PDF file, 709KB, The list of primers used for Real Time RT-PCR are shown in this table.

A 69-year-old man with a history of prostate cancer status post radiation/hormone therapy, hypertension, hyperlipidemia, and diabetes presented to the gastroenterology clinic for evaluation of bloody diarrhea and constant right-lower-quadrant abdominal pain for 3 weeks. He reported having a laparoscopic cholecystectomy 5 months prior for gangrenous cholecystitis. A colonoscopy 3 years prior revealed mild radiation proctopathy and a tubular adenoma. Physical examination, complete blood count, comprehensive metabolic panel, and stool culture were unremarkable.

Introduction: Retained gallstones is a complication of cholecystectomy which can lead to the formation of intra-abdominal abscesses. In the following case, we describe a patient who developed abdominal pain and bloody stools post-cholecystectomy, found to have a retained gallstone and abscess eroding into the liver parenchyma and colon. Case Description/Methods: A 69-year-old male with a past medical history significant for prostate cancer status post radiation and hormone therapy, hypertension, hyperlipidemia, and diabetes presented to the gastroenterology clinic for evaluation of bloody diarrhea and right lower quadrant abdominal pain of three weeks duration. He described the pain as constant and endorsed decreased appetite and three-pound weight loss over the same time period. Surgical history was significant for a laparoscopic cholecystectomy five months prior for gangrenous cholecystitis. A colonoscopy performed three years prior revealed radiation colonopathy and a tubular adenoma, but no other significant findings. Physical exam was unremarkable with no abdominal tenderness. Stool cultures and giardia were negative, and calprotectin was 8 mcg/g. Computed tomography of the abdomen and pelvis was subsequently performed, revealing a 3.5 × 2 cm peritoneal abscess with a 14 mm retained gallstone and gallstone fragments eroding into the liver parenchyma and the hepatic flexure of the colon. Given these findings, the patient was advised to present to the emergency department. He subsequently underwent a diagnostic laparoscopy with removal of the stone and drainage of the surrounding abscess. A Jackson Pratt drain was placed, and fluid cultures subsequently grew Escherichia coli. The patient was discharged with antibiotics on post-operative day two. On two-week follow up, the patient reported feeling well with complete resolution of his abdominal pain. Discussion: Gallstone spillage and subsequent abscess formation is a known risk of cholecystectomy. This most frequently occurs when laparoscopic cholecystectomy is complicated by gallbladder perforation. Symptoms of retained stones can present months to years after cholecystectomy. Definitive treatment generally requires both drainage of the abscess and removal of the retained gallstone to eliminate infection and prevent future repeat infection.Figure 1.: Computed tomography of the abdomen and pelvis (coronal view) demonstrating a 3.5 x 2 cm peritoneal abscess with a 14 mm retained gallstone (arrow) and gallstone fragments eroding into the liver parenchyma.

Cancer stem cells (CSCs) appear to explain many aspects of the neoplastic evolution of tumors and likely account for enhanced therapeutic resistance following treatment. Dysregulated Notch signaling, which affects CSCs plays an important role in pancreatic cancer progression. We have determined the ability of Quinomycin to inhibit CSCs and the Notch signaling pathway. Quinomycin treatment resulted in significant inhibition of proliferation and colony formation in pancreatic cancer cell lines, but not in normal pancreatic epithelial cells. Moreover, Quinomycin affected pancreatosphere formation. The compound also decreased the expression of CSC marker proteins DCLK1, CD44, CD24 and EPCAM. In addition, flow cytometry studies demonstrated that Quinomycin reduced the number of DCLK1+ cells. Furthermore, levels of Notch 1-4 receptors, their ligands Jagged1, Jagged2, DLL1, DLL3, DLL4 and the downstream target protein Hes-1 were reduced. The.-secretase complex proteins, Presenilin 1, Nicastrin, Pen2, and APH-1, required for Notch activation also exhibited decreased expression. Ectopic expression of the Notch Intracellular Domain (NICD) partially rescued the cells from Quinomycin mediated growth suppression. To determine the effect of Quinomycin on tumor growth in vivo, nude mice carrying tumor xenografts were administered Quinomycin intraperitoneally every day for 21 days. Treatment with the compound significantly inhibited tumor xenograft growth, coupled with significant reduction in the expression of CSC markers and Notch signaling proteins. Together, these data suggest that Quinomycin is a potent inhibitor of pancreatic cancer that targets the stem cells by inhibiting Notch signaling proteins.

Abstract Background: Pancreatic cancer (PCa) remains a leading cause of death in the United States. Cancer stem cells (CSC) are responsible for tumor behavior, and therapeutic resistance. Quinomycin (Qui) is an orally administered quinoxaline antibiotic that bifunctionally intercalates with double stranded DNA. As a first step for repurposing this drug, we determined whether Qui affects PCa growth, and if so whether this is by suppressing stem cells. Method: Growth and apoptosis of PCa lines (MiaPaCa-2, PanC-1, BxPC-3) and normal ductal epithelial cells (HPNE) was measured by hexosaminidase and clonogenicity, and caspase 3/7 assays, respectively. Pancosphere formation and FACS sorting were used for identifying effects on stem cells. For in vivo effects, MiaPaCa-2 xenografts were developed in the flanks of nude mice. Immunohistochemistry was performed for stem cell markers and Notch signaling proteins. Results: Qui treatment resulted in a dose- and time-dependent inhibition of proliferation and colony formation in all three PCa lines but not HPNE cells. Qui also induced PCa cells to undergo apoptosis. Qui also significantly reduced the number and size of pancospheres, suggesting effects on stem cells. In addition, flow cytometry and western blot analyses showed that Qui suppressed PCa stem cell marker proteins Doublecortin Calmodulin-like kinase 1 (DCLK1), CD44 and CD24. We next determined whether Qui affects the Notch signaling pathway, a pathway that is important in maintaining CSC population. Notch receptor and its ligands are up-regulated in human PCa tissues. Qui treatment significantly downregulated Notch-1, 2 and 3 expression and that of its ligand Jagged-1. Notch activation requires cleavage by the γ-secretase complex. Qui inhibits the expression of members of the complex Presenilin 1 and Nicastrin. Moreover, ectopic expression of the Notch Intracellular domain (NICD) rescued the cells from Qui -mediated growth suppression. These data demonstrate that Qui mediated effects of PCa stem cells is in part through downregulating Notch1 activation. To determine the effect of Qui on tumor growth in vivo, mice carrying MiaPaCa-2 tumor xenografts were administered the compound intraperitoneally (20 μg/kg bw) every day for 21 days. Qui treatment significantly suppressed tumor xenograft growth, with notably lower tumor volume and weight. Western blot and immunohistochemistry analyses demonstrated significant inhibition of CSC marker proteins DCLK1, CD44 and CD24 and also the Notch signaling related proteins in the Qui-treated xenograft tissues. Conclusion: Together, these data suggest that Qui suppresses PCa growth by inhibiting the Notch signaling pathway. Qui may therefore be a novel compound to target pancreatic cancers. Citation Format: Dharmalingam Subramaniam, Sivapriya Ponnurangam, Afreen Sayed, Animesh Dhar, Dan A. Dixon, Ossama Tawfik, Rajashri R. Parab, Prabhu Dutt Mishra, Prafull Ranadive, Rajiv Sharma, Girish Mahajan, Aravind Sugumar, Scott J. Weir, Roy A. Jensen, Arun Balakrishnan, Shrikant Anant. Quinomycin A affects pancreatic cancer stem cells in part through suppression of notch signaling pathway. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4214. doi:10.1158/1538-7445.AM2015-4214

Pancreatic ductal adenocarcinoma is a poorly understood cancer that is often fatal. It has the worst prognosis of any know solid tumor. Unfortunately this has not changed in the last 40 years. Symptoms such as abdominal pain and weight loss arise in the late stages of the disease and often preclude surgery. There is no screening test for pancreatic cancer at the present time. There are risk factors which have been identified but a lot remains to be elucidated. A better understanding of the basic mechanism involved in cancer initiation and progression in the coming years will afford better screening and treatment prospects.

Vishal R Aggarwal A Ahmed O Airaksinen Luis Alguacil Armando Almeida Anna Maria Aloisi Kevin N Alschuler Johan H Andersen Martin Angst Andrea Antal Fernand Anton AV Apkarian Thomas Armstrong Curtis Oware Asante Pernilla Asenlof Ali Asghari Sadaf Ashraf Anne Astrom Nadine Attal S Azad T Aziz Ana Baamonde Flemming W Bach Misha-Miroslav Backonja Ewa Balkowiec-Iskra Elisa Ballini Giovanni Barbara Karen Barker M Barrot Jennifer Barton Helene Bastuji Subrata Basu Ray Ulf Baumgärtner Pierre Beaulieu J Gayle Beck Susanne Becker P Beek Simon Beggs Inna Belfer Marie Hoeger Bement Fabrizio Benedetti A Benham Dan Benhamou Gary Bennett Odd-Geir Berge Stefan Bergman Sonia F Bernardes Andy Billinton Andreas Binder Dale Bjorling Fiona Blyth Michael Karl Boettger Jörgen Boivie Kristian Borg David Borsook Alexander Brack Markus Breimhorst Harald Breivik Timothy Brennan Stephen Bruehl Francesco Cacciola Brian Cairns Laura Calza Antonio Canedo Annmarie Cano Nicholas Carleton Susan M Carlton Daniel B Carr Earl Carstens B Carvalho Loris Chahl George Chalkiadis Luis Enrique Chaparro Martin Cheatle Yuefeng Chen Dan Cherkin Lih-Chu Chiou Jill Chorney D Ciampi de Andrade Eva Lucia Cignacco Michael Clark Chassaing Claude FR Clemente Steven Paul Cohen Lindsey L Cohen Beverly Collett Alex Collie Miguel Condes Lara M Costigan Christine Courteix Kenneth Craig Bud Craig Peter Croft Celia Cruz Albert Dahan Ola Dale Radhouane Dallel Lauren Daniel Erin Dannecker Monika Daubländer Margaret Frances Davies Andrew Neil Davies Ric Osborne Day G De Oliveira Maria de Tommaso Silvia Deandrea Isabelle Decosterd Ruth Defrin Joost Dekker J Dennerlein Jules Desmeules D Dessem Luda Diatchenko Sulayman D Dib-Hajj Anthony Dickenson Raymond Dionne Clermont E Dionne Josef Donnerer Jonathan Dostrovsky Peter Drummond P Dubovy John Dunlop Justin Durham Robert F Dworkin Samual Dworkin Christopher Eccleston Laura Eggermont Alison Elliott Jens Ellrich E Engelman Edzard Ernst Anne-Laure Fauchais Sally Ferguson Cesar Fernandez de las Penas Victor Fernandez-Duenas M Fetzner Roger Fillingrim Nanna Brix Finnerup Dennis Fisher Dominique Fletcher Pamela Flood Herta Flor Clemens Forster Nicolai Bang Foss Nadine Foster Mark Fox Janetti N Francischi Felipe Fregni Douglas French Rainer Freynhagen Stefan J Friedrichsdorf Perry Fuchs Uwe Fuhr Lucia Gagliese Xavier Gasull Jeremy Gauntlett-Gilbert Claire Gaveriaux-Ruff Narender Gavva Robert Gear Christian Geber Rinie Geenen A Geers Michael Edward Geisser Gerd Geisslinger Louis Gendron

Autoimmune pancreatitis is a rare, newly recognized type of chronic pancreatitis. Its histopathology, clinical presentation, and diagnostic profile differ from those of other types of pancreatitis. Although its clinical presentation can vary, it most closely resembles pancreatic cancer. Numerous publications from Japan, United States, and Europe have helped define this hitherto ill-defined disease and described two histologically distinct subtypes. Both are exquisitely sensitive to steroid therapy. Type 1 has been well described in the literature and multiple diagnostic criteria exist. Less is known about type 2, and although it can be suspected clinically, histologic confirmation is needed for definitive diagnosis.

BACKGROUND:There is a paucity of data on long-term management of type 1 autoimmune pancreatitis (AIP), a relapsing steroid-responsive disorder. OBJECTIVE:We describe our experience with treatment of relapses and maintenance of remission using steroid-sparing immunomodulators (IMs) and induction of remission using rituximab (RTX). METHODS:We obtained details of disease relapse and treatment in 116 type 1 AIP patients from clinic visits, medical records and telephone interviews. We compared relapse free survival in those treated with IMs versus those treated with steroids alone, assessed patients' response to RTX, and identified treatment-related complications. RESULTS:During a median follow-up of 47 months, 52/116 AIP patients experienced 76 relapse episodes. The first relapse was treated with another course of steroids in 24 patients, and with steroids plus IM in another 27 patients; subsequent relapse-free survival until a second relapse was similar in the two groups (p=0.23). 38 patients received an IM for >2 months; failure or intolerance of IM therapy occurred in 17 (45%). 12 patients with steroid or IM intolerance/resistance were treated with RTX, an antiCD20 antibody; 10 (83%) experienced complete remission and had no relapses while on maintenance therapy. Treatment-limiting side effects related to RTX were uncommon. CONCLUSIONS:In type 1 AIP relapses are common. Relapse-free survival is similar in those treated with steroids plus IM compared to those treated with steroids alone. Nearly half the patients on IMs will relapse during treatment. RTX is effective in the treatment of both IM resistant and steroid intolerant patients.

BACKGROUND:Autoimmune pancreatitis (AIP) has been classified into type 1 and type 2 subtypes. Serum immunoglobulin G4 (IgG4) elevation characterizes type 1 AIP. Type 2 AIP and a subset of type 1 AIP are seronegative, i.e., have normal serum IgG4 levels. AIM:We compared the profiles of the three subsets of AIP to identify the unique characteristics of seronegative type 1 AIP and type 2 AIP. METHODS:We compared the clinical profiles of 69 seropositive type 1 AIP patients, 21 seronegative type 1 AIP patients and 22 type 2 AIP patients. RESULTS:Among type 1 AIP, seronegative group had similar clinical profiles when compared to seropositive group except that they were more likely to undergo surgical resection than seropositive patients (p = 0.001). Seronegative type I AIP patients were older (61.9 ± 13.7 vs 45.3 ± 17.4; p = 0.004), and differed in the occurrence of other organ involvement (OOI) (71.4% vs 0%; p < 0.001) and disease relapse (33.3% vs 0%; p = 0.005) when compared with type 2 AIP. All seronegative type 1 AIP patients had at least one of the following -OOI, disease relapse, and age >50 years while none of the type 2 AIP had OOI or disease relapse. CONCLUSIONS:Seronegative and seropositive type 1 AIP patients have similar clinical profiles, which are distinct from that of type 2 AIP. Among the seronegative AIP group, patients are more likely to have type 1 AIP rather than type 2 AIP if they are older than 50 years or have OOI or disease relapse.

increasing cell viability by 50% while decreasing apoptosis by 50% in response to 5-FU in comparison to empty vector control transfected MIP/SP cells.Not surprisingly, the reverse was observed following GRP78 knock-down with siRNA, with a reduction in cell viability of 50%.Overexpression of GRP78 protects cells from ER-stress by association with ER sensors and re-establishment of homeostasis for normal ER function.Interestingly, exposure of MIP/SP cells to tunicamycin promoted ER-stress mediated apoptosis by upregulating pPERK, p-eIF2α and CHOP, while the opposite was observed in cells that underexpress SPARC.Conclusion: This study reveals a novel interaction between SPARC and GRP78, and demonstrates that SPARC's ability to reverse chemotherapy resistance In Vitro and In Vivo to also involve an attenuation of GRP78's ability to induce drug resistance by promoting ER-stress mediated apoptosis.

Abstract Despite advances in molecular pathogenesis, pancreatic cancer remains a major unsolved health problem. It is a rapidly invasive, metastatic tumor that is resistant to standard therapies. The phosphatidylinositol-3-kinase/Akt and mTOR signaling pathways are frequently dysregulated in pancreatic cancer. Gemcitabine is the mainstay treatment for metastatic pancreatic cancer. P276 is a novel CDK inhibitor that induces G2/M arrest and inhibits tumor growth in vivo models. Here, we determined that P276 sensitizes pancreatic cancer cells to gemcitabine-induced apoptosis, a mechanism-mediated through inhibition of Akt-mTOR signaling. In vitro, the combination of P276 and gemcitabine resulted in a dose- and time-dependent inhibition of proliferation and colony formation of pancreatic cancer cells but not with normal pancreatic ductal cells. This combination also induced apoptosis, as seen by activated caspase-3 and increased Bax/Bcl2 ratio. Gene profiling studies showed that this combination downregulated Akt-mTOR signaling pathway, which was confirmed by Western blot analyses. There was also a downregulation of VEGF and interleukin-8 expression suggesting effects on angiogenesis pathway. In vivo, intraperitoneal administration of the P276-Gem combination significantly suppressed the growth of pancreatic cancer tumor xenografts. There was a reduction in CD31-positive blood vessels and reduced VEGF expression, again suggesting an effect on angiogenesis. Taken together, these data suggest that P276-Gem combination is a novel potent therapeutic agent that can target the Akt-mTOR signaling pathway to inhibit both tumor growth and angiogenesis. Mol Cancer Ther; 11(7); 1598–608. ©2012 AACR.

The purpose of this review is to provide a concise view of the existing knowledge of autoimmune pancreatitis (AIP) for practicing clinicians. AIP is a rare disease whose recognition and understanding are evolving. It is a type of chronic pancreatitis that often presents as obstructive jaundice, has a distinctive histology, and is exquisitely sensitive to steroid therapy. This form of chronic pancreatitis has a unique clinical, biochemical, and radiological profile. The term “AIP” encompasses two subtypes: types 1 and 2. Type 1 AIP is the pancreatic manifestation of a systemic fibro‐inflammatory disease called immunoglobulin G4‐associated systemic diseases. Type 2 AIP has been shown to be associated with inflammatory bowel disease. Existing criteria are geared towards the diagnosis of type 1 AIP. At present, pancreatic histology is a requirement for the definitive diagnosis of type 2 AIP. AIP can mimic most other pancreatic diseases in its presentation, but in clinical practice, it often has to be differentiated from pancreatic cancer. There are established criteria and algorithms not only to diagnose AIP, but also to differentiate it from pancreatic cancer. The utility of these algorithms and the approach to management are discussed here.

The purpose of this review is to provide a concise view of the existing knowledge of autoimmune pancreatitis (AIP) for practicing clinicians. AIP is a rare disease whose recognition and understanding are evolving. It is a type of chronic pancreatitis that often presents as obstructive jaundice, has a distinctive histology, and is exquisitely sensitive to steroid therapy. This form of chronic pancreatitis has a unique clinical, biochemical, and radiological profile. The term "AIP" encompasses two subtypes: types 1 and 2. Type 1 AIP is the pancreatic manifestation of a systemic fibro-inflammatory disease called immunoglobulin G4-associated systemic diseases. Type 2 AIP has been shown to be associated with inflammatory bowel disease. Existing criteria are geared towards the diagnosis of type 1 AIP. At present, pancreatic histology is a requirement for the definitive diagnosis of type 2 AIP. AIP can mimic most other pancreatic diseases in its presentation, but in clinical practice, it often has to be differentiated from pancreatic cancer. There are established criteria and algorithms not only to diagnose AIP, but also to differentiate it from pancreatic cancer. The utility of these algorithms and the approach to management are discussed here.

The type of colonoscope used (pediatric vs adult) for a given patient is often subjective and is a matter of preference. There is very limited data to guide a trainee in choosing the appropriate type of colonoscope. To study the performance characters of the adult and pediatric colonoscopes and to compare the cecal intubation times of concordant assignment versus discordant assignment. We enrolled 62 consecutive patients who underwent routine screening colonoscopy. These patients were randomly assigned to undergo examination with either an adult or a pediatric colonoscope.In addition to the actual scope assigned we also noted the hypothetical preference of colonoscope the trainee would have used based on predetermined strategy. This predetermined strategy was based on sex and BMI. Assignments were considered concordant if the hypothetical choice of colonoscope matched the random assignment and discordant when dissimilar. All 62 colonoscopies were done by a single third year gastroenterology fellow. Patients with a history of colonic surgery were excluded from the study. Demographic data, cecal intubation times, success in intubating the terminal ilium, BMI, BSA, patient comfort, type of scope used,polypectomy rates and choice colonoscope were collected. The primary outcome of interest was the mean cecal intubation time. We also compared the mean cecal intubation times of concordant and discordant assignments. We used the PASW (Predictive Analytics Software) to carry out the descriptive statistics and calculating the independent corelation coefficients. The baseline demographics are show in Table 1. When an adult colonoscope was used height (−.589, p=.01), weight (.432, p=.017), BMI (−0.565, p =.001), BSA (0.417, p=0.02) independently correlated with cecal intubation time. When a pediatric colonoscope was used, height (−.064, p=.767), weight (−.027, p=.9), BMI (−0.051, p=.91), BSA (.022, p=.918) did not independently correlate with cecal intubation time. Over all mean cecal intubation times were not significantly different for concordant and discordant assignments (p = 0.1). But a subset of discordant assignment i.e. preferring a pediatric scope while assigned an adult colonoscope when compared with the subset having the lowest cecal intubation time was significant.(p =.04).Tabled 1General Statisticsn62AgeMean 60.82, Median 59SexM (58.1%), F (41.9%)Scope UsedA (54.8%), P (45.2%)CI Time (min)Mean 11.87, Median 10TI IntubationPositive (40.3%), Negative (59. 7%)% AgreementYes (67.7%), No (32.3%) Open table in a new tab Height,weight BMI and BSA are independent determinants of mean cecal intubation times with an adult but not pediatric colonoscope. Mean cecal intubation times are significantly longer in a subset of patients with discordant colonoscopic assignment.

AbstractThe purpose of this review is to provide a concise view of the existing knowledge of autoimmune pancreatitis (AIP) for practicing clinicians. AIP is a rare disease whose recognition and understanding are evolving. It is a type of chronic pancreatitis that often presents as obstructive jaundice, has a distinctive histology, and is exquisitely sensitive to steroid therapy. This form of chronic pancreatitis has a unique clinical, biochemical, and radiological profile. The term “AIP” encompasses two subtypes: types 1 and 2. Type 1 AIP is the pancreatic manifestation of a systemic fibro‐inflammatory disease called immunoglobulin G4‐associated systemic diseases. Type 2 AIP has been shown to be associated with inflammatory bowel disease. Existing criteria are geared towards the diagnosis of type 1 AIP. At present, pancreatic histology is a requirement for the definitive diagnosis of type 2 AIP. AIP can mimic most other pancreatic diseases in its presentation, but in clinical practice, it often has to be differentiated from pancreatic cancer. There are established criteria and algorithms not only to diagnose AIP, but also to differentiate it from pancreatic cancer. The utility of these algorithms and the approach to management are discussed here.

The purpose of this review is to provide a concise view of the existing knowledge of autoimmune pancreatitis (AIP) for practicing clinicians. AIP is a rare disease whose recognition and understanding are evolving. It is a type of chronic pancreatitis that often presents as obstructive jaundice, has a distinctive histology, and is exquisitely sensitive to steroid therapy. This form of chronic pancreatitis has a unique clinical, biochemical, and radiological profile. The term "AIP" encompasses two subtypes: types 1 and 2. Type 1 AIP is the pancreatic manifestation of a systemic fibro-inflammatory disease called immunoglobulin G4-associated systemic diseases. Type 2 AIP has been shown to be associated with inflammatory bowel disease. Existing criteria are geared towards the diagnosis of type 1 AIP. At present, pancreatic histology is a requirement for the definitive diagnosis of type 2 AIP. AIP can mimic most other pancreatic diseases in its presentation, but in clinical practice, it often has to be differentiated from pancreatic cancer. There are established criteria and algorithms not only to diagnose AIP, but also to differentiate it from pancreatic cancer. The utility of these algorithms and the approach to management are discussed here.

Question: A 52-year-oldwoman with no past medical history presented for further evaluation of a 2-year history of intermittent melena. She initially presented to her primary physician 2 years prior with pica and fatigue and was found to have iron-deficiency anemia. Evaluation had included upper endoscopy with small bowel biopsy, colonoscopy, and abdominal comuted tomography (CT), which were unrevealing. She was placed on oral iron supplementation and did well for a short period of time; owever, the episodes of melena increased. A small-bowel-follow-through and a capsule endoscopy were performed and were normal. Her nemia became transfusion dependent and she was referred to our clinic. Physical examination was unremarkable except for conjunctival allor. CT enterography showed a 2-cm enhancing mass in the jejunum (Figure A, arrow). The patient underwent laparoscopic jejunal esection at which time a pedunculated polyp was removed (Figure B). What is the cause of her obscure gastrointestinal (GI) bleeding and what historical information is important for the future care f this patient? Look on page 1533 for the answer and see the GASTROENTEROLOGY web site (www.gastrojournal.org) for more information n submitting your favorite image to Clinical Challenges and Images in GI. Conflicts of interest: The authors disclose no conflicts. © 2011 by the AGA Institute 0016-5085/$36.00 doi:10.1053/j.gastro.2009.10.062