of therapy–3 were treated 4-8 wks and 3 were treated with an additional 12 wks pIFN+RBV–while all in the comparator group received ≥ 24 weeks of therapy. A higher percentage Histidine ammonia-lyase of men in the TVR vs comparator group had IL28B CC (63% vs 42%), which may have contributed to the higher SVR rate. No one in the TVR group had HIV VL break-through and the overall safety profile was similar to that known for the TVR+pIFN+RBV regimen. Conclusions: Incorporating TVR into treatment of acute gt 1 HCV in HIV-infected men reduced treatment duration to 12 wks in most patients while maintaining a very high SVR rate. The absence of relapses suggests that 12 wks triple therapy is sufficient if HCV VL < 5 by wk 4.Larger studies should be done to confirm these findings. Nonetheless, this triple drug regimen appears to be a substantive improvement in the treatment of acute gt 1 HCV in HIV-infected men. Disclosures: Douglas T.

9 ROS formation was measured using a multiwell fluorescence scanner (CytoFluor 2300; Millipore, Bedford, MA). Liver extracts were obtained in a modified radioimmunoprecipitation buffer as described.18 Western blotting was performed using standard protocols. An antibody against αSMA (Sigma-Aldrich) was used at the concentration of 1:1000. Horseradish peroxidase–conjugated secondary antibodies were used and visualized with enhanced chemiluminescence. Bone marrow transplantation (BMT) was performed as described.25 Mice received an intravenous injection

of liposomal clodronate (200 μL intravenously) before irradiation to deplete KCs.27 Tibias and femurs of donor mice were Ivacaftor clinical trial flushed to obtain bone marrow (BM). BM cells (1 × 107) were injected into

the tail veins of lethally irradiated (11 Gy) recipient mice. BDL was performed 12 weeks after BMT. To determine successful BMT in p47phox-deficient and p47phox-sufficient mice, spleen cells were isolated from BDL chimeric mice and analyzed by quantitative real-time polymerase chain reaction (RT-PCR) to measure p47phox messenger RNA (mRNA) expression (data not shown). RT-PCR was used for measuring mRNA levels of fibrogenic markers (collagen α1(I) and αSMA). Extraction of RNA from total liver of mice was performed by a combination of TRIzol (Invitrogen, Carlsbad, CA) and RNeasy columns (Qiagen, Valencia, CA). Complementary DNA was obtained using the Amersham Deforolimus chemical structure kit for complementary DNA synthesis.11 Results are expressed as mean ± standard error of the mean. The results were analyzed using RVX-208 the unpaired Student t test or the Newman-Keuls test. A P value < 0.05 was considered statistically significant. To assess the role of the NOX in liver fibrosis, p47phox knockout (KO) mice were subjected to two different models of hepatic damage: BDL as a model of cholestatic liver injury and CCl4 treatment as a model of toxic liver injury. Consistent with our previous studies,9 mice deficient for the p47phox component of NOX had reduced fibrosis after 3 weeks of BDL, as evaluated by collagen deposition and αSMA staining (Fig. 1A,B). Furthermore, the

critical role of NOX in liver fibrosis was confirmed in mice subjected to intraperitoneal injection of CCl4. Mice received 16 injections of CCl4 (0.5 μL/g body weight; twice weekly) and were sacrificed 2 days after the last injection. WT mice displayed a significant increase in collagen deposition and αSMA staining following treatment with CCl4 compared to vehicle-treated mice (Fig. 1C,D). The increase in fibrotic parameters was significantly reduced in p47phox-deficient mice (Fig. 1C,D). In addition, mRNA levels of collagen α1(I) and αSMA were significantly reduced in p47phox-deficient mice compared to p47phox-sufficient mice either after 3 weeks of BDL or after 16 injections of CCl4, as evaluated by RT-PCR (Fig. 1E,F).

He described similar

episodes on two previous occasions. On examination of the abdomen, the only abnormality was mild tenderness on palpation over the right upper quadrant. Screening blood tests including liver function tests and serum amylase were within the reference range. His pain settled with analgesia and he was given an outpatient appointment for an upper abdominal ultrasound scan. The gallbladder was poorly seen but the possibility was raised of a contracted gallbladder with multiple stones. Because of continuing minor symptoms, he was STA-9090 in vivo advised to proceed with elective laparoscopic cholecystectomy. At operation, it was not possible to identify the gallbladder. The appearance of the gallbladder fossa is shown in Figure 1. Magnetic resonance cholangiopancreatography (MRCP) was performed after surgery and showed congenital absence of the cystic duct and gallbladder (Figure 2). An incidental finding was that of pancreas divisum. Agenesis of the gallbladder Temsirolimus is a rare congenital anomaly with an estimated prevalence of between 1 and 10 per 10,000 people in the general population. The anomaly is usually sporadic although there are occasional reports of two affected members within families. Embryologically, the anomaly is presumed to arise because of a defect in the development of the gallbladder

bud that arises from the caudal portion of the hepatic bud. Most patients do not have a cystic duct stump. At surgery, gallbladder agenesis should only be diagnosed after a careful search of ectopic

locations, particularly an intrahepatic or left-sided gallbladder. Intraoperative cholangiography may also be helpful if the bile duct can be readily identified. However, extensive surgical dissection of the area should be avoided as this may result in injury to hilar structures. MRCP either before or after surgery may also be helpful in those patients with uncertain results from ultrasound or computed tomography scans. In the above patient, possible causes for pain include an atypical irritable bowel syndrome, a motility disorder of the sphincter of Oddi and L-gulonolactone oxidase perhaps pancreas divisum. There are also rare reports of agenesis of the gallbladder with primary bile duct stones. Contributed by “
“A woman, aged 64, was investigated because of upper abdominal discomfort. An upper abdominal ultrasound study and computed tomography (CT) scan showed a cystic mass, 3 cm in diameter, in the head of the pancreas. Endoscopic retrograde cholangiopancreatography revealed a cystic lesion in a major branch of the main pancreatic duct. There was also a filling-defect within the cystic lesion and this was confirmed by endoscopic ultrasound. The diagnosis was that of an intraductal papillary mucinous neoplasm of the head of the pancreas.

He described similar

episodes on two previous occasions. On examination of the abdomen, the only abnormality was mild tenderness on palpation over the right upper quadrant. Screening blood tests including liver function tests and serum amylase were within the reference range. His pain settled with analgesia and he was given an outpatient appointment for an upper abdominal ultrasound scan. The gallbladder was poorly seen but the possibility was raised of a contracted gallbladder with multiple stones. Because of continuing minor symptoms, he was www.selleckchem.com/products/acalabrutinib.html advised to proceed with elective laparoscopic cholecystectomy. At operation, it was not possible to identify the gallbladder. The appearance of the gallbladder fossa is shown in Figure 1. Magnetic resonance cholangiopancreatography (MRCP) was performed after surgery and showed congenital absence of the cystic duct and gallbladder (Figure 2). An incidental finding was that of pancreas divisum. Agenesis of the gallbladder Proteasome inhibitor is a rare congenital anomaly with an estimated prevalence of between 1 and 10 per 10,000 people in the general population. The anomaly is usually sporadic although there are occasional reports of two affected members within families. Embryologically, the anomaly is presumed to arise because of a defect in the development of the gallbladder

bud that arises from the caudal portion of the hepatic bud. Most patients do not have a cystic duct stump. At surgery, gallbladder agenesis should only be diagnosed after a careful search of ectopic

locations, particularly an intrahepatic or left-sided gallbladder. Intraoperative cholangiography may also be helpful if the bile duct can be readily identified. However, extensive surgical dissection of the area should be avoided as this may result in injury to hilar structures. MRCP either before or after surgery may also be helpful in those patients with uncertain results from ultrasound or computed tomography scans. In the above patient, possible causes for pain include an atypical irritable bowel syndrome, a motility disorder of the sphincter of Oddi and Paclitaxel mouse perhaps pancreas divisum. There are also rare reports of agenesis of the gallbladder with primary bile duct stones. Contributed by “
“A woman, aged 64, was investigated because of upper abdominal discomfort. An upper abdominal ultrasound study and computed tomography (CT) scan showed a cystic mass, 3 cm in diameter, in the head of the pancreas. Endoscopic retrograde cholangiopancreatography revealed a cystic lesion in a major branch of the main pancreatic duct. There was also a filling-defect within the cystic lesion and this was confirmed by endoscopic ultrasound. The diagnosis was that of an intraductal papillary mucinous neoplasm of the head of the pancreas.