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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.cghjournal.org/?rss=yes"><title>Clinical Gastroenterology and Hepatology</title><description>Clinical Gastroenterology and Hepatology RSS feed: Current Issue. The mission of  Clinical Gastroenterology and Hepatology  is to provide readers with a broad spectrum of themes in clinical 
gastroenterology and hepatology, including the diagnostic , endoscopic, interventional, and therapeutic advances in cancer, inflammatory 
diseases, functional gastrointestinal disorders, nutrition, absorption, and secretion. This peer-reviewed journal includes original articles 
as well as scholarly reviews, with the goal that all articles published will be immediately relevant to practice of the specialties of 
gastroenterology and hepatology. In addition to peer-reviewed articles, the journal includes invited key reviews and articles on endoscopy/practice-based 
technology and health policy/practice management. 
 
The journal is abstracted and indexed in Current Contents/Clinical Medicine, Excerpta 
Medica/EMBASE, Index Medicus/MEDLINE, and Science Citation Index Expanded.</description><link>http://www.cghjournal.org/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2010 AGA Institute. Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:issn>1542-3565</prism:issn><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:publicationDate>February 2010</prism:publicationDate><prism:copyright> © 2010 AGA Institute. Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509008787/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509008337/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509006557/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509008908/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509009951/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509012737/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509012750/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509013135/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509011380/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509006739/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509010763/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509008933/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509013275/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509010751/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509010441/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509010842/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509006569/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509010118/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509010829/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509010799/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509010428/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509010131/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509009938/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509010854/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509009549/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509008921/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS154235650901009X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS154235650901043X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509007411/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509012774/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS154235650901235X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509002365/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509002377/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509002316/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509003322/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509003188/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509012403/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509012373/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509012385/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509012397/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509008787/abstract?rss=yes"><title>Pancreaticoduodenal Artery and Superior Mesenteric Artery Pseudoaneurysm Associated With Hemosuccus Pancreaticus</title><link>http://www.cghjournal.org/article/PIIS1542356509008787/abstract?rss=yes</link><description>A 24-year-old man who underwent a second partial gastrectomy was admitted to our hospital with gastrointestinal (GI) bleeding. In autumn 2005, he had several episodes of GI bleeding after epigastric intermittent pain. There were 1 or 2 attacks every year. Three years later, he suddenly vomited about 1000 mL blood on a bus and was sent to a hospital; his hemoglobin had dropped to 40 g/L. One month later, he underwent first partial gastrectomy for duodenal bulb ulcer associated with active bleeding. Then the second gastrectomy was performed for 2 episodes of anastomotic ulcer bleeding in December 2008. On February 4, 2009, he had hematemesis again. Computed tomography (CT) scanning showed splenomegaly and signs of portal hypertension, and magnetic resonance cholangiopancreatography (MRCP) image revealed normal biliary tract and pancreas. On March 9, he was admitted to our hospital; the serum gastrin and amylase levels were normal. MRCP image showed normal common bile duct. CT scanning revealed a slightly distended pancreatic tube and a normal size pancreas.</description><dc:title>Pancreaticoduodenal Artery and Superior Mesenteric Artery Pseudoaneurysm Associated With Hemosuccus Pancreaticus</dc:title><dc:creator>Shilong Jin, Xiaolin Dong, Chen Ping</dc:creator><dc:identifier>10.1016/j.cgh.2009.08.032</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-09-14</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-09-14</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Electronic Images of the Month</prism:section><prism:startingPage>e11</prism:startingPage><prism:endingPage>e12</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509008337/abstract?rss=yes"><title>A Case of Recurrent Abdominal Pain Due to a Gossypiboma With Spontaneous Resolution</title><link>http://www.cghjournal.org/article/PIIS1542356509008337/abstract?rss=yes</link><description>Although gossypiboma is an old term, many physicians are not familiar with it. Retained surgical sponge has been referred to as a gossypiboma, which is derived from gossypium (Latin, cotton) and boma (Swahili, place of concealment).</description><dc:title>A Case of Recurrent Abdominal Pain Due to a Gossypiboma With Spontaneous Resolution</dc:title><dc:creator>Erick Alayo, Bashar Attar, Benjamin Go</dc:creator><dc:identifier>10.1016/j.cgh.2009.08.029</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-09-07</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-09-07</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Electronic Images of the Month</prism:section><prism:startingPage>e13</prism:startingPage><prism:endingPage>e14</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509006557/abstract?rss=yes"><title>Acute Lymphoblastic Leukemia Presenting as Painless Jaundice</title><link>http://www.cghjournal.org/article/PIIS1542356509006557/abstract?rss=yes</link><description>A 52-year-old woman was admitted with fatigue and jaundice. Two weeks before admission she developed malaise and dyspnea on exertion. Initially, her primary care provider prescribed azithromycin for presumed bronchitis. Her symptoms did not improve, and she subsequently developed jaundice, prompting further evaluation.</description><dc:title>Acute Lymphoblastic Leukemia Presenting as Painless Jaundice</dc:title><dc:creator>Darryn Potosky, William Twaddell, Sandeep Khurana</dc:creator><dc:identifier>10.1016/j.cgh.2009.07.007</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-07-15</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-07-15</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Electronic Images of the Month</prism:section><prism:startingPage>e15</prism:startingPage><prism:endingPage>e16</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509008908/abstract?rss=yes"><title>Hepatocellular Carcinoma Mimicking Bile Duct Stone</title><link>http://www.cghjournal.org/article/PIIS1542356509008908/abstract?rss=yes</link><description>   See related articles, Lok AS et al, on page 493 in Gastroenterology and, Miura H, on page xxiv in this issue of CGH.</description><dc:title>Hepatocellular Carcinoma Mimicking Bile Duct Stone</dc:title><dc:creator>Koji Miyahara, Kazuhiro Nouso, Kazuhide Yamamoto</dc:creator><dc:identifier>10.1016/j.cgh.2009.09.007</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-09-18</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-09-18</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Electronic Images of the Month</prism:section><prism:startingPage>e17</prism:startingPage><prism:endingPage>e17</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509009951/abstract?rss=yes"><title>Pancreatic Cystosis Complicating Cystic Fibrosis</title><link>http://www.cghjournal.org/article/PIIS1542356509009951/abstract?rss=yes</link><description>A 16-year-old African American boy with cystic fibrosis presented with a 3-day history of abdominal pain, constipation, and increased cough. The pain was poorly characterized, diffuse, and continuous, without exacerbating or relieving factors. He denied nausea and vomiting, but did report recent onset of anorexia with a 4-pound weight loss. He reported worsening constipation, with no bowel movement for 3 days despite increasing doses of milk of magnesia. Past medical history was significant for cystic fibrosis, pancreatic insufficiency, pulmonary disease, and severe constipation. Past surgical history revealed no abdominal surgeries. Medications included pancreatic enzyme supplements, proton-pump inhibitor, β-agonist, fat-soluble vitamin supplements, dornase alpha, and inhaled tobramycin. Physical examination was significant for diffuse abdominal tenderness to light palpation; no hepatosplenomegaly or masses were felt. Pulmonary examination revealed poor respiratory effort but clear breath sounds.</description><dc:title>Pancreatic Cystosis Complicating Cystic Fibrosis</dc:title><dc:creator>Alvin J. Freeman, Henry W. Giles, Michael J. Nowicki</dc:creator><dc:identifier>10.1016/j.cgh.2009.09.027</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-10-05</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-10-05</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Electronic Images of the Month</prism:section><prism:startingPage>e18</prism:startingPage><prism:endingPage>e19</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509012737/abstract?rss=yes"><title>Exam 1: Antiviral Therapy Reduces Risk of Hepatocellular Carcinoma in Patients With Hepatitis C–Related Cirrhosis</title><link>http://www.cghjournal.org/article/PIIS1542356509012737/abstract?rss=yes</link><description></description><dc:title>Exam 1: Antiviral Therapy Reduces Risk of Hepatocellular Carcinoma in Patients With Hepatitis C–Related Cirrhosis</dc:title><dc:creator>Joseph R. Bloomer</dc:creator><dc:identifier>10.1016/j.cgh.2009.12.003</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-12-14</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-12-14</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>CME Activities</prism:section><prism:startingPage>e20</prism:startingPage><prism:endingPage>e21</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509012750/abstract?rss=yes"><title>Exam 2: Mucin-Producing Neoplasms of the Pancreas: An Analysis of Distinguishing Clinical and Epidemiologic Characteristics</title><link>http://www.cghjournal.org/article/PIIS1542356509012750/abstract?rss=yes</link><description></description><dc:title>Exam 2: Mucin-Producing Neoplasms of the Pancreas: An Analysis of Distinguishing Clinical and Epidemiologic Characteristics</dc:title><dc:creator>Joseph R. Bloomer</dc:creator><dc:identifier>10.1016/j.cgh.2009.12.004</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-12-14</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-12-14</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>CME Activities</prism:section><prism:startingPage>e22</prism:startingPage><prism:endingPage>e22</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509013135/abstract?rss=yes"><title>Abstracts from Around the World</title><link>http://www.cghjournal.org/article/PIIS1542356509013135/abstract?rss=yes</link><description>The administration of propofol by nonanesthesiologists for gastrointestinal endoscopic procedures remains highly controversial. This statement, issued jointly by our 4 societies, is based upon a systematic literature review from an experienced, 4 member committee. To date, over 460,000 published cases of nonanesthesiologist administered propofol (NAAP) have been reported. Of these, there have been 3 deaths, all of which occurred during or after upper endoscopy. No mortalities have been reported in those undergoing colonoscopy or in those classified as American Society of Anesthesiology (ASA) Class I or II. When examining economic models, cost effectiveness appears to be improved for gastroenterologist administered propofol for advanced procedures (eg, endoscopic retrograde cholangiopancreatography [ERCP] or endoscopic ultrasonography [EUS]). Anesthesiologist administered sedation for healthy low risk patients was not proven to be beneficial. The overall safety profile of NAAP is equivalent to standard sedation for routine procedures and may be equivalent for advanced procedures, although more data are needed. Training guidelines were offered for those physicians who wish to provide propofol and were comprised of 4 components: didactic training, airway workshop, simulation training, and preceptorship.</description><dc:title>Abstracts from Around the World</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/j.cgh.2009.12.009</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2010-01-04</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2010-01-04</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Abstracts From Around the World</prism:section><prism:startingPage>101</prism:startingPage><prism:endingPage>102</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509011380/abstract?rss=yes"><title>Anesthesia-Mediated Sedation for Advanced Endoscopic Procedures and Cardiopulmonary Complications: Of Mountains and Molehills</title><link>http://www.cghjournal.org/article/PIIS1542356509011380/abstract?rss=yes</link><description>Anesthesiologist-administered sedation for gastrointestinal endoscopy has become an indelible and somewhat controversial part of our practice landscape. I am not here to expound upon the pharmacoeconomic and regulatory maelstrom that propofol-mediated sedation has created or tout the fact that the safety record for endoscopist-directed propofol is impressive. Instead, I would invite the reader to step into the world where anesthesiologist-assisted sedation may play an important role: procedures such as endoscopic retrograde cholangiopancreatography (ERCP) and endoscopic ultrasonography (EUS) where deep sedation or general anesthesia for extended periods is the rule. Even this indication for anesthesiologist-administered sedation is controversial. Numerous studies have shown that gastroenterologist-directed propofol sedation for ERCP and EUS results in improvements in throughput, recovery, and patient satisfaction. The cumulative numbers, however, are not robust enough to render a final opinion on safety as they are for upper endoscopy and colonoscopy. Surprisingly, the same can be said for monitored anesthesia care for endoscopy.</description><dc:title>Anesthesia-Mediated Sedation for Advanced Endoscopic Procedures and Cardiopulmonary Complications: Of Mountains and Molehills</dc:title><dc:creator>John J. Vargo</dc:creator><dc:identifier>10.1016/j.cgh.2009.11.001</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-11-13</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-11-13</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Editorial</prism:section><prism:startingPage>103</prism:startingPage><prism:endingPage>104</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509006739/abstract?rss=yes"><title>Effects of Helicobacter pylori Eradication on Early Stage Gastric Mucosa–Associated Lymphoid Tissue Lymphoma</title><link>http://www.cghjournal.org/article/PIIS1542356509006739/abstract?rss=yes</link><description>Background &amp; Aims: Different remission rates of gastric low-grade, B-cell, mucosa–associated lymphoid tissue (MALT) lymphoma have been reported after Helicobacter pylori eradication. We assessed the long-term remission and relapse rates of early stage MALT lymphoma in patients treated only by H pylori eradication and identified factors that might predict outcome.Methods: This systematic review analyzed data from 32 studies, including 1408 patients.Results: The MALT lymphoma remission rate was 77.5% (95% confidence interval, 75.3−79.7), and was significantly higher in patients with stage I than stage II1 lymphoma (78.4% vs 55.6%; P = .0003) and in Asian than in Western groups (84.1% vs 73.8%; P = .0001). Neoplasia confined to the submucosa regressed more frequently than that with deeper invasion (82.2% vs 54.5%; P = .0001); patients with lymphoma localized to the distal stomach experienced regression more frequently than those with lymphoma of the proximal stomach (91.8% vs 75.7%; P = .0037). The remission rate was higher among patients without the API2–MALT1 translocation than in those with this translocation (78% vs 22.2%; P = .0001). In an analysis of data from 994 patients, 7.2% experienced lymphoma relapse during 3253 patient-years of follow-up evaluation, with a yearly recurrence rate of 2.2%. Infection and lymphoma were cured by additional eradication therapy in all patients with H pylori recurrence (16.7%). Five (0.05%) of the patients initially cured of lymphoma developed high-grade lymphoma within 6 to 25 months of therapy.Conclusions: H pylori eradication is effective in treating approximately 75% of patients with early stage gastric lymphoma. Long-term follow-up evaluation of these patients is needed to detect early lymphoma relapse or progression.</description><dc:title>Effects of Helicobacter pylori Eradication on Early Stage Gastric Mucosa–Associated Lymphoid Tissue Lymphoma</dc:title><dc:creator>Angelo Zullo, Cesare Hassan, Francesca Cristofari, Alessandro Andriani, Vincenzo De Francesco, Enzo Ierardi, Silverio Tomao, Manfred Stolte, Sergio Morini, Dino Vaira</dc:creator><dc:identifier>10.1016/j.cgh.2009.07.017</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-07-23</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-07-23</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Review</prism:section><prism:startingPage>105</prism:startingPage><prism:endingPage>110</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509010763/abstract?rss=yes"><title>Nuclear Medicine Hepatobiliary Imaging</title><link>http://www.cghjournal.org/article/PIIS1542356509010763/abstract?rss=yes</link><description>Nuclear medicine hepatobilary imaging (HIDA) is a time proven imaging methodology that uses radioactive drugs and specialized cameras to make imaging diagnoses based on physiology. HIDA radiopharmaceuticals are extracted by hepatocytes in the liver and cleared through the biliary system similar to bilirubin. The most common indication for HIDA imaging is acute cholecystitis, diagnosed by nonfilling of the gallbladder due to cystic duct obstruction. HIDA can detect high grade biliary obstruction prior to ductal dilatation; images reveal a persistent hepatogram without biliary clearance due to the high backpressure. HIDA also aids in the diagnosis of partial biliary obstruction due to stones, biliary stricture, and sphincter of Oddi obstruction. It can confirm biliary leakage postcholecystectomy and hepatic transplantation. Calculation of a gallbladder ejection fraction after cholecystokinin infusion is commonly used to diagnose chronic acalculous gallbladder disease. Diseased gallbladders do not contract. There are many other less common but valuable diagnostic indications for HIDA imaging.</description><dc:title>Nuclear Medicine Hepatobiliary Imaging</dc:title><dc:creator>Harvey A. Ziessman</dc:creator><dc:identifier>10.1016/j.cgh.2009.10.017</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-11-02</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-11-02</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Clinical Imaging</prism:section><prism:startingPage>111</prism:startingPage><prism:endingPage>116</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509008933/abstract?rss=yes"><title>Severe Gastroparesis: Medical Therapy or Gastric Electrical Stimulation</title><link>http://www.cghjournal.org/article/PIIS1542356509008933/abstract?rss=yes</link><description>A 33-year-old woman is referred for evaluation of refractory nausea and vomiting of 8 months' duration. She has a 20-year history of type I diabetes mellitus complicated by retinopathy and peripheral neuropathy. Her glycemic control is suboptimal and occasionally blood sugars are in the 20-mmol/L (360 mg/dL) range and the recent hemoglobin A1c level is 9.8%. Her symptoms occur postprandially about 30 minutes after a meal and are characterized by nausea, epigastric fullness, bloating, and pain. Vomiting is less frequent (2–3 days/wk); however, when it does occur, it is usually 2 to 4 hours after eating and on several occasions she has identified food in the vomitus that she consumed the previous day. Her severe nausea and vomiting have led to 12 emergency department visits and 4 hospitalizations in the past year. She is not able to work and take care of her family because of those symptoms. She spends most of her day lying in bed or sitting in a chair. She also lost 9 kg in this time frame.</description><dc:title>Severe Gastroparesis: Medical Therapy or Gastric Electrical Stimulation</dc:title><dc:creator>Savio C. Reddymasu, Irene Sarosiek, Richard W. McCallum</dc:creator><dc:identifier>10.1016/j.cgh.2009.09.010</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-09-17</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-09-17</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Education Practice</prism:section><prism:startingPage>117</prism:startingPage><prism:endingPage>124</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509013275/abstract?rss=yes"><title>Do the Symptom-Based, Rome Criteria of Irritable Bowel Syndrome Lead to Better Diagnosis and Treatment Outcomes?</title><link>http://www.cghjournal.org/article/PIIS1542356509013275/abstract?rss=yes</link><description>Irritable bowel syndrome (IBS) is an extraordinarily prevalent condition, remaining one of the most common disorders gastroenterologists treat. Because there is no specific test for diagnosing IBS, experts have devised criteria to guide the clinician and researcher in making a diagnosis. Despite their widespread adoption, the Rome III criteria still engender debate regarding their utility and symptom-guided approach. Herein, 2 experts with divergent views explore this debate. A third expert concludes the article, outlining the strengths and weaknesses of each viewpoint.</description><dc:title>Do the Symptom-Based, Rome Criteria of Irritable Bowel Syndrome Lead to Better Diagnosis and Treatment Outcomes?</dc:title><dc:creator>Robin Spiller, Michael Camilleri, George F. Longstreth</dc:creator><dc:identifier>10.1016/j.cgh.2009.12.018</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2010-02-01</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2010-02-01</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Perspective</prism:section><prism:startingPage>125</prism:startingPage><prism:endingPage>125</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509010751/abstract?rss=yes"><title>The Pro Argument</title><link>http://www.cghjournal.org/article/PIIS1542356509010751/abstract?rss=yes</link><description>Irritable bowel syndrome (IBS) patients are at risk of being subjected to numerous investigations only to be told “I can find nothing wrong with you.” This produces an undesirable uncertainty, anxiety, and demand for further tests which can be prevented by a positive symptom-based diagnosis. Several criteria including the Manning, Kruis, and Rome I criteria have been validated and give useful positive likelihood ratios of 2.9–5.9. However, sensitivity remains low at 0.65–0.84, meaning that some patients who clinicians feel should be labeled IBS are not. Nonetheless, given the high prevalence of IBS, the positive predictive value of clinical criteria is high and the diagnosis can be made with some authority if patients meet the criteria in the absence of alarm features. There is a consensus that making a firm symptom-based diagnosis reduces patient anxiety and allows better management. Future developments of the criteria which could involve adding the results of laboratory tests might improve their clinical performance. Furthermore adding biomarkers of underlying mechanisms could improve their usefulness as a guide to treatment. Their use in clinical trials has undoubtedly proved valuable in improving the consistency of the results but all recent IBS trials have shown large numbers needed to treat (NNT) suggesting that further refinement is needed if we are to achieve our aim of targeting our treatments to the patients who will specifically benefit.</description><dc:title>The Pro Argument</dc:title><dc:creator>Robin Spiller</dc:creator><dc:identifier>10.1016/j.cgh.2009.10.016</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-11-02</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-11-02</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Perspective</prism:section><prism:startingPage>125</prism:startingPage><prism:endingPage>129</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509010441/abstract?rss=yes"><title>The Con Argument</title><link>http://www.cghjournal.org/article/PIIS1542356509010441/abstract?rss=yes</link><description>Some claim that symptom-based Rome criteria are diagnostic and enhance clinical practice and choice of therapy for patients presenting with gastrointestinal symptoms. This overview focuses on lower gastrointestinal symptoms: constipation, diarrhea, pain, and bloating. The main con arguments for using such criteria for diagnosis are insufficient specificity, overlap of symptom-based categories or disorders, insufficient and therefore nonspecific characterization of pain in the criteria, inability to differentiate the “mimics” of irritable bowel syndrome (IBS) with constipation (IBS-C) and IBS with diarrhea (IBS-D), and inability to optimize treatment for IBS with mixed or alternating bowel function (IBS-M) or bloating in the absence of objective measurements.</description><dc:title>The Con Argument</dc:title><dc:creator>Michael Camilleri</dc:creator><dc:identifier>10.1016/j.cgh.2009.10.009</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-10-21</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-10-21</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Perspective</prism:section><prism:startingPage>129</prism:startingPage><prism:endingPage>132</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509010842/abstract?rss=yes"><title>Symptoms and Tests for Irritable Bowel Syndrome: Diagnosing a Complex Disorder</title><link>http://www.cghjournal.org/article/PIIS1542356509010842/abstract?rss=yes</link><description>Use of symptom criteria for diagnosing irritable bowel syndrome (IBS) is complicated by issues concerning the selection of terms for nociceptive sensations, possible interaction of language with cognition, gender-based variation in pain description, language translation problems, bowel habit classification, and the role of bloating and abdominal distension, and other symptoms and factors. Limited symptom validation and extensive patient follow-up indicate that IBS symptom criteria are accurate. However, symptom overlap between constipation-predominant IBS and functional constipation occurs, and special tests are required to identify a functional defecation disorder. Fluctuating IBS symptoms and the complex pathophysiology could be associated with limited durability of some test abnormalities, including transit studies. Unnecessary testing has a negative impact on patient outcome. Most patients can be managed on the basis of symptoms.</description><dc:title>Symptoms and Tests for Irritable Bowel Syndrome: Diagnosing a Complex Disorder</dc:title><dc:creator>George F. Longstreth</dc:creator><dc:identifier>10.1016/j.cgh.2009.10.025</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-11-02</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-11-02</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Perspective</prism:section><prism:startingPage>133</prism:startingPage><prism:endingPage>136</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509006569/abstract?rss=yes"><title>Incidence of Sedation-Related Complications With Propofol Use During Advanced Endoscopic Procedures</title><link>http://www.cghjournal.org/article/PIIS1542356509006569/abstract?rss=yes</link><description>Background &amp; Aims: Propofol is an effective sedative in advanced endoscopy. However, the incidence of sedation-related complications is unclear. We sought to define the frequency of sedation-related adverse events, particularly the rate of airway modifications (AMs), with propofol use during advanced endoscopy. We also evaluated independent predictors of AMs.Methods: Patients undergoing sedation with propofol for advanced endoscopic procedures, including endoscopic retrograde cholangiopancreatography, endoscopic ultrasound, and small-bowel enteroscopy, were studied prospectively. Sedative dosing was determined by a certified registered nurse anesthetist with the goal of achieving deep sedation. Sedation-related complications included AMs, hypoxemia (pulse oximetry [SpO2] &lt; 90%), hypotension requiring vasopressors, and early procedure termination. AMs were defined as chin lift, modified face mask ventilation, and nasal airway. We performed a regression analysis to compare characteristics of patients requiring AMs (AM+) with those who did not (AM−).Results: A total of 799 patients were enrolled over 7 months. Procedures included endoscopic ultrasound (423), endoscopic retrograde cholangiopancreatography (336), and small-bowel enteroscopy (40). A total of 87.2% of patients showed no response to endoscopic intubation. Hypoxemia occurred in 12.8%, hypotension in 0.5%, and premature termination in 0.6% of the patients. No patients required bag-mask ventilation or endotracheal intubation. There were 154 AMs performed in 115 (14.4%) patients, including chin lift (12.1%), modified face mask ventilation (3.6%), and nasal airway (3.5%). Body mass index, male sex, and American Society of Anesthesiologists class of 3 or higher were independent predictors of AMs.Conclusions: Propofol can be used safely for advanced endoscopic procedures when administered by a trained professional. Independent predictors of AMs included male sex, American Society of Anesthesiologists class of 3 or higher, and increased body mass index.</description><dc:title>Incidence of Sedation-Related Complications With Propofol Use During Advanced Endoscopic Procedures</dc:title><dc:creator>Gregory A. Coté, Robert M. Hovis, Michael A. Ansstas, Lawrence Waldbaum, Riad R. Azar, Dayna S. Early, Steven A. Edmundowicz, Daniel K. Mullady, Sreenivasa S. Jonnalagadda</dc:creator><dc:identifier>10.1016/j.cgh.2009.07.008</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-07-15</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-07-15</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Endoscopy Corner</prism:section><prism:startingPage>137</prism:startingPage><prism:endingPage>142</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509010118/abstract?rss=yes"><title>Algorithms Outperform Metabolite Tests in Predicting Response of Patients With Inflammatory Bowel Disease to Thiopurines</title><link>http://www.cghjournal.org/article/PIIS1542356509010118/abstract?rss=yes</link><description>Background &amp; Aims: Levels of the thiopurine metabolites 6-thioguanine nucleotide (6-TGN) and 6-methylmercaptopurine commonly are monitored during thiopurine therapy for inflammatory bowel disease despite this test's high cost and poor prediction of clinical response (sensitivity, 62%; specificity, 72%). We investigated whether patterns in common laboratory parameters might be used to identify appropriate immunologic responses to thiopurine and whether they are more accurate than measurements of thiopurine metabolites in identifying patients who respond to therapy.Methods: We identified 774 patients with inflammatory bowel disease on thiopurine therapy using metabolite and standard laboratory tests over a 24-hour time period. Machine learning algorithms were developed using laboratory values and age in a random training set of 70% of the cases; these algorithms were tested in the remaining 30% of the cases.Results: A random forest algorithm was developed based on laboratory and age data; it differentiated clinical responders from nonresponders in the test set with an area under the receiver operating characteristic (AUROC) curve of 0.856. In contrast, 6-TGN levels differentiated clinical responders from nonresponders with an AUROC of 0.594 (P &lt; .001). Algorithms developed to identify thiopurine nonadherence (AUROC, 0.813) and thiopurine shunters (AUROC, 0.797) were accurate.Conclusions: Algorithms that use age and laboratory values can differentiate clinical response, nonadherence, and shunting of thiopurine metabolism among patients who take thiopurines. This approach was less costly and more accurate than 6-TGN metabolite measurements in predicting clinical response. If validated, this approach would provide a low-cost, rapid alternative to metabolite measurements for monitoring thiopurine use.</description><dc:title>Algorithms Outperform Metabolite Tests in Predicting Response of Patients With Inflammatory Bowel Disease to Thiopurines</dc:title><dc:creator>Akbar K. Waljee, Joel C. Joyce, Sijian Wang, Aditi Saxena, Margaret Hart, Ji Zhu, Peter D.R. Higgins</dc:creator><dc:identifier>10.1016/j.cgh.2009.09.031</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-10-15</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-10-15</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Original Articles-Alimentary Tract</prism:section><prism:startingPage>143</prism:startingPage><prism:endingPage>150</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509010829/abstract?rss=yes"><title>Long-term Outcome of Patients With Obscure Gastrointestinal Bleeding Investigated by Double-Balloon Endoscopy</title><link>http://www.cghjournal.org/article/PIIS1542356509010829/abstract?rss=yes</link><description>Background &amp; Aims: It is often difficult to determine the cause of obscure gastrointestinal bleeding (OGIB). We evaluated the diagnostic yield and long-term outcome of patients with OGIB by using double-balloon endoscopy (DBE).Methods: In this large, retrospective cohort study, DBE was performed in 200 consecutive patients with OGIB. Follow-up data were available from 151 patients for 29.7 months (range, 6–78 months), and clinical outcome was assessed.Results: DBE detected bleeding sources in 155 of 200 patients (77.5%). The most frequent source detected was small intestine ulcers/erosions (64 patients). Patients who underwent DBE within 1 month after the last episode of overt bleeding had a better yield of positive findings than those who did not (84%, 107/128 patients vs 57%, 24/42; P = .002). The overall rate of control of OGIB was 64% (97/151 patients). Patients with vascular lesions of the small intestine had a significantly lower rate of control of OGIB than those with other small intestine lesions (40%, 12/30 patients vs 74%, 52/70; P = .001). A requirement for a large transfusion before DBE (P = .012), multiple lesions (P = .010), and suspicious (not definite) lesions (P = .038) each significantly increased the likelihood of overt rebleeding in patients with vascular lesions of the small intestine.Conclusions: DBE is useful for the diagnosis of patients with OGIB and should be performed as soon as possible after overt OGIB. Patients with vascular lesions of the small intestine should be followed with particular care.</description><dc:title>Long-term Outcome of Patients With Obscure Gastrointestinal Bleeding Investigated by Double-Balloon Endoscopy</dc:title><dc:creator>Satoshi Shinozaki, Hironori Yamamoto, Tomonori Yano, Keijiro Sunada, Tomohiko Miyata, Yoshikazu Hayashi, Masayuki Arashiro, Kentaro Sugano</dc:creator><dc:identifier>10.1016/j.cgh.2009.10.023</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-11-02</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-11-02</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Original Articles-Alimentary Tract</prism:section><prism:startingPage>151</prism:startingPage><prism:endingPage>158</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509010799/abstract?rss=yes"><title>Effects of Chenodeoxycholate and a Bile Acid Sequestrant, Colesevelam, on Intestinal Transit and Bowel Function</title><link>http://www.cghjournal.org/article/PIIS1542356509010799/abstract?rss=yes</link><description>Background &amp; Aims: Di-α hydroxy bile salt, sodium chenodeoxycholate (CDC), and bile acid binding have unclear effects on colonic transit in health and disease.Methods: We performed 2 randomized, double-blind, placebo-controlled studies. In healthy volunteers (20 per group), we evaluated the effects of oral placebo, 500 mg, or 1000 mg of CDC (delayed-release, each given for 4 days) on gastrointestinal and colonic transit. A second trial compared the effects of colesevelam (1.875 g, twice daily) versus placebo in 24 patients (12 per group) with diarrhea-predominant irritable bowel syndrome (IBS-D) on transit, daily bowel frequency and consistency, and colonic mucosal permeability. Serum fasting 7α-hydroxy-4-cholesten-3-one (7αC4) was measured to screen for bile acid malabsorption. Effects of treatments on transit were compared using analysis of covariance with body mass index and 7αC4 as covariates.Results: In healthy volunteers, CDC significantly accelerated colonic transit (at 24 and 48 hours, P = .01 and P &lt; .0001, respectively), increased stool frequency and ease of passage (both P &lt; .001), and evacuation (P = .02), and decreased stool consistency (P &lt; .001). Four of the 24 IBS-D patients had increased serum 7αC4 levels. In IBS-D, colesevelam modestly affected overall colonic transit (24 h; P = .22). Emptying of the ascending colon took an average of 4 hours longer in patients given colesevelam compared with placebo; treatment effect was associated with baseline serum 7αC4 levels (P = .0025). Colesevelam was associated with greater ease of stool passage (P = .048) and somewhat firmer stool consistency (P = .12). No effects on mucosal permeability or safety were identified.Conclusions: Sodium chenodeoxycholate in health and colesevelam in IBS-D patients have opposite effects on colonic transit and fecal parameters.</description><dc:title>Effects of Chenodeoxycholate and a Bile Acid Sequestrant, Colesevelam, on Intestinal Transit and Bowel Function</dc:title><dc:creator>Suwebatu T. Odunsi–Shiyanbade, Michael Camilleri, Sanna McKinzie, Duane Burton, Paula Carlson, Irene A. Busciglio, Jesse Lamsam, Ravinder Singh, Alan R. Zinsmeister</dc:creator><dc:identifier>10.1016/j.cgh.2009.10.020</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-11-02</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-11-02</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Original Articles-Alimentary Tract</prism:section><prism:startingPage>159</prism:startingPage><prism:endingPage>165.e5</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509010428/abstract?rss=yes"><title>Serious Complications Within 30 Days of Screening and Surveillance Colonoscopy Are Uncommon</title><link>http://www.cghjournal.org/article/PIIS1542356509010428/abstract?rss=yes</link><description>Background &amp; Aims: The risk of serious complications after colonoscopy has important implications for the overall benefits of colorectal cancer screening programs. We evaluated the incidence of serious complications within 30 days after screening or surveillance colonoscopies in diverse clinical settings and sought to identify potential risk factors for complications.Methods: Patients age 40 and over undergoing colonoscopy for screening, surveillance, or evaluation based an abnormal result from another screening test were enrolled through the National Endoscopic Database (CORI). Patients completed a standardized telephone interview approximately 7 and 30 days after their colonoscopy. We estimated the incidence of serious complications within 30 days of colonoscopy and identified risk factors associated with complications using logistic regression analyses.Results: We enrolled 21,375 patients. Gastrointestinal bleeding requiring hospitalization occurred in 34 patients (incidence 1.59/1000 exams; 95% confidence interval [CI], 1.10–2.22). Perforations occurred in 4 patients (0.19/1000 exams; 95% CI, 0.05–0.48), diverticulitis requiring hospitalization in 5 patients (0.23/1000 exams; 95% CI, 0.08–0.54), and postpolypectomy syndrome in 2 patients (0.09/1000 exams; 95% CI, 0.02–0.30). The overall incidence of complications directly related to colonoscopy was 2.01 per 1000 exams (95% CI, 1.46–2.71). Two of the 4 perforations occurred without biopsy or polypectomy. The risk of complications increased with preprocedure warfarin use and performance of polypectomy with cautery.Conclusions: Complications after screening or surveillance colonoscopy are uncommon. Risk factors for complications include warfarin use and polypectomy with cautery.</description><dc:title>Serious Complications Within 30 Days of Screening and Surveillance Colonoscopy Are Uncommon</dc:title><dc:creator>Cynthia W. Ko, Stacy Riffle, Leann Michaels, Cynthia Morris, Jennifer Holub, Jean A. Shapiro, Marcia A. Ciol, Michael B. Kimmey, Laura C. Seeff, David Lieberman</dc:creator><dc:identifier>10.1016/j.cgh.2009.10.007</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-10-21</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-10-21</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Original Articles-Alimentary Tract</prism:section><prism:startingPage>166</prism:startingPage><prism:endingPage>173</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509010131/abstract?rss=yes"><title>Efficacy of Annual Colonoscopic Surveillance in Individuals With Hereditary Nonpolyposis Colorectal Cancer</title><link>http://www.cghjournal.org/article/PIIS1542356509010131/abstract?rss=yes</link><description>Background &amp; Aims: Individuals with hereditary nonpolyposis colorectal cancer (HNPCC; Lynch syndrome) have a high risk for developing colorectal cancer (CRC). We evaluated the efficacy of annual surveillance colonoscopies to detect adenomas and CRCs.Methods: In a prospective, multicenter cohort study, 1126 individuals underwent 3474 colonoscopies. We considered individuals from 3 groups of HNPCC families: those with a pathogenic germline mutation in a mismatch repair gene (MUT group), those without a mutation but with microsatellite instability (MSI group), and those who fufilled the Amsterdam criteria without microsatellite instability (MSS group).Results: Compliance to annual intervals was good, with 81% of colonoscopies completed within 15 months. Ninety-nine CRC events were observed in 90 patients. Seventeen CRCs (17%) were detected through symptoms (8 before baseline colonoscopy, 8 at intervals &gt;15 months to the preceding colonoscopy, and 1 interval cancer). Only 2 of 43 CRCs detected by follow-up colonoscopy were regionally advanced. Tumor stages were significantly lower among CRCs detected by follow-up colonoscopies compared with CRCs detected by symptoms (P = .01). Cumulative CRC risk at the age of 60 years was similar in the MUT and MSI groups (23.0% combined; 95% confidence interval [CI], 14.8%–31.2%) but considerably lower in the MSS group (1.8%; 95% CI, 0.0%–5.1%). Adenomas at baseline colonoscopy predicted an earlier occurrence of subsequent adenoma (hazard ratio, 2.6; 95% CI, 1.7–4.0) and CRC (hazard ratio, 3.9; 95% CI, 1.7–8.5), providing information about interindividual heterogeneity of adenomas and kinetics of CRC formation.Conclusions: Annual colonoscopic surveillance is recommended for individuals with HNPCC. Less intense surveillance might be appropriate for MSS families.</description><dc:title>Efficacy of Annual Colonoscopic Surveillance in Individuals With Hereditary Nonpolyposis Colorectal Cancer</dc:title><dc:creator>Christoph Engel, Nils Rahner, Karsten Schulmann, Elke Holinski–Feder, Timm O. Goecke, Hans K. Schackert, Matthias Kloor, Verena Steinke, Holger Vogelsang, Gabriela Möslein, Heike Görgens, Stefan Dechant, Magnus von Knebel Doeberitz, Josef Rüschoff, Nicolaus Friedrichs, Reinhard Büttner, Markus Loeffler, Peter Propping, Wolff Schmiegel, German HNPCC Consortium</dc:creator><dc:identifier>10.1016/j.cgh.2009.10.003</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-10-15</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-10-15</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Original Articles-Alimentary Tract</prism:section><prism:startingPage>174</prism:startingPage><prism:endingPage>182</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509009938/abstract?rss=yes"><title>Prevalence and Factors Associated With Liver Test Abnormalities Among Human Immunodeficiency Virus–Infected Persons</title><link>http://www.cghjournal.org/article/PIIS1542356509009938/abstract?rss=yes</link><description>Background &amp; Aims: Liver disease is a major cause of morbidity and mortality among human immunodeficiency virus (HIV)-infected persons. We evaluated the prevalence, etiology, and factors associated with liver dysfunction in patients during the highly active antiretroviral therapy era.Methods: We performed liver tests (baseline and after a 6-month follow-up period) in HIV-infected patients treated at a large clinic. Comprehensive laboratory and ultrasound analyses were performed. Factors associated with liver test abnormalities were assessed using multivariate logistic regression models.Results: Eighty of 299 HIV-positive patients (27%) had abnormal liver test results during the 6-month study period. The majority of abnormalities were grade 1. Of those with liver test abnormalities, the most common diagnosis was nonalcoholic fatty liver disease (30%), followed by excessive alcohol use (13%), chronic hepatitis B (9%), chronic active hepatitis C (5%), and other (hemochromatosis and autoimmune hepatitis, 2%); 8 participants (10%) had more than 1 diagnosis. In total, 39 HIV patients with abnormal liver test results (49%) had a defined underlying liver disease. Despite laboratory tests and ultrasound examination, 41 abnormal liver test results (51%) were unexplained. Multivariate analyses of this group found that increased total cholesterol levels (odds ratio, 1.6 per 40-mg/dL increase; P = .01) were associated with liver abnormalities.Conclusions: Liver test abnormalities are common among HIV patients during the highly active antiretroviral therapy era. The most common diagnosis was nonalcoholic fatty liver disease. Despite laboratory and radiologic investigations into the cause of liver dysfunction, 51% were unexplained, but might be related to unrecognized fatty liver disease.</description><dc:title>Prevalence and Factors Associated With Liver Test Abnormalities Among Human Immunodeficiency Virus–Infected Persons</dc:title><dc:creator>Nancy Crum–Cianflone, Gary Collins, Sheila Medina, Dean Asher, Richard Campin, Mary Bavaro, Braden Hale, Charles Hames</dc:creator><dc:identifier>10.1016/j.cgh.2009.09.025</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-10-05</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-10-05</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Original Articles-Liver, Pancreas, and Biliary Tract</prism:section><prism:startingPage>183</prism:startingPage><prism:endingPage>191</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509010854/abstract?rss=yes"><title>Antiviral Therapy Reduces Risk of Hepatocellular Carcinoma in Patients With Hepatitis C Virus–Related Cirrhosis</title><link>http://www.cghjournal.org/article/PIIS1542356509010854/abstract?rss=yes</link><description>Background &amp; Aims: The effects of antiviral therapy on prevention of hepatocellular carcinoma (HCC) in patients with hepatitis C virus (HCV)-related cirrhosis are unclear. We performed a systematic review and meta-analysis to assess HCC risk reduction in patients with HCV-related cirrhosis who have received antiviral therapy.Methods: Twenty studies (4700 patients) were analyzed that compared untreated patients with those given interferon (IFN) alone or ribavirin. Risk ratios (RRs) determined effect size using a random effects model.Results: Pooled data showed reduced HCC risk in the treatment group (RR, 0.43; 95% confidence interval [CI], 0.33–0.56), although the data were heterogenous (χ2 = 59.10). Meta-regression analysis showed that studies with follow-up durations of more than 5 years contributed to heterogeneity. Analysis of 14 studies (n = 3310) reporting sustained virologic response (SVR) rates with antiviral treatment showed reduced HCC risk in patients with an SVR, compared with nonresponders (RR, 0.35; 95% CI, 0.26–0.46); the maximum benefits were observed in patients treated with ribavirin-based regimens (RR, 0.25; 95% CI, 0.14–0.46). Meta-analysis of 4 studies assessing the role of maintenance IFN in nonresponders did not show HCC risk reduction (RR, 0.58; 95% CI, 0.33–1.03). No publication bias was detected by the Egger test analysis (P &gt; 0.1).Conclusions: The risk of HCC is reduced among patients with HCV who achieve an SVR with antiviral therapy. Maintenance therapy with IFN does not reduce HCC risk among patients who do not respond to initial therapy.View this article's video abstract at www.cghjournal.org.</description><dc:title>Antiviral Therapy Reduces Risk of Hepatocellular Carcinoma in Patients With Hepatitis C Virus–Related Cirrhosis</dc:title><dc:creator>Ashwani K. Singal, Amanpal Singh, Sathya Jaganmohan, Praveen Guturu, Rajasekhara Mummadi, Yong–Fang Kuo, Gagan K. Sood</dc:creator><dc:identifier>10.1016/j.cgh.2009.10.026</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-11-02</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-11-02</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Original Articles-Liver, Pancreas, and Biliary Tract</prism:section><prism:startingPage>192</prism:startingPage><prism:endingPage>199</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509009549/abstract?rss=yes"><title>Survival and Recurrence in Patients With Splanchnic Vein Thromboses</title><link>http://www.cghjournal.org/article/PIIS1542356509009549/abstract?rss=yes</link><description>Background &amp; Aims: Hepatic, splenic, portal, and mesenteric veins are confluent elements within the splanchnic system. It is therefore unclear whether thromboses of isolated segments represent unique entities. We compared etiologies, recurrence, and survival of patients with thromboses of different splanchnic venous segments.Methods: An inception cohort of individuals was identified with first lifetime incident of splanchnic vein thrombosis between 1980 and 2000. We performed a case-controlled comparison of recurrent thrombosis and survival data with those of patients with deep venous thrombosis (DVT).Results: The study (832 patients; mean age, 53 ± 17 years; 42% women) included patients with isolated portal (n = 329), mesenteric (n = 76), splenic (n = 62), and hepatic (n = 45) vein thrombosis and patients with multisegment involvement (n = 320). Malignancy (27%) and cirrhosis (24%) were the most common etiologies. Recurrence-free survival 10 years after splanchnic vein thrombosis (76%) was comparable with that after DVT (68%) and not improved by anticoagulant therapy. Hormone therapy was the only independent predictor of recurrence (hazard ratio [HR], 2.2; 95% confidence interval [CI], 1.09–4.45; P = .03). Major bleeding was 6.9/100 patient-years. Gastroesophageal varices (HR, 2.63; 95% CI, 1.72–4.03; P &lt; .001) and warfarin therapy (HR, 1.91, 95% CI, 1.25–2.92; P = .003) were independent predictors of bleeding. The 10-year survival rate of patients with splanchnic vein thrombosis (60%) was lower than that of patients with DVT (68%, P &lt; .05). Older age (HR, 1.03; 95% CI, 1.02–1.03), active cancer (HR, 2.23; 95% CI, 1.78–2.78), and myeloproliferative disorder (HR, 1.92; 95% CI, 1.41–2.61) were independent determinants of mortality (P &lt; .001).Conclusions: Splanchnic vein thrombosis depends on the pathology of the organ supplied. On the basis of the low rate of recurrence and substantial rate of major hemorrhage, prolonged anticoagulant therapy does not appear to be justified.</description><dc:title>Survival and Recurrence in Patients With Splanchnic Vein Thromboses</dc:title><dc:creator>Mallikarjun R. Thatipelli, Robert D. McBane, David O. Hodge, Waldemar E. Wysokinski</dc:creator><dc:identifier>10.1016/j.cgh.2009.09.019</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-09-27</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-09-27</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Original Articles-Liver, Pancreas, and Biliary Tract</prism:section><prism:startingPage>200</prism:startingPage><prism:endingPage>205</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509008921/abstract?rss=yes"><title>Pathology Analysis Reveals That Dysplastic Pancreatic Ductal Lesions Are Frequent in Patients With Hereditary Pancreatitis</title><link>http://www.cghjournal.org/article/PIIS1542356509008921/abstract?rss=yes</link><description>Background &amp; Aims: Hereditary pancreatitis (HP) is a risk factor for pancreatic adenocarcinoma. We performed a retrospective, multicenter study to characterize and evaluate the frequency of pancreatic intraepithelial neoplasia (PanIN) and to describe the characteristics of fibrosis in pancreatic surgical specimens from patients with HP.Methods: Samples from partial pancreatectomies (n = 13) of patients with HP complications (n = 12; 7 males; mean age, 24 y; 1 patient underwent 2 surgeries over 16 years) were analyzed by histologic and immunohistologic analyses; patients with suspected or proven pancreatic adenocarcinoma were excluded. HP diagnosis was confirmed by analysis of PRSS1 mutations. Dysplastic lesions were described according to the PanIN classification.Results: Eleven patients were found to have the R122H mutation in PRSS1 and 1 patient was found to have the N29I mutation in PRSS1. Fifty-one PanIN lesions were observed in 10 specimens (77%): PanIN lesions 1a, 1b, 2, and 3 were observed in 8, 5, 8, and 5 specimens, respectively. The median number of PanIN lesions was 3.5 for each specimen. The density of the lesions was 2.6 per 10 cm2. The size of lesions was greater than 0.5 mm in 55% of the samples. Two patients with PanIN-3 developed pancreatic cancer, 18 months and 44 years after surgery.Conclusions: PanIN lesions are frequent, severe, and occur early in the course of HP. Among patients with PanINs, 50% had PanIN-3 lesions. Pancreatectomy could be considered as a prophylactic against pancreatic cancer in patients with high-grade dysplasia.</description><dc:title>Pathology Analysis Reveals That Dysplastic Pancreatic Ductal Lesions Are Frequent in Patients With Hereditary Pancreatitis</dc:title><dc:creator>Vinciane Rebours, Philippe Lévy, Jean–François Mosnier, Jean–Yves Scoazec, Marie–Sophie Soubeyrand, Jean–François Fléjou, Bruno Turlin, Pascal Hammel, Philippe Ruszniewski, Pierre Bedossa, Anne Couvelard</dc:creator><dc:identifier>10.1016/j.cgh.2009.09.009</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-09-17</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-09-17</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Original Articles-Liver, Pancreas, and Biliary Tract</prism:section><prism:startingPage>206</prism:startingPage><prism:endingPage>212</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS154235650901009X/abstract?rss=yes"><title>Mucin-Producing Neoplasms of the Pancreas: An Analysis of Distinguishing Clinical and Epidemiologic Characteristics</title><link>http://www.cghjournal.org/article/PIIS154235650901009X/abstract?rss=yes</link><description>Background &amp; Aims: Mucin-producing neoplasms (MPNs) of the pancreas include mucinous cystic neoplasms (MCNs) and main-duct, branch-duct, and combined intraductal papillary mucinous neoplasms (IPMNs). MCNs and branch-duct IPMNs are frequently confused; it is unclear whether main-duct, combined, and branch-duct IPMNs are a different spectrum of the same disease. We evaluated their clinical and epidemiologic characteristics.Methods: Patients who underwent resection for histologically confirmed MPNs were identified (N = 557); specimens were reviewed and eventually reclassified.Results: One hundred sixty-eight patients (30%) had MCNs, 159 (28.5%) had branch-duct IPMNs, 149 (27%) had combined IPMNs, and 81 (14.5%) had main-duct IPMNs. Patients with MCNs were significantly younger and almost exclusively women; 44% of patients with main-duct or combined IPMNs and 57% of those with branch-duct IPMNs were women. MCNs were single lesions located in the distal pancreas (95%); 11% were invasive. IPMNs were more frequently found in the proximal pancreas; invasive cancer was found in 11%, 42%, and 48% of branch-duct, combined, and main-duct IPMNs, respectively (P = .001). Patients with invasive MCN and those with combined and main-duct IPMNs were older than those with noninvasive tumors. The 5-year disease-specific survival rate approached 100% for patients with noninvasive MPNs. The rates for those with invasive cancer were 58%, 56%, 51%, and 64% for invasive MCNs, branch-duct IPMNs, main-duct IPMNs, and combined IPMNs, respectively.Conclusions: MPNs comprise 3 different neoplasms: MCNs, branch-duct IPMNs, and main-duct IPMNs, including the combined type. These tumors have specific clinical, epidemiologic, and morphologic features that allow a reasonable degree of accuracy in preoperative diagnosis.</description><dc:title>Mucin-Producing Neoplasms of the Pancreas: An Analysis of Distinguishing Clinical and Epidemiologic Characteristics</dc:title><dc:creator>Stefano Crippa, Carlos Fernández–del Castillo, Roberto Salvia, Dianne Finkelstein, Claudio Bassi, Ismael Domínguez, Alona Muzikansky, Sarah P. Thayer, Massimo Falconi, Mari Mino–Kenudson, Paola Capelli, Gregory Y. Lauwers, Stefano Partelli, Paolo Pederzoli, Andrew L. Warshaw</dc:creator><dc:identifier>10.1016/j.cgh.2009.10.001</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-10-15</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-10-15</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Original Articles-Liver, Pancreas, and Biliary Tract</prism:section><prism:startingPage>213</prism:startingPage><prism:endingPage>219.e4</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS154235650901043X/abstract?rss=yes"><title>Personality Traits and Impaired Health-Related Quality of Life in Patients With Functional Gastrointestinal Disorders</title><link>http://www.cghjournal.org/article/PIIS154235650901043X/abstract?rss=yes</link><description>Background &amp; Aims: Negative affectivity and social isolation (Type D personality) are personality traits associated with poor health-related quality of life (HRQoL). We hypothesized these traits would be associated with impaired HRQoL and increased gastrointestinal symptom severity in functional gastrointestinal disorders.Methods: Data were collected from patients undergoing breath testing. Patients completed the Type D Scale-14, Gastrointestinal Symptoms Severity Index and Short-Form Health Survey 12.Results: Of 230 patients evaluated, 37% met criteria for Type D personality. Type D was associated with a decreased Mental Component score on the Short-Form Health Survey 12 (mean difference = −8.29; 95% confidence interval, 5.2–11.4; P &lt; .001). On the Gastrointestinal Symptoms Severity Index, severity of symptoms was significantly higher in Type D patients compared with non Type D patients (P &lt; .001).Conclusions: Type D personality was associated with decreased perceived HRQoL and reporting of more severe gastrointestinal symptoms. Type D personality construct may be an important consideration when assessing HRQoL outcomes. Consideration of personality traits could improve risk stratification in research and clinical practice in this patient group.</description><dc:title>Personality Traits and Impaired Health-Related Quality of Life in Patients With Functional Gastrointestinal Disorders</dc:title><dc:creator>Stephanie L. Hansel, Sarah B. Umar, Tisha N. Lunsford, Lucinda A. Harris, John K. Dibaise, Michael D. Crowell</dc:creator><dc:identifier>10.1016/j.cgh.2009.10.008</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-10-21</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-10-21</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Brief Communication</prism:section><prism:startingPage>220</prism:startingPage><prism:endingPage>222</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509007411/abstract?rss=yes"><title>Comments on Nonsteroidal Anti-Inflammatory Drug Enteropathy</title><link>http://www.cghjournal.org/article/PIIS1542356509007411/abstract?rss=yes</link><description>Dear Editor:   We read the recent articles by Watanabe et al and Smecuol et al on the likely small bowel toxicity of low dose aspirin (ASA) with great interest. Our observational study of 40 cases of likely Nonsteroidal Anti-Inflammatory Drug (NSAID)–induced ulcerative ileitis found a strong association with not only nonselective NSAIDs but, surprisingly, selective cyclooxygenase-2 inhibitors as well. Our suggested causative associations have been subsequently supported by elegant wireless capsule endoscopy (WCE) studies. We also found an unanticipated high association of ulcerative ileitis (class 4 damage by the classification of Smecuol et al) with aspirin (ASA) in doses of no greater than 325 mg/d in 55% of cases, specifically the enteric-coated variety in 48% (4 took only 81 mg/d), and 8% with regular ASA. In 38% of cases, ASA was the only NSAID taken. In what might be the largest pathologic series of NSAID enteropathy, we found changes that shared similarities with Crohn's disease, although this condition did not develop in clinical and colonoscopic follow-up averaging over 3 years, and none have developed such to this date. Therefore, these recent works and others have corroborated our contention that low dose aspirin, especially the enteric-coated variety, causes NSAID enteropathy, and all the aforementioned studies now establish with fair clinical certainty that NSAIDs of all types and even in small doses cause frequent small bowel damage with acute (within 2 weeks) and chronic ingestion in the majority of users. Once these changes occur, as seen in a published study but also in our clinical experience, they might persist off the offending agents for months to years. These observations have far reaching implications that we briefly discussed in our article and would like to elaborate on at this time in light of this subsequent body of research.</description><dc:title>Comments on Nonsteroidal Anti-Inflammatory Drug Enteropathy</dc:title><dc:creator>Randall W. Lengeling, Konrad S. Schulze</dc:creator><dc:identifier>10.1016/j.cgh.2009.07.029</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-08-10</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-08-10</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>223</prism:startingPage><prism:endingPage>224</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509012774/abstract?rss=yes"><title>Reply</title><link>http://www.cghjournal.org/article/PIIS1542356509012774/abstract?rss=yes</link><description>We appreciate the interest of Drs Lengeling and Schulze in our recently published article describing the association of the short-term administration of low-dose aspirin (acetylsalicylic acid [ASA]) and the occurrence of small intestinal mucosal damage.</description><dc:title>Reply</dc:title><dc:creator>Edgardo Smecuol, Julio C. Bai, Angel Lanas</dc:creator><dc:identifier>10.1016/j.cgh.2009.12.006</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-12-16</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-12-16</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>224</prism:startingPage><prism:endingPage>225</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS154235650901235X/abstract?rss=yes"><title>Cover</title><link>http://www.cghjournal.org/article/PIIS154235650901235X/abstract?rss=yes</link><description></description><dc:title>Cover</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1542-3565(09)01235-X</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2010-02-01</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2010-02-01</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>OFC</prism:startingPage><prism:endingPage>OFC</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509002365/abstract?rss=yes"><title>Primary Epiploic Appendagitis</title><link>http://www.cghjournal.org/article/PIIS1542356509002365/abstract?rss=yes</link><description>A 42-year-old female patient presented with vomiting, bloating, diarrhea, and a dull constant abdominal pain at admission. She reported a history of recurrent complaints and intermittent febrile temperature up to 38.5°C. Her symptoms included tenderness in the right upper abdominal quadrant, postprandial fullness, epigastric discomfort, early satiety, and weight loss of 5 kg during the preceding 4 months. Gastrointestinal examinations including abdominal ultrasound, colonoscopy with terminal ileum intubation, gastroscopy, and lactose-intolerance test provided no explanation for her symptoms. At admission, abnormal laboratory parameters included C-reactive protein 33 mg/L (normal, &lt;5 mg/L) and 83% (normal, 42%–75%) neutrophil leukocytes. Routine laboratory parameters including all other parameters of white blood count, erythrocyte sedimentation rate, and liver and pancreas enzymes were within normal limits. Abdominal computed tomography (CT) with intravenous contrast medium demonstrated an oval lesion, maximum diameter 2.7 cm, with fat attenuation, located close below the liver and adjacent to the ascending colon (), and the diagnosis of primary epiploic appendagitis (PEA) was completed.</description><dc:title>Primary Epiploic Appendagitis</dc:title><dc:creator>Wolfgang J. Schnedl, Manfred Tillich, Rainer W. Lipp</dc:creator><dc:identifier>10.1016/j.cgh.2009.03.009</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-03-23</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-03-23</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Images of the Month</prism:section><prism:startingPage>A16</prism:startingPage><prism:endingPage>A16</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509002377/abstract?rss=yes"><title>Massive Cerebral Air Embolism During Esophagogastroduodenoscopy</title><link>http://www.cghjournal.org/article/PIIS1542356509002377/abstract?rss=yes</link><description>After an unsuccessful Mason vertical gastroplasty for morbid obesity, a 46-year-old woman underwent a biliopancreatic diversion according to Scopinaro et al. On the 7th postoperative day, the patient developed a gastric fistula that got infected and needed multiple hospital stays for surgical correction during the following months.</description><dc:title>Massive Cerebral Air Embolism During Esophagogastroduodenoscopy</dc:title><dc:creator>Marco Vinetti, Sophie De Roock, Philippe Hantson</dc:creator><dc:identifier>10.1016/j.cgh.2009.03.008</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-03-23</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-03-23</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Images of the Month</prism:section><prism:startingPage>A20</prism:startingPage><prism:endingPage>A20</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509002316/abstract?rss=yes"><title>Intestinal Spirochetosis: An Unusual Cause of Asymptomatic Colonic Ulceration</title><link>http://www.cghjournal.org/article/PIIS1542356509002316/abstract?rss=yes</link><description>A 55-year-old homosexual man with human immunodeficiency virus (HIV) on highly active antiretroviral therapy presented for screening colonoscopy. He denied recent fevers, chills, weight loss, abdominal pain, blood in stool, constipation, or diarrhea. Also, he denied NSAID intake. Laboratory results were notable for a cluster of differentiation 4 count of 237 cells/μL and HIV RNA by polymerase chain reaction &lt;50 copies/mL. A colonoscopy was normal except for a nonbleeding 5-mm ulcer in the cecum (, arrow). Pathology of the ulcer biopsy specimens demonstrated mild acute cryptitis with a prominent luminal brush border. No viral inclusions were identified. A Warthin-Starry stain showed luminal spirochetes on the surface epithelium (, arrow). Intestinal spirochetosis (IS) was diagnosed, and the patient was treated with metronidazole. Repeat colonoscopy after a course of metronidazole showed a complete resolution of the cecal ulcer, and random colonic biopsies were without evidence of spirochetes or other colonic pathology. The patient remained asymptomatic for more than 1 year of follow-up.</description><dc:title>Intestinal Spirochetosis: An Unusual Cause of Asymptomatic Colonic Ulceration</dc:title><dc:creator>Mouen Khashab, Spencer Wilson, Won Kyoo Cho</dc:creator><dc:identifier>10.1016/j.cgh.2009.03.014</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-03-23</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-03-23</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Images of the Month</prism:section><prism:startingPage>A22</prism:startingPage><prism:endingPage>A22</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509003322/abstract?rss=yes"><title>Synchronous Hepatocellular Carcinoma and Metastatic Squamous Cell Carcinoma With Life-Threatening Hypercalcemia</title><link>http://www.cghjournal.org/article/PIIS1542356509003322/abstract?rss=yes</link><description>   See related articles, Lok AS et al, on page 493 in Gastroenterology and, Miyahara K et al, on page e17 in this issue of CGH.</description><dc:title>Synchronous Hepatocellular Carcinoma and Metastatic Squamous Cell Carcinoma With Life-Threatening Hypercalcemia</dc:title><dc:creator>Hideaki Miura</dc:creator><dc:identifier>10.1016/j.cgh.2009.04.006</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-04-17</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-04-17</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Images of the Month</prism:section><prism:startingPage>A24</prism:startingPage><prism:endingPage>A24</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509003188/abstract?rss=yes"><title>Dysphagia—Unusual Presentation</title><link>http://www.cghjournal.org/article/PIIS1542356509003188/abstract?rss=yes</link><description>   See related article, Kiewe P et al, on page e5 in Gastroenterology.</description><dc:title>Dysphagia—Unusual Presentation</dc:title><dc:creator>Mark Prince</dc:creator><dc:identifier>10.1016/j.cgh.2009.03.030</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2009-04-13</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-04-13</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Images of the Month</prism:section><prism:startingPage>A25</prism:startingPage><prism:endingPage>A25</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509012403/abstract?rss=yes"><title>Copyright Assignment, Authorship Responsibility, NIH Funding, Financial Disclosure, Institutional Review Board/Animal Care Committee Approval, and Sponsorship</title><link>http://www.cghjournal.org/article/PIIS1542356509012403/abstract?rss=yes</link><description>In consideration of the American Gastroenterological Association (AGA) Institute (the “AGA Institute”) taking action to review and credit the below-identified submission (the “Manuscript”), and for other valuable consideration, the receipt and sufficiency of which is hereby acknowledged, the undersigned authors and/or creators (the “Authors”), jointly and severally, hereby transfer, convey, and assign to the AGA Institute, free and clear of any liens, licenses or encumbrances, the entire right, title, and interest in and to the Manuscript throughout the world, including without limitation in and to any and all copyrights for the Manuscript (including but not limited to rights to copy, publish, excerpt, collect royalties and make derivative works) in print, electronic, Internet, broadcast, and all other forms and media now or hereafter known, and for any and all causes of action heretofore accrued in Authors' favor for infringement of the aforesaid copyrights, to have and to hold the same unto the AGA Institute, its successors and assigns, for and during the existence of the aforesaid copyrights, and all renewals and extensions thereof. At any time and from time to time hereafter, the Authors shall upon the AGA Institute's written request take any and all steps and execute, acknowledge and deliver to the AGA Institute any and all further instruments and assurances necessary or expedient in order to vest the aforesaid copyrights and causes of action more effectively in the AGA Institute. The Authors retain the nonexclusive permission to use all or part of the Manuscript in future works of their own in a noncompeting way, provided proper copyright credit is given to the AGA Institute. Should the AGA Institute finally determine that it will not publish the Manuscript, the AGA Institute agrees to assign its rights therein back to the Authors. (Note: material prepared by employees of the federal government in the course of their official duties may not be copyrightable.)</description><dc:title>Copyright Assignment, Authorship Responsibility, NIH Funding, Financial Disclosure, Institutional Review Board/Animal Care Committee Approval, and Sponsorship</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1542-3565(09)01240-3</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2010-02-01</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2010-02-01</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Electronic Images of the Month</prism:section><prism:startingPage>A26</prism:startingPage><prism:endingPage>A26</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509012373/abstract?rss=yes"><title>Editorial Board</title><link>http://www.cghjournal.org/article/PIIS1542356509012373/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1542-3565(09)01237-3</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2010-02-01</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2010-02-01</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>A4</prism:startingPage><prism:endingPage>A4</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509012385/abstract?rss=yes"><title>Contents</title><link>http://www.cghjournal.org/article/PIIS1542356509012385/abstract?rss=yes</link><description></description><dc:title>Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1542-3565(09)01238-5</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2010-02-01</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2010-02-01</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>A7</prism:startingPage><prism:endingPage>A10</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509012397/abstract?rss=yes"><title>Information for Authors and Readers</title><link>http://www.cghjournal.org/article/PIIS1542356509012397/abstract?rss=yes</link><description>Clinical Gastroenterology and Hepatology is the go-to resource on a broad spectrum of themes in clinical gastroenterology and hepatology. The official clinical practice journal of the AGA Institute brings you the best original research in the field with a unique combination of reviews, editorials, podcasts, video abstracts, and outcomes research—Mall supporting clinical practice. Articles on education, policy, and practice management highlight issues pertinent to clinicians.</description><dc:title>Information for Authors and Readers</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1542-3565(09)01239-7</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 2 (2010)</dc:source><dc:date>2010-02-01</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2010-02-01</prism:publicationDate><prism:volume>8</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1542-3565(09)X0014-5</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>A13</prism:startingPage><prism:endingPage>A14</prism:endingPage></item></rdf:RDF>