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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>3</prism:number><prism:publicationDate>March 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/PIIS1542356509009963/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509009847/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509010192/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509010180/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509010209/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356510000443/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356510000455/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356510000789/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509012294/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509013032/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509010453/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509010106/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509012178/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509012038/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509011355/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509012348/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509010817/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509012191/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509011379/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS154235650901218X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509010805/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509012336/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509009860/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509010866/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356510000431/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356510000029/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509003127/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS154235650900319X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509003218/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509003747/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356509004881/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356510000042/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356510000054/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356510000066/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cghjournal.org/article/PIIS1542356510000078/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509009963/abstract?rss=yes"><title>Surprise Finding at Endoscopic Retrograde Cholangiopancreatography</title><link>http://www.cghjournal.org/article/PIIS1542356509009963/abstract?rss=yes</link><description>A 47-year-old woman was admitted with right upper-quadrant pain, radiating to her back, with nausea and fever. She was known to have had gallstones and had undergone open cholecystectomy 9 years earlier. She developed epilepsy after an intracerebral hemorrhage at the age of 22, for which she was on treatment with phenytoin and carbamazepine, and had mild asthma.</description><dc:title>Surprise Finding at Endoscopic Retrograde Cholangiopancreatography</dc:title><dc:creator>Kirstin Mary Taylor, Matthew Foxton, Alistair McNair</dc:creator><dc:identifier>10.1016/j.cgh.2009.09.028</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (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>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Electronic Images of the Month</prism:section><prism:startingPage>e24</prism:startingPage><prism:endingPage>e25</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509009847/abstract?rss=yes"><title>Masquerading Primary Liver Leiomyosarcoma as a Hemorrhagic Hepatoma</title><link>http://www.cghjournal.org/article/PIIS1542356509009847/abstract?rss=yes</link><description>A 78-year-old woman presented with 2 months of pleuritic right upper quadrant abdominal pain associated with a 12-pound weight loss. Abdominal exam showed moderate right upper quadrant tenderness, with a palpable liver edge up to 3 inches below the right costal margin; no discrete mass was palpated. Computed tomography scan enhanced triple phase of the liver subsequently demonstrated a 13-cm mass in the right lobe, a 3-cm mass in the posterior and inferior subcapsular region of segment 3 of the left hepatic lobe, and a 2-cm focal lesion in segment 3 of the left hepatic lobe near the fissure of the round ligament ( A). Follow-up magnetic resonance image with gadolinium showed the largest lesion in right lobe measuring 13.4 × 11.1 × 17.4 cm with heterogeneous enhancement and low peripheral and high central T1 and T2 signal, consistent with necrosis or hemorrhage, impressing on, but not originating from, the inferior vena cava ( B). Histologic evaluation stained with hematoxylin-eosin from a liver biopsy showed a spindle cell malignant tumor ( C). In addition, this tumor immunohistochemically stained positive for desmin, and there was coexpression of keratin, yet it stained negative for DF31, CD 68, S100, and hepatocellular antigen. The tumor was diagnosed as a high-grade sarcoma consistent with primary liver leiomyosarcoma. The patient was referred to oncology for further medical management because she was determined to be a nonsurgical candidate.</description><dc:title>Masquerading Primary Liver Leiomyosarcoma as a Hemorrhagic Hepatoma</dc:title><dc:creator>Carol Jamie Morris, Ravi Ghanta</dc:creator><dc:identifier>10.1016/j.cgh.2009.09.021</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (2010)</dc:source><dc:date>2009-09-28</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-09-28</prism:publicationDate><prism:volume>8</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Electronic Images of the Month</prism:section><prism:startingPage>e26</prism:startingPage><prism:endingPage>e26</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509010192/abstract?rss=yes"><title>Fish Bone-Induced Pancreatitis</title><link>http://www.cghjournal.org/article/PIIS1542356509010192/abstract?rss=yes</link><description>   See related article, Nazaki Y et al, on page xxii in this issue of CGH.</description><dc:title>Fish Bone-Induced Pancreatitis</dc:title><dc:creator>Yu–Hui Chiu, Chorng–Kuang How, Jen–Dar Chen</dc:creator><dc:identifier>10.1016/j.cgh.2009.09.037</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (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>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Electronic Images of the Month</prism:section><prism:startingPage>e27</prism:startingPage><prism:endingPage>e27</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509010180/abstract?rss=yes"><title>Cryptococcal Gastroduodenitis: A Rare Location of the Disease</title><link>http://www.cghjournal.org/article/PIIS1542356509010180/abstract?rss=yes</link><description>A 26-year-old woman originating from Zambia presented at the emergency room with a 3-week history of epigastric abdominal pain and biliary vomiting. She returned from Zambia 3 weeks earlier. She had complained of fever, and had been treated with an antimalaric drug which was stopped because of a negative blood smear. Epigastric pain was constant, not relieved by proton pump inhibitors, and accompanied by diarrhea. She had lost 10 kg in the last 3 months. Past medical history included pulmonary tuberculosis (2 years earlier) and human immunodeficiency virus (HIV) infection diagnosed 3 years earlier. Physical examination revealed an altered general condition, pale conjunctiva, oral candidosis, diffuse infracentimetric adenopathies, and epigastric tenderness. Laboratory exams gave the followings results: C-reactive protein 11 mg/L (normal range, 0–10); hemoglobin 85 g/L (normal range, 120–160); white blood cell count 2.2 × 109/L (normal range, 4–11); platelets 125 × 109/L (normal range, 150–350); CD4+ cell count 3/μL (normal range, 600–1950); HIV viral load 8.7 × 104 copies/mL. Kidney and liver function tests were normal. Abdominal computerized tomography scan showed a thickened third part of the duodenum with an infiltrated mesentery as well as some free liquid between intestinal loops suggesting duodenitis ( A). Upper gastrointestinal endoscopy showed patchy lesions in the second duodenum suggestive of swollen, whitish villi ( B). Duodenal biopsies showed a slightly atrophic intestinal mucosa with a neutrophilic and eosinophilic polnuclear infiltrate within the lamina propria. Numerous circular bodies (arrows) were present in the lamina propria and in the submucosa at H&amp;E coloration ( C). They were periodic acid–Schiff positive and the alcian blue coloration highlighted mucopolysaccharides surrounding the circular bodies ( D). The positive reaction of these inclusions at alcian blue staining, indicating mucopolysaccharides production, is considered to be highly suggestive of cryptococcal disease. A few days later, the patient was diagnosed with meningitis along with a very high titer of cryptococcal antigen in the cerebrospinal fluid.</description><dc:title>Cryptococcal Gastroduodenitis: A Rare Location of the Disease</dc:title><dc:creator>Marc Girardin, Vincent Greloz, Antoine Hadengue</dc:creator><dc:identifier>10.1016/j.cgh.2009.09.036</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (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>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Electronic Images of the Month</prism:section><prism:startingPage>e28</prism:startingPage><prism:endingPage>e29</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509010209/abstract?rss=yes"><title>Ectopic Pancreas in Duodenal Bulb</title><link>http://www.cghjournal.org/article/PIIS1542356509010209/abstract?rss=yes</link><description>A 43-year-old woman underwent gastroscopy for evaluation of indigestion. A 1.5 cm, elevated, central dimpling submucosal mass was found endoscopically at the duodenal bulb (). Histologic evaluation showed small intestinal mucosa with marked chronic and acute inflammation as lymphocyte infiltration and fragments of pancreatic tissue ().</description><dc:title>Ectopic Pancreas in Duodenal Bulb</dc:title><dc:creator>Sun Young Yi</dc:creator><dc:identifier>10.1016/j.cgh.2009.10.005</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (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>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Electronic Images of the Month</prism:section><prism:startingPage>e30</prism:startingPage><prism:endingPage>e30</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356510000443/abstract?rss=yes"><title>Exam 1: Risk of Esophageal Adenocarcinoma and Mortality in Patients With Barrett's Esophagus: A Systematic Review and Meta-analysis</title><link>http://www.cghjournal.org/article/PIIS1542356510000443/abstract?rss=yes</link><description></description><dc:title>Exam 1: Risk of Esophageal Adenocarcinoma and Mortality in Patients With Barrett's Esophagus: A Systematic Review and Meta-analysis</dc:title><dc:creator>C. Mel Wilcox</dc:creator><dc:identifier>10.1016/j.cgh.2010.01.004</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (2010)</dc:source><dc:date>2010-01-22</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2010-01-22</prism:publicationDate><prism:volume>8</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>CME Activities</prism:section><prism:startingPage>e31</prism:startingPage><prism:endingPage>e32</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356510000455/abstract?rss=yes"><title>Exam 2: Acute Pancreatitis: Computed Tomography Utilization and Radiation Exposure Are Related to Severity but Not Patient Age</title><link>http://www.cghjournal.org/article/PIIS1542356510000455/abstract?rss=yes</link><description></description><dc:title>Exam 2: Acute Pancreatitis: Computed Tomography Utilization and Radiation Exposure Are Related to Severity but Not Patient Age</dc:title><dc:creator>C. Mel Wilcox</dc:creator><dc:identifier>10.1016/j.cgh.2010.01.005</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (2010)</dc:source><dc:date>2010-01-21</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2010-01-21</prism:publicationDate><prism:volume>8</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>CME Activities</prism:section><prism:startingPage>e33</prism:startingPage><prism:endingPage>e33</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356510000789/abstract?rss=yes"><title>Abstracts From Around the World</title><link>http://www.cghjournal.org/article/PIIS1542356510000789/abstract?rss=yes</link><description>The rising incidence of adenocarcinoma of the esophagus and the link between symptomatic gastroesophageal reflux and obesity with this cancer are well recognized. This nationwide case-control study of esophageal cancer from Australia sought to identify factors associated with gastroesophageal reflux symptoms and esophageal cancer, as well as any modification by nonsteroidal anti-inflammatory drugs (NSAIDs), smoking, and proton pump inhibitor use. Symptomatic reflux was associated with an increased risk of 6.4 times for esophageal cancer, 4.6 times for gastroesophageal junction cancer (adenocarcinoma), and 2.2 times for squamous cell cancer. Heavy smokers had a markedly higher risk for esophageal cancer than non-smokers (odds ratio, 12.3 vs 6.8), with similar patterns for gastroesophageal junction cancer and squamous cell cancer. Regular use of aspirin or NSAIDs was associated with two thirds lower risk of esophageal cancer, while no difference was observed with use of acid suppressants.</description><dc:title>Abstracts From Around the World</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/j.cgh.2010.01.015</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (2010)</dc:source><dc:date>2010-02-05</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2010-02-05</prism:publicationDate><prism:volume>8</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Abstracts From Around the World</prism:section><prism:startingPage>227</prism:startingPage><prism:endingPage>230</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509012294/abstract?rss=yes"><title>Personalized Dose Reduction for Computed Tomography Scanning: Size Matters, so Does Prior Radiation Exposures</title><link>http://www.cghjournal.org/article/PIIS1542356509012294/abstract?rss=yes</link><description>The article, “Acute Pancreatitis: Computed Tomography Utilization and Radiation Exposure Are Related to Severity but Not Patient Age” by Morgan et al is timely and a valuable addition to the existing literature written on the subject of radiation dose in patients undergoing repetitive computed tomography (CT) scans. We agree with the points made by the authors and several other investigators who recently have written and commented on the subject of excessive radiation dose caused by imaging and its reduction. In this clinical setting, the referring physicians, gastroenterologists, surgeons, and radiologists should work together as a team to eliminate unnecessary routine CT scanning and utilize ultrasound or magnetic resonance imaging (MRI) if the needed information can be obtained with these nonionizing imaging modalities. However, if the desired information can be obtained only with CT, dose reduction techniques should be used that effectively reduce radiation dose to the patient without sacrificing diagnostic information.</description><dc:title>Personalized Dose Reduction for Computed Tomography Scanning: Size Matters, so Does Prior Radiation Exposures</dc:title><dc:creator>Mannudeep K. Kalra, Isaac R. Francis</dc:creator><dc:identifier>10.1016/j.cgh.2009.12.001</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (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>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Editorials</prism:section><prism:startingPage>231</prism:startingPage><prism:endingPage>232</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509013032/abstract?rss=yes"><title>Risk and Reason in Barrett's Esophagus</title><link>http://www.cghjournal.org/article/PIIS1542356509013032/abstract?rss=yes</link><description>   Podcast interview: www.gastro.org/cghpodcast.</description><dc:title>Risk and Reason in Barrett's Esophagus</dc:title><dc:creator>Nicholas J. Shaheen</dc:creator><dc:identifier>10.1016/j.cgh.2009.12.007</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (2010)</dc:source><dc:date>2009-12-18</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-12-18</prism:publicationDate><prism:volume>8</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Editorials</prism:section><prism:startingPage>233</prism:startingPage><prism:endingPage>234</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509010453/abstract?rss=yes"><title>Risk of Esophageal Adenocarcinoma and Mortality in Patients With Barrett's Esophagus: A Systematic Review and Meta-analysis</title><link>http://www.cghjournal.org/article/PIIS1542356509010453/abstract?rss=yes</link><description>Background &amp; Aims: As the risk of esophageal adenocarcinoma (EAC) and mortality in patients with Barrett's esophagus (BE) are important determinants of the potential yield and cost-effectiveness of BE surveillance, clarification of these factors is essential. We therefore performed a systematic review and meta-analysis to determine the incidence of EAC and mortality due to EAC in BE under surveillance.Methods: Databases were searched for relevant cohort studies in English language that reported EAC risk and mortality due to EAC in BE. Studies had to include patients with histologically proven BE, documented follow-up, and histologically proven EAC on surveillance. A random effects model was used with assessment of heterogeneity by the I2-statistic and of publication bias by Begg's and Egger's tests.Results: Fifty-one studies were included in the main analysis. The overall mean age of BE patients was 61 years; the mean overall proportion of males was 64%. The pooled estimate for EAC incidence was 6.3/1000 person-years of follow-up (95% confidence interval, 4.7–8.4) with considerable heterogeneity (P &lt; .001; I2 = 79%). Nineteen studies reported data on mortality due to EAC. The pooled incidence of fatal EAC was 3.0/1000 person-years of follow-up (95% confidence interval, 2.2–3.9) with no evidence for heterogeneity (P = .4; I2 = 7%). No evidence of publication bias was found.Conclusions: Patients with BE are at low risk of malignant progression and predominantly die due to causes other than EAC. This undermines the cost-effectiveness of BE surveillance and supports the search for valid risk stratification tools to identify the minority of patients that are likely to benefit from surveillance.</description><dc:title>Risk of Esophageal Adenocarcinoma and Mortality in Patients With Barrett's Esophagus: A Systematic Review and Meta-analysis</dc:title><dc:creator>Marjolein Sikkema, Pieter J.F. de Jonge, Ewout W. Steyerberg, Ernst J. Kuipers</dc:creator><dc:identifier>10.1016/j.cgh.2009.10.010</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (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>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Review</prism:section><prism:startingPage>235</prism:startingPage><prism:endingPage>244</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509010106/abstract?rss=yes"><title>A 53-Year-Old Woman With Recurrent Vomiting and Migraine Headache</title><link>http://www.cghjournal.org/article/PIIS1542356509010106/abstract?rss=yes</link><description>A 53-year-old woman was referred to the Gastroenterology clinic after 5 admissions to the hospital for intractable nausea and vomiting during a period of 8 months. On questioning, the patient describes recurrent episodes of similar symptoms. These begin with the sudden onset of nausea. Often the nausea will be constant for days. During a matter of hours her symptoms will progress to include nonbloody emesis. Often she will vomit 4–6 times a day. Occasionally she will experience nonbloody diarrhea associated with these episodes. She can identify no triggering events or exacerbating factors, although she attributes the recent increase in her symptoms to stress from a family conflict. Warm baths seem to improve her symptoms somewhat. Typically her symptoms are preceded by an aura and migraine headache. Often her headache will resolve before the nausea and vomiting. These episodes have been occurring for about the last 1 1/2 years. She has no history of functional gastrointestinal disorders.</description><dc:title>A 53-Year-Old Woman With Recurrent Vomiting and Migraine Headache</dc:title><dc:creator>Jonathan Nass, Nathaniel S. Winstead</dc:creator><dc:identifier>10.1016/j.cgh.2009.10.002</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (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>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Education Practice</prism:section><prism:startingPage>245</prism:startingPage><prism:endingPage>247</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509012178/abstract?rss=yes"><title>Depth of Submucosal Invasion Does Not Predict Lymph Node Metastasis and Survival of Patients With Esophageal Carcinoma</title><link>http://www.cghjournal.org/article/PIIS1542356509012178/abstract?rss=yes</link><description>Background &amp; Aims: There is controversy over the outcomes of esophageal adenocarcinoma with superficial submucosal invasion. We evaluated the impact of depth of submucosal invasion on the presence of metastatic lymphadenopathy and survival in patients with esophageal adenocarcinoma.Methods: Pathology reports of esophagectomy samples collected from 1997 to 2007 were reviewed. Specimens from patients with esophageal adenocarcinoma and submucosal invasion were reviewed and classified as superficial (upper 1 third, sm1) or deep (middle third, sm2 or deepest third, sm3) invasion. Outcomes studied were presence of metastatic lymphadenopathy and overall survival. Variables of interest were analyzed as factors that affect overall and cancer-free survival using Cox proportional hazards modeling. A multivariate model was constructed to establish independent associations with survival.Results: The study included 80 patients; 31 (39%) had sm1 carcinoma, 23 (29%) had sm2 carcinoma, and 26 (33%) had sm3 carcinoma. Superficial and deep submucosal invasion were associated with substantial rates of metastatic lymphadenopathy (12.9% and 20.4%, respectively). The mean follow-up time was 40.5 ± 4 months and the mean overall unadjusted survival time was 53.8 ± 4.1 months. Factors significantly associated with reduced survival time included the presence of metastatic lymph nodes (hazard ratio [HR], 2.89; confidence interval [CI], 1.13–6.88) and esophageal cancer recurrence (HR 6.39, CI 2.40–16.14), but not depth of submucosal invasion.Conclusions: Patients with sm1 esophageal carcinoma have substantial rates of metastatic lymphadenopathy. Endoscopic treatment of superficial submucosal adenocarcinoma is not advised for patients that are candidates for surgery.</description><dc:title>Depth of Submucosal Invasion Does Not Predict Lymph Node Metastasis and Survival of Patients With Esophageal Carcinoma</dc:title><dc:creator>Rami J. Badreddine, Ganapathy A. Prasad, Jason T. Lewis, Lori S. Lutzke, Lynn S. Borkenhagen, Kelly T. Dunagan, Kenneth K. Wang</dc:creator><dc:identifier>10.1016/j.cgh.2009.11.016</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (2010)</dc:source><dc:date>2009-11-30</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-11-30</prism:publicationDate><prism:volume>8</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Original Articles-Alimentary Tract</prism:section><prism:startingPage>248</prism:startingPage><prism:endingPage>253</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509012038/abstract?rss=yes"><title>A Cytologic Assay for Diagnosis of Food Hypersensitivity in Patients With Irritable Bowel Syndrome</title><link>http://www.cghjournal.org/article/PIIS1542356509012038/abstract?rss=yes</link><description>Background &amp; Aims: A percentage of patients with symptoms of irritable bowel syndrome (IBS) suffer from food hypersensitivity (FH) and improve on a food-elimination diet. No assays have satisfactory levels of sensitivity for identifying patients with FH. We evaluated the efficacy of an in vitro basophil activation assay in the diagnosis of FH in IBS-like patients.Methods: Blood samples were collected from 120 consecutive patients diagnosed with IBS according to Rome II criteria. We analyzed in vitro activation of basophils by food allergens (based on levels of CD63 expression), as well as total and food-specific immunoglobulin (Ig)E levels in serum. Effects of elimination diets and double-blind food challenges were used as standards for FH diagnosis.Results: Twenty-four of the patients (20%) had FH (cow's milk and/or wheat hypersensitivity); their symptom scores improved significantly when they were placed on an elimination diet. Patients with FH differed from other IBS patients in that they had a longer duration of clinical history, a history of FH as children, and an increased frequency of self-reported FH; they also had hypersensitivities to other antigens (eg, egg or soy). The basophil activation assay diagnosed FH with 86% sensitivity, 88% specificity, and 87% accuracy; this level of sensitivity was significantly higher than that of serum total IgE or food-specific IgE assays.Conclusions: A cytometric assay that quantifies basophils after stimulation with food antigens based on cell-surface expression of CD63 had high levels of sensitivity, specificity, and accuracy in diagnosing FH. This assay might be used to diagnose FH in patients with IBS-like symptoms.</description><dc:title>A Cytologic Assay for Diagnosis of Food Hypersensitivity in Patients With Irritable Bowel Syndrome</dc:title><dc:creator>Antonio Carroccio, Ignazio Brusca, Pasquale Mansueto, Giuseppe Pirrone, Maria Barrale, Lidia Di Prima, Giuseppe Ambrosiano, Giuseppe Iacono, Maria Letizia Lospalluti, Stella M. La Chiusa, Gaetana Di Fede</dc:creator><dc:identifier>10.1016/j.cgh.2009.11.010</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (2010)</dc:source><dc:date>2009-11-23</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-11-23</prism:publicationDate><prism:volume>8</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Original Articles-Alimentary Tract</prism:section><prism:startingPage>254</prism:startingPage><prism:endingPage>260</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509011355/abstract?rss=yes"><title>Cost Effectiveness of Alternative Imaging Strategies for the Diagnosis of Small-Bowel Crohn's Disease</title><link>http://www.cghjournal.org/article/PIIS1542356509011355/abstract?rss=yes</link><description>Background &amp; Aims: The cost effectiveness of alternative approaches to the diagnosis of small-bowel Crohn's disease is unknown. This study evaluates whether computed tomographic enterography (CTE) is a cost-effective alternative to small-bowel follow-through (SBFT) and whether capsule endoscopy is a cost-effective third test in patients in whom a high suspicion of disease remains after 2 previous negative tests.Methods: A decision-analytic model was developed to compare the lifetime costs and benefits of each diagnostic strategy. Patients were considered with low (20%) and high (75%) pretest probability of small-bowel Crohn's disease. Effectiveness was measured in quality-adjusted life-years (QALYs) gained. Parameter assumptions were tested with sensitivity analyses.Results: With a moderate to high pretest probability of small-bowel Crohn's disease, and a higher likelihood of isolated jejunal disease, follow-up evaluation with CTE has an incremental cost-effectiveness ratio of less than $54,000/QALY-gained compared with SBFT. The addition of capsule endoscopy after ileocolonoscopy and negative CTE or SBFT costs greater than $500,000 per QALY-gained in all scenarios. Results were not sensitive to costs of tests or complications but were sensitive to test accuracies.Conclusions: The cost effectiveness of strategies depends critically on the pretest probability of Crohn's disease and if the terminal ileum is examined at ileocolonoscopy. CTE is a cost-effective alternative to SBFT in patients with moderate to high suspicion of small-bowel Crohn's disease. The addition of capsule endoscopy as a third test is not a cost-effective third test, even in patients with high pretest probability of disease.</description><dc:title>Cost Effectiveness of Alternative Imaging Strategies for the Diagnosis of Small-Bowel Crohn's Disease</dc:title><dc:creator>Barrett G. Levesque, Lauren E. Cipriano, Steven L. Chang, Keane K. Lee, Douglas K. Owens, Alan M. Garber</dc:creator><dc:identifier>10.1016/j.cgh.2009.10.032</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (2010)</dc:source><dc:date>2009-11-06</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-11-06</prism:publicationDate><prism:volume>8</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Original Articles-Alimentary Tract</prism:section><prism:startingPage>261</prism:startingPage><prism:endingPage>267.e4</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509012348/abstract?rss=yes"><title>Increased Risk for Non-Melanoma Skin Cancer in Patients With Inflammatory Bowel Disease</title><link>http://www.cghjournal.org/article/PIIS1542356509012348/abstract?rss=yes</link><description>Background &amp; Aims: Patients with inflammatory bowel disease (IBD) might be at increased risk for certain malignancies. We evaluated the risk of non-melanoma skin cancer (NMSC) in patients with IBD and determined how immunosuppressive and biologic medications affect this risk.Methods: We performed retrospective cohort and nested case-control studies by using administrative data from PharMetrics Patient Centric Database. In the cohort study, 26,403 patients with Crohn's disease (CD) and 26,974 patients with ulcerative colitis (UC) were each matched to 3 non-IBD controls. NMSC risk was evaluated by incidence rate ratio (IRR). In the nested case-control study, 387 CD patients and 355 UC patients with NMSC were each matched to 4 IBD patients without NMSC by using incidence density sampling. Conditional logistic regression was used to determine the association between specific IBD medication use and NMSC.Results: In the cohort study, the incidence of NMSC was higher among patients with IBD compared with controls (IRR, 1.64; 95% confidence interval [CI], 1.51–1.78). In the nested-case control study, recent thiopurine use (≤90 days) was associated with NMSC (adjusted odds ratio [OR], 3.56; 95% CI, 2.81–4.50), as was recent biologic use among patients with CD (adjusted OR, 2.07; 95% CI, 1.28–3.33). Persistent thiopurine use (&gt;365 days) was associated with NMSC (adjusted OR, 4.27; 95% CI, 3.08–5.92), as was persistent biologic use among patients with CD (adjusted OR, 2.18; 95% CI, 1.07–4.46).Conclusions: Patients with IBD, especially those who receive thiopurines, are at risk for NMSC. Appropriate counseling and monitoring of such patients with IBD are recommended.</description><dc:title>Increased Risk for Non-Melanoma Skin Cancer in Patients With Inflammatory Bowel Disease</dc:title><dc:creator>Millie D. Long, Hans H. Herfarth, Clare A. Pipkin, Carol Q. Porter, Robert S. Sandler, Michael D. Kappelman</dc:creator><dc:identifier>10.1016/j.cgh.2009.11.024</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (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>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Original Articles-Alimentary Tract</prism:section><prism:startingPage>268</prism:startingPage><prism:endingPage>274</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509010817/abstract?rss=yes"><title>Endoscopist Specialty Is Associated With Incident Colorectal Cancer After a Negative Colonoscopy</title><link>http://www.cghjournal.org/article/PIIS1542356509010817/abstract?rss=yes</link><description>Background &amp; Aims: The incidence of colorectal cancer (CRC) is reduced for at least 10 years after a negative colonoscopy, compared with the general population. However, CRCs do occur in individuals after a negative colonoscopy. We investigated whether the colonoscopy volume and specialty of the endoscopists who perform the exam are associated with CRC after a negative complete colonoscopy.Methods: A cohort of Ontario residents, 50–80 years old, who had a negative complete colonoscopy between January 1, 1992, and December 31, 1997, was identified by using linked administrative databases. Cohort members had no history of CRC or inflammatory bowel disease or a recent colonic resection. Each individual was followed through December 31, 2006, and those with a new diagnosis of CRC were identified. Multivariable analysis was used to evaluate the association of patient, endoscopist, and procedure setting characteristics with incident CRC.Results: A cohort of 110,402 individuals with a negative complete colonoscopy was identified; the majority (86%) had their procedures performed in hospitals. During the 15-year follow-up period, 1596 (14.5%) developed CRC. There was no association between endoscopist colonoscopy volume and incident CRC. Among persons who had their colonoscopies at a hospital, those who had their procedures performed by a non-gastroenterologist were at significantly increased risk for developing subsequent CRC.Conclusions: Endoscopist specialty is an important determinant of the effectiveness of colonoscopy in usual clinical practice. After a negative colonoscopy, those who have had their procedures performed by a gastroenterologist are less likely to develop CRC.</description><dc:title>Endoscopist Specialty Is Associated With Incident Colorectal Cancer After a Negative Colonoscopy</dc:title><dc:creator>Linda Rabeneck, Lawrence F. Paszat, Refik Saskin</dc:creator><dc:identifier>10.1016/j.cgh.2009.10.022</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (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>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Original Articles-Alimentary Tract</prism:section><prism:startingPage>275</prism:startingPage><prism:endingPage>279</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509012191/abstract?rss=yes"><title>A Sustained Viral Response Is Associated With Reduced Liver-Related Morbidity and Mortality in Patients With Hepatitis C Virus</title><link>http://www.cghjournal.org/article/PIIS1542356509012191/abstract?rss=yes</link><description>Background &amp; Aims: The incidences of decompensated cirrhosis (defined by ascites, hepatic encephalopathy, or bleeding esophageal varices), hepatocellular carcinoma (HCC), and liver-related mortality among patients infected with hepatitis C virus (HCV) who achieve a sustained viral response (SVR), compared with patients who fail treatment (treatment failure), are unclear. We performed a meta-analysis to quantify the incidences of these outcomes.Methods: This meta-analysis included observational cohort studies that followed HCV treatment failure patients; data were collected regarding the incidence of decompensated cirrhosis, HCC, or liver-related mortality and stratified by SVR status. Two investigators independently extracted data on patient populations, study methods, and results by using standardized forms. The agreement between investigators in data extraction was greater than 95%. Data analysis was performed separately for studies that enrolled only HCV patients with advanced fibrosis.Results: We identified 26 appropriate studies for meta-analysis. Among treatment failure patients with advanced fibrosis, rates of liver-related mortality (2.73%/year; 95% confidence interval [CI], 1.38–4.080), HCC (3.22%/year, 95% CI, 2.02–4.42), and hepatic decompensation (2.92%/year; 95% CI, 1.61–4.22) were substantial. Patients with SVR are significantly less likely than patients who experienced treatment failure to develop liver-related mortality (relative risk [RR], 0.23; 95% CI, 0.10–0.52), HCC (RR, 0.21; 95% CI, 0.16–0.27), or hepatic decompensation (RR, 0.16; 95% CI, 0.04–0.59).Conclusions: HCV patients with advanced fibrosis who do not undergo an SVR have substantial liver-related morbidity and mortality. Achieving SVR is associated with substantially lower liver-related morbidity and mortality.</description><dc:title>A Sustained Viral Response Is Associated With Reduced Liver-Related Morbidity and Mortality in Patients With Hepatitis C Virus</dc:title><dc:creator>Amit G. Singal, Michael L. Volk, Donald Jensen, Adrian M. Di Bisceglie, Philip S. Schoenfeld</dc:creator><dc:identifier>10.1016/j.cgh.2009.11.018</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (2010)</dc:source><dc:date>2009-11-30</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-11-30</prism:publicationDate><prism:volume>8</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Original Articles-Liver, Pancreas, and Biliary Tract</prism:section><prism:startingPage>280</prism:startingPage><prism:endingPage>288.e1</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509011379/abstract?rss=yes"><title>Histologic Predictors of Fibrosis Progression in Liver Allografts in Patients With Hepatitis C Virus Infection</title><link>http://www.cghjournal.org/article/PIIS1542356509011379/abstract?rss=yes</link><description>Background &amp; Aims: Recurrent hepatitis C with ensuing fibrosis is the leading cause of liver allograft loss. We investigated whether histologic features in early posttransplant liver biopsies could predict the rate of fibrosis progression in this population.Methods: From 1999 to 2007 there were 476 liver transplants performed for hepatitis C at our center. We reviewed all available posttransplant biopsies for these patients; patients were categorized as rapid, intermediate, or slow fibrosers based on their METAVIR fibrosis score at 24 months. Stage F0 biopsies for rapid and slow fibrosers were analyzed histologically and immunohistochemically.Results: We identified 52 rapid fibrosers and 61 slow fibrosers in our cohort. There was a significant increase in the fibrosis progression rate in the group transplanted between 2003 and 2007 compared with between 1999 and 2002. The course of fibrosis progression was determined early in the posttransplant period and the rate was constant. Rapid fibrosers had more hepatocyte apoptosis than slow fibrosers (P = .001), but no difference in hepatitis activity on stage F0 biopsies. Rapid fibrosers also experienced more episodes of acute rejection after transplantation (P &lt; .001). Cytokeratin 19 (CK19) and vimentin expression on F0 stage biopsies could distinguish rapid from slow fibrosers (CK19: area under the curve, 0.71; P = .0034; vimentin: P = .0219).Conclusions: CK19, vimentin, and hepatocellular apoptosis are promising early markers of rapid fibrosis progression in patients transplanted for hepatitis C. The rate of fibrosis progression is established early in the posttransplant period; this initial rate dictates long-term outcome.</description><dc:title>Histologic Predictors of Fibrosis Progression in Liver Allografts in Patients With Hepatitis C Virus Infection</dc:title><dc:creator>Zina Meriden, Kimberly A. Forde, Theresa L. Pasha, Jia–Ji Hui, K. Rajender Reddy, Emma E. Furth, Rebecca G. Wells</dc:creator><dc:identifier>10.1016/j.cgh.2009.10.034</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (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>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Original Articles-Liver, Pancreas, and Biliary Tract</prism:section><prism:startingPage>289</prism:startingPage><prism:endingPage>296.e8</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS154235650901218X/abstract?rss=yes"><title>Associations Among Behavior-Related Susceptibility Factors in Porphyria Cutanea Tarda</title><link>http://www.cghjournal.org/article/PIIS154235650901218X/abstract?rss=yes</link><description>Background &amp; Aims: Porphyria cutanea tarda (PCT) is the most common of the human porphyrias and results from an acquired deficiency of hepatic uroporphyrinogen decarboxylase (UROD). Some susceptibility factors have been identified; we examined associations among multiple factors in a large cohort of patients.Methods: Multiple known or suspected susceptibility factors and demographic and clinical features of 143 patients (mean age 52 years, 66% male, 88% Caucasian) with documented PCT (mean onset at 41 ± 8.8 years) were tabulated; associations were examined by contingency tables, classification and regression tree (CART) analysis, and logistic regression.Results: The most common susceptibility factors for PCT were ethanol use (87%), smoking (81%), chronic hepatitis C virus (HCV) infection (69%), and HFE mutations (53%; 6% C282Y/C282Y and 8% C282Y/H63D). Of those who underwent hepatic biopsy or ultrasound, 56% had evidence of hepatic steatosis. Of those with PCT, 66% of females took estrogen, 8% were diabetic, 13% had human immunodeficiency virus (HIV) infection, and 17% had inherited uroporphyrinogen decarboxylase (UROD) deficiency (determined by low erythrocyte UROD activity). Three or more susceptibility factors were identified in 70% of patients. HCV infection in patients with PCT was significantly associated with other behavior-related factors such as ethanol use (odds ratio [OR], 6.3) and smoking (OR, 11.9).Conclusions: Susceptibility factors for PCT were similar to previous studies; most patients had 3 or more susceptibility factors. Associations between PCT and HCV, ethanol or smoking could be accounted for by a history of multiple substance abuse; other factors are distributed more randomly among patients.</description><dc:title>Associations Among Behavior-Related Susceptibility Factors in Porphyria Cutanea Tarda</dc:title><dc:creator>Sajid Jalil, James J. Grady, Chul Lee, Karl E. Anderson</dc:creator><dc:identifier>10.1016/j.cgh.2009.11.017</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (2010)</dc:source><dc:date>2009-11-30</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-11-30</prism:publicationDate><prism:volume>8</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Original Articles-Liver, Pancreas, and Biliary Tract</prism:section><prism:startingPage>297</prism:startingPage><prism:endingPage>302.e1</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509010805/abstract?rss=yes"><title>Acute Pancreatitis: Computed Tomography Utilization and Radiation Exposure Are Related to Severity but Not Patient Age</title><link>http://www.cghjournal.org/article/PIIS1542356509010805/abstract?rss=yes</link><description>Background &amp; Aims: A goal of radiologists is to use computed tomography (CT) imaging less frequently in younger patients because of radiation exposure. We evaluated abdominal CT use among patients hospitalized for acute pancreatitis at a tertiary care hospital and compared estimated radiation doses with disease severity and patient age.Methods: We performed a retrospective analysis of numbers and types of CTs performed on patients with acute pancreatitis (1036 admissions, 869 patients; mean age, 50.8 y); 566 had 1081 abdominopelvic CTs performed from October 1, 2001, to September 30, 2006. Effective dose estimates for abdominopelvic CTs were used to estimate exposure. Disease severities were stratified using Balthazar CT grades and severity indexes.Results: The mean number of abdominopelvic CTs per patient, per hospitalization, was 1.9 (range, 1–12); the mean number was 3.0 over the 5-year period (range, 1–19). During hospitalization, each patient was exposed to a mean estimated radiation dose of 31.03 ± 26.4 mSv (range, 14.7–176.9 mSv). Patients with pancreatitis grades D or E (n = 233) compared with grades A through C (n = 333) had longer periods of hospitalization (mean, 23.3 vs 10.8 d; P &lt; .001), more days as an inpatient (mean, 2.54 vs 1.45 d; P &lt; .001), more total CT scans (mean, 4.02 vs 2.37; P &lt; .001), and higher total effective radiation doses (mean, 53.5 vs 35 mSv; P &lt; .0001). Linear regression revealed a relationship between dose and disease grade, but not patient age.Conclusions: Regardless of age, patients with severe acute pancreatitis undergo more abdominopelvic CTs as inpatients and outpatients and are exposed to higher doses of radiation compared with patients with less severe disease. Awareness of CT ordering patterns for patients with acute pancreatitis may aid in the development of alternate imaging strategies to reduce radiation exposure in this population, especially for younger patients.</description><dc:title>Acute Pancreatitis: Computed Tomography Utilization and Radiation Exposure Are Related to Severity but Not Patient Age</dc:title><dc:creator>Desiree E. Morgan, Caroline M. Ragheb, Mark E. Lockhart, Barrett Cary, Naomi S. Fineberg, Lincoln L. Berland</dc:creator><dc:identifier>10.1016/j.cgh.2009.10.021</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (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>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Original Articles-Liver, Pancreas, and Biliary Tract</prism:section><prism:startingPage>303</prism:startingPage><prism:endingPage>308</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509012336/abstract?rss=yes"><title>Stool Polymerase Chain Reaction for Helicobacter pylori Detection and Clarithromycin Susceptibility Testing in Children</title><link>http://www.cghjournal.org/article/PIIS1542356509012336/abstract?rss=yes</link><description>Background &amp; Aims: This study was undertaken in a pediatric gastroenterology clinic to retrospectively evaluate a real-time polymerase chain reaction (PCR) for the detection and clarithromycin susceptibility testing of Helicobacter pylori using stool specimens.Methods: All consecutive children who underwent a gastroscopy between March 2006 and February 2009 and also having been examined by stool PCR were enrolled. Rapid urease test, histology, and culture were the reference methods for the detection of H pylori and E-test for susceptibility testing, respectively.Results: A total of 143 children (mean age, 10.8 y; range, 2.8–17.9; males:females, 1:1.5) were evaluable. Sensitivity, specificity, and test accuracy for the detection of H pylori were 83.8%, 98.4%, and 90.2%, respectively. Sensitivity, specificity, and accuracy for the detection of clarithromycin resistance were 89.2%, 100%, and 94.0%, respectively.Conclusions: Stool PCR was a reliable and useful noninvasive tool for detection and clarithromycin susceptibility testing of H pylori in a pediatric population with a high prevalence of clarithromycin-resistant strains.</description><dc:title>Stool Polymerase Chain Reaction for Helicobacter pylori Detection and Clarithromycin Susceptibility Testing in Children</dc:title><dc:creator>Andreas Vécsei, Albina Innerhofer, Christa Binder, Heidi Gizci, Karin Hammer, Andrea Bruckdorfer, Stefan Riedl, Helmut Gadner, Alexander M. Hirschl, Athanasios Makristathis</dc:creator><dc:identifier>10.1016/j.cgh.2009.12.002</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (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>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Brief Communication</prism:section><prism:startingPage>309</prism:startingPage><prism:endingPage>312</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509009860/abstract?rss=yes"><title>Efficacy of Esophageal Impedance/Ph Monitoring in Patients With Refractory Gastroesophageal Reflux Disease, on and off Therapy</title><link>http://www.cghjournal.org/article/PIIS1542356509009860/abstract?rss=yes</link><description>In July 2009 Pritchett et al compared impedance/pH (MII-pH) on-therapy with 48-hour wireless pH-monitoring off-therapy in those refractory to proton pump inhibitors (PPIs). They conclude MII-pH on-therapy might provide the single best strategy for evaluation of persistent reflux.</description><dc:title>Efficacy of Esophageal Impedance/Ph Monitoring in Patients With Refractory Gastroesophageal Reflux Disease, on and off Therapy</dc:title><dc:creator>Rami Sweis, Angela Anggiansah, Terry Wong</dc:creator><dc:identifier>10.1016/j.cgh.2009.09.023</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (2010)</dc:source><dc:date>2009-09-28</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-09-28</prism:publicationDate><prism:volume>8</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>313</prism:startingPage><prism:endingPage>313</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509010866/abstract?rss=yes"><title>“Power” of Selective Serotonin Reuptake Inhibitors in Irritable Bowel Syndrome</title><link>http://www.cghjournal.org/article/PIIS1542356509010866/abstract?rss=yes</link><description>We read the recent article by Ladabaum et al. A meta-analysis of randomized controlled trials (RCTs) suggested that antidepressants are effective in irritable bowel syndrome (IBS). Selective serotonin reuptake inhibitors (SSRIs) were superior to placebo, with a number needed to treat (NNT) of 3.5.</description><dc:title>“Power” of Selective Serotonin Reuptake Inhibitors in Irritable Bowel Syndrome</dc:title><dc:creator>Alexander C. Ford, Paul Moayyedi</dc:creator><dc:identifier>10.1016/j.cgh.2009.10.027</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (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>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>313</prism:startingPage><prism:endingPage>314</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356510000431/abstract?rss=yes"><title>Reply</title><link>http://www.cghjournal.org/article/PIIS1542356510000431/abstract?rss=yes</link><description>We thank Drs Ford and Moayyedi for their comment on our paper. This provides us with an opportunity to emphasize a principle that is important both for our paper and more generally: power is not relevant for interpreting completed studies. This has been discussed in several articles, and the explanation document for the Consolidated Standards of Reporting Trials (CONSORT) guidelines states, “There is little merit in calculating the statistical power once the results of the trial are known.”</description><dc:title>Reply</dc:title><dc:creator>Peter Bacchetti, Uri Ladabaum</dc:creator><dc:identifier>10.1016/j.cgh.2010.01.003</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (2010)</dc:source><dc:date>2010-01-21</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2010-01-21</prism:publicationDate><prism:volume>8</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>314</prism:startingPage><prism:endingPage>314</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356510000029/abstract?rss=yes"><title>Cover</title><link>http://www.cghjournal.org/article/PIIS1542356510000029/abstract?rss=yes</link><description></description><dc:title>Cover</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1542-3565(10)00002-9</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>8</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>OFC</prism:startingPage><prism:endingPage>OFC</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509003127/abstract?rss=yes"><title>Hemangioma of the Small Intestine Presenting With Recurrent Overt, Obscure Gastrointestinal Bleeding</title><link>http://www.cghjournal.org/article/PIIS1542356509003127/abstract?rss=yes</link><description>A 30-year-old man was referred to our institution for work up of iron deficiency anemia, with hemoglobin of 8.4 gm/dL and blood in the stools; he had an upper endoscopy and colonoscopy that failed to show the cause of bleeding and anemia. The patient underwent capsule endoscopy that showed multiple polypoid lesions () in the proximal jejunum. The differential diagnosis included Kaposi's sarcoma, blue rubber nevus syndrome, hemangioma/hemangiosarcoma, and melanoma. On the basis of the appearance alone, it was difficult to differentiate between a benign or malignant process.</description><dc:title>Hemangioma of the Small Intestine Presenting With Recurrent Overt, Obscure Gastrointestinal Bleeding</dc:title><dc:creator>Georg Elias, Nabil Toubia</dc:creator><dc:identifier>10.1016/j.cgh.2009.03.036</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (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>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Images of the Month</prism:section><prism:startingPage>A18</prism:startingPage><prism:endingPage>A18.e1</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS154235650900319X/abstract?rss=yes"><title>Usefulness of Positron Emission and Computed Tomography Scan in Early Evaluation of Treatment Response in Gastrointestinal Stromal Tumor</title><link>http://www.cghjournal.org/article/PIIS154235650900319X/abstract?rss=yes</link><description>   See related article, Chiu Y–H et al, on page e27 in this issue of CGH.</description><dc:title>Usefulness of Positron Emission and Computed Tomography Scan in Early Evaluation of Treatment Response in Gastrointestinal Stromal Tumor</dc:title><dc:creator>Yuichi Nozaki, Mikio Yanase, Naohiko Masaki</dc:creator><dc:identifier>10.1016/j.cgh.2009.03.029</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (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>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</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/PIIS1542356509003218/abstract?rss=yes"><title>Massive Rectal Prolapse with Small Bowel Involvement</title><link>http://www.cghjournal.org/article/PIIS1542356509003218/abstract?rss=yes</link><description>A 43-year-old man with a history of alcohol abuse presented to our hospital with complaints of rectal prolapse. The prolapse had been gradually worsening over a 3-year period and was associated with fecal incontinence and wetting of undergarments. The patient had no complaints of constipation and suffered only mild discomfort during prolapse. He denied history of receptive anal intercourse, childhood abuse, or other anal trauma. His prolapse was typically elicited by straining, and could be manually reduced with some difficulty. Rectal exam revealed trace prolapse at rest and decreased anal sphincter tone. Straining produced an external mass measuring approximately 12 × 15 cm ( A). Colonoscopy was performed and revealed a 2 × 4 cm patch of mild erythema along the anterior rectal wall approximately 6 cm from the anal verge, without ulceration or identifiable lead point.</description><dc:title>Massive Rectal Prolapse with Small Bowel Involvement</dc:title><dc:creator>William A. Hackworth, Alvin M. Zfass</dc:creator><dc:identifier>10.1016/j.cgh.2009.03.027</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (2010)</dc:source><dc:date>2009-04-10</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-04-10</prism:publicationDate><prism:volume>8</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</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/PIIS1542356509003747/abstract?rss=yes"><title>Simultaneous Occurrence of Obscure-Overt Gastrointestinal and Intraperitoneal Bleeding in Gastrointestinal Stromal Tumor</title><link>http://www.cghjournal.org/article/PIIS1542356509003747/abstract?rss=yes</link><description>A 67-year-old woman had a history of melena for 7 days and a sudden onset of lower abdominal pain 2 days earlier. The bowel sounds were normal, and the abdomen was soft and dull upon percussion. However, tenderness and rebound tenderness in the lower abdomen were revealed. No abnormal findings were found throughout laboratory tests except decreased hemoglobin (7.5 g/dL). Postcontrast computerized tomography scan of the abdominopelvis showed a heterogeneously enhanced, exophytic, round mass originating from the small intestine. The surrounding fluid in the peritoneal cavity which had a relatively high attenuation with a Hounsfield unit value of 60 represented partly clotted blood ( A, arrow). On the duodenoscopy and colonoscopy, no focus of gastrointestinal bleeding was found but a shifting blue hue sign was noted during colonoscopy. Laparoscopy revealed a large volume of bloody peritoneal fluid and a 3.5-cm exophytic, spherical, subepithelial tumor was found at the jejunum, accompanied with active intraperitoneal and gastrointestinal bleeding. The tumor was an extraluminally protruding, spherical, solid mass with several areas of central hemorrhagic necrosis extending up to the serosal surface ( B, arrowhead) and an active ulcer at the epithelial aspect ( B, arrow). The tumor was composed of spindle cells (mitosis 4/50 HFP) of fascicular pattern, involving proper muscle, and was positive for c-kit, consistent with the diagnosis of gastrointestinal stromal tumor (GIST) ( C).</description><dc:title>Simultaneous Occurrence of Obscure-Overt Gastrointestinal and Intraperitoneal Bleeding in Gastrointestinal Stromal Tumor</dc:title><dc:creator>Dong Yang Park, Won Moon</dc:creator><dc:identifier>10.1016/j.cgh.2009.04.014</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (2010)</dc:source><dc:date>2009-04-27</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-04-27</prism:publicationDate><prism:volume>8</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Images of the Month</prism:section><prism:startingPage>A28</prism:startingPage><prism:endingPage>A28</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356509004881/abstract?rss=yes"><title>Stercoral Ulcer Due to Chicken Bones in Rectum: Overtube Used as a Conduit for Endoscopic Removal</title><link>http://www.cghjournal.org/article/PIIS1542356509004881/abstract?rss=yes</link><description>A 68-year-old female complained of anal pain and bleeding for 1 day. Noticeably, she had a history of eating seasoned chicken feet as a side dish for several days, and recently experienced constipation. Digital rectal examination aggravated pain, with small, hard, contents palpable in lumen. Plain abdomen radiograph revealed massive fecal impaction. On computed tomography scan, diffusely scattered hyperdense materials were observed from the anal verge to the terminal ileum without evidence of absolute bowel obstruction ( A). To investigate the cause of anal pain and bleeding, sigmoidoscopy was performed. After glycerin enema, painful defecation released some feces admixed with bone-like materials. The endoscope was carefully inserted into the anus, showing small numerous feces-tainted materials reminiscent of phalangeal bones ( B). Foreign bodies nearly occluded the rectum, hindering further access into the proximal gut. In an effort to remove foreign bodies endoscopically and relieve pain, an overtube insertion was attempted. Numerous small bones were retracted through the overtube with a “rat tooth” forceps. After several hours, work of foreign body removal, a linear radiating ulcer of the rectum appeared ( C). The rectum was somewhat cleared and pain was greatly relieved, and the patient gradually improved by conservative therapy including sucralfate enema.</description><dc:title>Stercoral Ulcer Due to Chicken Bones in Rectum: Overtube Used as a Conduit for Endoscopic Removal</dc:title><dc:creator>Sanghoon Park, Bora Keum, Yoon Tae Jeen</dc:creator><dc:identifier>10.1016/j.cgh.2009.05.022</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (2010)</dc:source><dc:date>2009-06-04</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2009-06-04</prism:publicationDate><prism:volume>8</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Images of the Month</prism:section><prism:startingPage>A32</prism:startingPage><prism:endingPage>A32</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356510000042/abstract?rss=yes"><title>Editorial Board</title><link>http://www.cghjournal.org/article/PIIS1542356510000042/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1542-3565(10)00004-2</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>8</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A4</prism:startingPage><prism:endingPage>A4</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356510000054/abstract?rss=yes"><title>Contents</title><link>http://www.cghjournal.org/article/PIIS1542356510000054/abstract?rss=yes</link><description></description><dc:title>Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1542-3565(10)00005-4</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>8</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A9</prism:startingPage><prism:endingPage>A12</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356510000066/abstract?rss=yes"><title>Information for Authors and Readers</title><link>http://www.cghjournal.org/article/PIIS1542356510000066/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—all 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(10)00006-6</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>8</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A15</prism:startingPage><prism:endingPage>A16</prism:endingPage></item><item rdf:about="http://www.cghjournal.org/article/PIIS1542356510000078/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/PIIS1542356510000078/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(10)00007-8</dc:identifier><dc:source>Clinical Gastroenterology and Hepatology 8, 3 (2010)</dc:source><dc:date>2010-03-01</dc:date><prism:publicationName>Clinical Gastroenterology and Hepatology</prism:publicationName><prism:publicationDate>2010-03-01</prism:publicationDate><prism:volume>8</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1542-3565(10)X0002-7</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A17</prism:startingPage><prism:endingPage>A17</prism:endingPage></item></rdf:RDF>