Gastroenterology RSS feed: Current Issue. Gastroenterology is the most prominent journal in the field of gastrointestinal disease. As the official journal of the AGA Institute, Gastroenterology delivers up-to-date and authoritative coverage of both basic and clinical gastroenterology. Regular features include articles by leading authorities and reports on the latest treatments for diseases. Original research is organized by clinical and basic-translational content, as well as by alimentary tract, liver, pancreas, and biliary content. Gastroenterology also bridges the gap between basic and clinical science by publishing comprehensive reviews and perspectives on important topics such as pancreatitis and liver disease. Additional features include Covering the Cover; Mentoring, Training, and Education Corner; Press Highlights; Imaging and Advanced Technology; Clinical Challenges and Images in GI; Selected Summaries; Print and Digital Media Reviews; Continuing Medical Education Activities; Editorials; and Correspondence. Multimedia offerings include images, video abstracts, and podcasts. Gastroenterology also provides updates and commentary via Facebook, Twitter, LinkedIn, and its research blog "The AGA Journals Blog". Gastroenterology is recommended for initial purchase in the Brandon-Hill study, Selected List of Books and Journals for the Small Medical Library. Gastroenterology is ranked 1st of 71 journals in the Gastroenterology and Hepatology category on the 2011 Journal Citation Reports®, published by Thomson Reuters, and has an Impact Factor of 12.032. Its immediacy index, which is a measure of how topical and urgent work published Gastroenterology is, is 2.868, the highest in the field. On average, authors receive decisions on their manuscripts within 25 days. Gastroenterology is circulated to 19,000 individuals and institutions worldwide. http://www.gastrojournal.org/?rss=yesElsevier Inc.en © 2012 Published by Elsevier Inc. All rights reserved. Gastroenterology0016-50851426May 2012 © 2012 Published by Elsevier Inc. All rights reserved. healthpermissions@elsevier.comhttp://www.gastrojournal.org/article/PIIS0016508512004635/abstract?rss=yesCover 110.1053/S0016-5085(12)00463-5Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5OFCOFChttp://www.gastrojournal.org/article/PIIS0016508512003435/abstract?rss=yes Every May, Gastroenterology publishes a supplementary issue, the “13th Issue”, that is devoted to a specific topic or theme. When the 2012 theme was discussed by the new Board of Editors (each member of which desperately tried to avoid having his or her favorite topic be chosen, as this would undoubtedly mean a considerable amount of additional work), the topic of viral hepatitis emerged unanimously. It must be acknowledged that no other field in Hepatology and Gastroenterology has grown more rapidly than viral hepatitis during the past 15 years, thanks to the considerable interest of the scientific community for diseases that involve over 500 million patients worldwide, active support for research from governments in the United States, Europe, Japan, and Australia, among other regions, and major drug industry investment for what promises to be an incredibly rewarding market for antiviral drugs. Viral hepatitis care and research are now at a crossroad. After many years of investigation aimed at understanding the life cycle of hepatitis viruses, the immunology of acute and chronic infection and the pathophysiology of related liver and extra-hepatic disorders, the field is poised with powerful therapeutic and preventive strategies that will efficiently control these infections. With entecavir and tenofovir now approved in most areas of the world, hepatitis B virus (HBV) replication can be controlled in the long-term in the vast majority of chronically infected patients. In addition, the universal HBV vaccination of newborns in high endemic areas has proven to reduce not only HBV infection but also HBV-related hepatocellular carcinoma (HCC). After some false starts, the search for antiviral drugs targeting hepatitis C virus (HCV) is now moving at an incredible pace with more than 100 compounds currently at the preclinical, or early-to-late clinical developmental stages. After 10 years of stagnation with pegylated interferon alfa and ribavirin therapy, 2 specific inhibitors of the HCV NS3/4A protease, telaprevir and boceprevir, were approved in 2011 in the United States and Europe for the treatment of patients infected with HCV genotype 1. Many other compounds are likely to be approved within the next 5 years. Most importantly, the hope that very high rates of viral eradication will be achieved soon with all-oral, interferon-free regimens is no longer a fantasy. Reasonably, one can now foresee that most chronic HCV infections will be cured, at least in countries that will be able to afford the high price of the new drug combinations.Viral Hepatitis at a CrossroadAnna S.F. Lok, Jean-Michel Pawlotsky10.1053/j.gastro.2012.03.007Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5Introduction12611263http://www.gastrojournal.org/article/PIIS001650851200220X/abstract?rss=yes Most cases of hepatocellular carcinoma (HCC) are associated with cirrhosis related to chronic hepatitis B virus (HBV) or hepatitis C virus (HCV) infection. Changes in the time trends of HCC and most variations in its age-, sex-, and race-specific rates among different regions are likely to be related to differences in hepatitis viruses that are most prevalent in a population, the timing of their spread, and the ages of the individuals the viruses infect. Environmental, host genetic, and viral factors can affect the risk of HCC in individuals with HBV or HCV infection. This review summarizes the risk factors for HCC among HBV- or HCV-infected individuals, based on findings from epidemiologic studies and meta-analyses, as well as determinants of patient outcome and the HCC disease burden, globally and in the United States. Epidemiology of Viral Hepatitis and Hepatocellular CarcinomaHashem B. El-Serag10.1053/j.gastro.2011.12.061Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5Review12641273.e1http://www.gastrojournal.org/article/PIIS0016508512002193/abstract?rss=yes No one would argue with the notion that chronic infection with hepatitis C virus (HCV) causes hepatocellular carcinoma (HCC). Early observations of the association between post-transfusion non-A, non-B hepatitis and HCC in Japan from the 1980s have, unfortunately, proved to be all too true, and in many industrialized countries (including the United States and Japan), HCV infection is now the leading risk factor for HCC. The age-adjusted incidence rate of HCC has tripled in the United States over the past 30 years, reflecting the spread of HCV among Americans decades earlier. Most cases occur in patients with well-established cirrhosis, by itself a very strong risk factor for liver cancer. However, this is not always the case. Eight percent of patients developing HCC in the prospective Hepatitis C Antiviral Long-term Treatment against Cirrhosis (HALT-C) study lacked any evidence of cirrhosis, although all had an Ishak fibrosis score of at least 3 when enrolled in the study. Adjusting for other risk factors, such as alcohol intake, active HCV infection increases the risk of HCC about 18-fold. Thus, the question is not whether HCV infection causes liver cancer, but rather how it does this. Is HCV directly carcinogenic? Or does infection simply set in motion a brisk inflammatory and profibrotic response that causes cancer?Is Hepatitis C Virus Carcinogenic?Stanley M. Lemon, David R. McGivern10.1053/j.gastro.2012.01.045Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5Commentary12741278http://www.gastrojournal.org/article/PIIS0016508512002296/abstract?rss=yes Hepatitis C virus (HCV) causes liver-related death in more than 300,000 people annually. Treatments for patients with chronic HCV are suboptimal, despite the introduction of directly acting antiviral agents. There is no vaccine that prevents HCV infection. Relevant animal models are important for HCV research and development of drugs and vaccines. Chimpanzees are the best model for studies of HCV infection and related innate and adaptive host immune responses. They can be used in immunogenicity and efficacy studies of HCV vaccines. The only small animal models of robust HCV infection are T- and B- cell deficient mice with human chimeric livers. Although these mice cannot be used in studies of adaptive immunity, they have provided new insights into HCV neutralization, interactions between virus and receptors, innate host responses, and therapeutic approaches. Recent progress in developing genetically humanized mice is exciting, but these models only permit studies of specific steps in the HCV life cycle and have limited or no viral replication. Animal Models for the Study of Hepatitis C Virus Infection and Related Liver DiseaseJens Bukh10.1053/j.gastro.2012.02.016Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5Review12791287.e3http://www.gastrojournal.org/article/PIIS0016508512002223/abstract?rss=yes Hepatitis C virus (HCV) causes chronic hepatitis, which can progress to cirrhosis and hepatocellular carcinoma. The World Health Organization estimates that approximately 2.35% of the world population (∼160 million individuals) is infected with HCV. Another widespread disorder, metabolic syndrome, comprises a group of correlated clinical features that have insulin resistance as a common pathogenic determinant; it can lead to type 2 diabetes mellitus, nonalcoholic fatty liver disease, cardiovascular disorders, and many types of cancer, including hepatocellular carcinoma. Metabolic syndrome is pandemic; its estimated prevalence in the United States is ∼25%. It is important to determine the relationship between HCV infection and metabolic syndrome.HCV Infection and Metabolic Syndrome: Which Is the Chicken and Which Is the Egg?Francesco Negro10.1053/j.gastro.2011.12.063Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5Commentary12881292http://www.gastrojournal.org/article/PIIS0016508512002302/abstract?rss=yes The prognosis and management of patients with chronic viral hepatitis B and C depend on the amount and progression of liver fibrosis and the risk for cirrhosis. Liver biopsy, traditionally considered to be the reference standard for staging of fibrosis, has been challenged over the past decade by the development of noninvasive methodologies. These methods rely on distinct but complementary approaches: a biologic approach, which quantifies serum levels of biomarkers of fibrosis, and a physical approach, which measures liver stiffness by ultrasound or magnetic resonance elastography. Noninvasive methods were initially studied and validated in patients with chronic hepatitis C but are now used increasingly for patients with hepatitis B, reducing the need for liver biopsy analysis. We review the advantages and limitations of the noninvasive methods used to manage patients with chronic viral hepatitis B or C infection. Noninvasive Methods to Assess Liver Disease in Patients With Hepatitis B or CLaurent Castera10.1053/j.gastro.2012.02.017Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5Review12931302.e4http://www.gastrojournal.org/article/PIIS0016508512002405/abstract?rss=yes Molecular biology techniques are routinely used to diagnose and monitor treatment of patients with chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. These tools can detect and quantify viral genomes and analyze their sequence to determine their genotype or subtype and to identify nucleotide or amino acid substitutions associated with resistance to antiviral drugs. They include real-time target amplification methods, which have been standardized and are widely used in clinical practice to diagnose and monitor HBV and HCV infections, and next-generation sequencing techniques, which are still restricted to research laboratories. In addition, new enzyme immunoassays can quantify hepatitis B surface and hepatitis C core antigens, and point-of-care tests and alternatives to biologic tests that require whole-blood samples obtained by venipuncture have been developed. We review these new virologic methods and their clinical and research applications to HBV and HCV infections. New Virologic Tools for Management of Chronic Hepatitis B and CStéphane Chevaliez, Christophe Rodriguez, Jean–Michel Pawlotsky10.1053/j.gastro.2012.02.027Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5Review13031313.e1http://www.gastrojournal.org/article/PIIS0016508512002259/abstract?rss=yes Recently developed drugs and innovative strategies for the treatment of chronic infection with genotype 1 hepatitis C virus (HCV) have become the standard of care. The protease inhibitors telaprevir (Incivek) and boceprevir (Victrelis) are the first direct-acting antiviral (DAA) agents approved, and many more are being developed. These drugs substantially increased rates of sustained virologic response in treatment-naïve and -experienced patients, in conjunction with peginterferon and ribavirin (triple therapy), in phase 3 trials. The efficacy of triple therapy depends on appropriate selection of patients, although the population of patients that receive triple therapy could be expanded as the risk/benefit ratio improves. Attention to details that reflect the standard of care, such as appropriate dosing, anticipation of adverse effects, and strict adherence to stopping rules, will insure the success of these drugs and lead the way for new combination therapies. Maximizing Opportunities and Avoiding Mistakes in Triple Therapy for Hepatitis C VirusA. Sidney Barritt, Michael W. Fried10.1053/j.gastro.2012.02.013Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5Review13141323.e1http://www.gastrojournal.org/article/PIIS0016508512002247/abstract?rss=yes With the development of effective therapies against human immunodeficiency virus (HIV), hepatitis C virus (HCV) infection has become a major cause of morbidity and mortality among patients with both infections (coinfection). In addition to the high prevalence of chronic HCV, particularly among HIV-infected injection drug users, the rate of incident HIV infections is increasing among HIV-infected men who have sex with men, leading to recommendations for education and screening for HCV in this population. Liver disease is the second leading and, in some cases, a preventable cause of death among coinfected patients. Those at risk for liver disease progression are usually treated with a combination of interferon (IFN) and ribavirin (RBV), which is not highly effective; it has low rates of sustained virologic response (SVR), especially for coinfected patients with HCV genotype 1 and those of African descent. Direct-acting antivirals might overcome factors such as immunodeficiency that can reduce the efficacy of IFN. However, for now it remains challenging to treat coinfected patients due to interactions among drugs, additive drug toxicities, and the continued need for combination therapies that include pegylated IFN. Recently developed HCV protease inhibitors such as telaprevir and boceprevir, given in combination with pegylated IFN and RBV, could increase the rate of SVR with manageable toxicity and drug interactions. We review the latest developments and obstacles to treating coinfected patients. Management of Patients Coinfected With HCV and HIV: A Close Look at the Role for Direct-Acting AntiviralsSusanna Naggie, Mark S. Sulkowski10.1053/j.gastro.2012.02.012Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5Review13241334.e3http://www.gastrojournal.org/article/PIIS0016508512002260/abstract?rss=yes It is now possible to comprehensively screen the human genome for genetic variation that influences the outcomes of human disease and pharmacotherapy. The most popular approach remains the genome-wide association study (GWAS), in which many hundreds of thousands of genetic markers, representing common variation across the genome, are tested for association with disease. Two success stories of the GWAS era are reviewed here: the discoveries of the association between interleukin-28B (IL28B) polymorphism and peginterferon-α (pegIFN) and ribavirin (RBV) treatment response for genotype 1 HCV, as well as spontaneous clearance of acute HCV infection, and the association between inosine triphosphatase (ITPA) variation and RBV-induced hemolytic anemia.Genetic Factors and Hepatitis C Virus InfectionAlexander J. Thompson10.1053/j.gastro.2012.01.046Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5Commentary13351339http://www.gastrojournal.org/article/PIIS0016508512002284/abstract?rss=yes Development of robust cell culture models for hepatitis C viral infection has greatly increased our understanding of this virus and its life cycle. This knowledge has led to the development of many drugs that target specific elements of viral replication, including viral proteins and host factors required for replication. The NS3/4A serine protease inhibitors were the first of these to be used in the clinic, and reagents that target other elements of the viral lifecycle are in advanced stages of clinical development. These include new NS3/4A protease inhibitors, NS5B RNA-dependent RNA polymerase inhibitors, NS5A inhibitors, and host-directed antivirals, such as cyclophilin inhibitors. Alternative interferons with possibly improved tolerability, specifically interferon-λ1 (interleukin-29), are also under development. These new reagents against hepatitis C virus should lead to highly effective, well-tolerated, and likely interferon-sparing therapies in the next several years. Anti−Hepatitis C Virus Drugs in DevelopmentEsperance A.K. Schaefer, Raymond T. Chung10.1053/j.gastro.2012.02.015Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5Review13401350.e1http://www.gastrojournal.org/article/PIIS0016508512002211/abstract?rss=yes Many promising small molecule inhibitors directed against hepatitis C virus (HCV) proteins (direct-acting antiviral [DAA] agents) and compounds targeting host cell factors (host-targeting agents [HTAs]) are currently in the drug development and clinical trial pipeline, whereas contraindications and adverse effects limit the clinical applicability of peginterferon (Peg-IFN)-based therapies. The increasing number of alternative treatment options is driving the investigation of interferon-sparing regimens and paving the way for the question on the future place for interferon in HCV therapy. The recent approval of 2 DAAs by the US Food and Drug Administration and European Medicines Agency has opened a new era in the treatment of chronic HCV infection (CHC). The new standard of care is a triple therapy, combining the previous standard, Peg-IFN-α plus ribavirin (RBV), with a ketoamide protease inhibitor. The new standard of care is licensed for patients infected with genotype 1 HCV, the most prevalent genotype in Europe and North America. Ketoamide compounds, boceprevir (Victrelis, Merck & Co, Whitehouse Station, NJ) and telaprevir (Incivek, Vertex Pharmaceuticals, Cambridge, MA), are designed to mimic the natural NS3/4A protease substrate in genotype 1 HCV. Their addition to Peg-IFN/RBV significantly improves the sustained virologic response (SVR) rate.Will Interferon-Free Regimens Prevail?Christoph Welsch, Stefan Zeuzem10.1053/j.gastro.2011.12.062Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5Commentary13511355http://www.gastrojournal.org/article/PIIS0016508512002417/abstract?rss=yes The Protease Inhibition for Viral Evaluation (PROVE) 2 and PROVE 3 trials tested the efficacy of various regimens of telaprevir-combination therapy in treatment-naïve and treatment-experienced patients. Both studies included a ribavirin-free arm in which patients received telaprevir with peginterferon alone. The results were striking. In the PROVE 2 study, patients who received only peginterferon and telaprevir had a sustained virologic response (SVR) rate of only 36%, significantly lower than in those treated with standard peginterferon and ribavirin (SVR, 46%; P = .003). In treatment-experienced patients, replacement of ribavirin with telaprevir led to a very modest increase in SVR from 14% in the control group to only 24% in those treated with peginterferon plus telaprevir alone (P = .02). The serine protease inhibitor therapy 1 (SPRINT 1) trial evaluated boceprevir combination therapy and included an arm with low-dose ribavirin. Similar to the telaprevir studies, ribavirin proved to be very important. Only 36% of patients randomized to receive low-dose ribavirin achieved an SVR, a markedly worse outcome than in those treated with either the standard of care or with boceprevir with peginterferon and full-dose ribavirin. These trials clearly demonstrated that ribavirin will not disappear quite as quickly as some might have anticipated.Is There a Role for Ribavirin in the Era of Hepatitis C Virus Direct-Acting Antivirals?Jordan J. Feld10.1053/j.gastro.2011.12.064Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5Commentary13561359http://www.gastrojournal.org/article/PIIS001650851200217X/abstract?rss=yes It is important to examine the effectiveness of current therapies for chronic hepatitis B in clinical practice, given the therapeutic advances over the past 15 years. A 2010 Institute of Medicine report on hepatitis and liver cancer stated that the public and health care providers have a lack of knowledge and awareness about viral hepatitis, and that there is a gap between medical innovation and community care. We review the efficacy of hepatitis B treatment, based on results from clinical trials, and discuss the effectiveness of these treatments in clinical practice. We also discuss why having efficacious treatments alone would have a small impact on the global health burden of hepatitis B, and highlight the importance of educating the public and the medical community and coordination of care. Effectiveness of Hepatitis B Treatment in Clinical PracticeSteven J. Scaglione, Anna S.F. Lok10.1053/j.gastro.2012.01.044Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5Review13601368.e1http://www.gastrojournal.org/article/PIIS0016508512002181/abstract?rss=yes The onset of the acquired immune deficiency syndrome epidemic in the early 1980s led to successful antiviral drug discovery programs, which brought to the market a large number of antiretroviral drugs with different targets and mechanisms of action. However, it soon became apparent that human immunodeficiency virus (HIV) resistance to these drugs would be a problem in long-term antiretroviral therapy. A combination of drugs with different viral targets and no cross-resistance (highly active antiretroviral therapy [HAART]) was shown to be a valuable option to prevent HIV resistance in the long-term. Nevertheless, multidrug-resistant viruses emerge in some patients on HAART therapy, generally those who have been on treatment for many years and have received a number of different drugs during their life. These viruses escape the antiviral effect of all available drugs and their outgrowth is responsible for treatment failure, disease progression, and death.Is Hepatitis Virus Resistance to Antiviral Drugs a Threat?Jean–Michel Pawlotsky10.1053/j.gastro.2011.12.060Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5Commentary13691372http://www.gastrojournal.org/article/PIIS0016508512002235/abstract?rss=yes Liver transplantation is the only alternative for patients with end-stage liver disease. Viral hepatitis B and C are among the most common causes of cirrhosis and hepatocellular carcinoma and a frequent indication for liver transplantation. Hepatitis B virus immunoglobulin and nucleot(s)ide analogues have facilitated the management of patients with hepatitis B who have received liver transplants and resulted in excellent long-term outcomes. On the contrary, recurrence of hepatitis C is the main cause of graft loss in most transplant programs. Current therapeutic approaches are far from optimal, because sustained virologic responses are only achieved in one-third of treated patients, and adverse effects are common and severe. However, the rapid development of direct-acting antivirals against hepatitis C virus will change the management of this disease and in a few years prevent graft infection with this virus. Viral Hepatitis in Liver TransplantationGonzalo Crespo, Zoe Mariño, Miquel Navasa, Xavier Forns10.1053/j.gastro.2012.02.011Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5Review13731383.e1http://www.gastrojournal.org/article/PIIS0016508512002168/abstract?rss=yes The discovery of the hepatitis C virus (HCV) more than 20 years ago offered the promise of a vaccine to prevent life-long persistent infection and associated progressive liver diseases. To date, only a few candidate vaccines have been tested in human beings for safety and immunogenicity. None have yet been assessed for prevention of HCV infection or persistence. In the event that current vaccine candidates do not advance to efficacy trials, or fail to provide protection against HCV, the pipeline of alternatives appears to be very small. With a sharp reduction in new HCV infections because of effective screening of the blood supply, and the possibility that acute and chronic infections will be curable because of improving therapy, it is reasonable to ask if the considerable effort to develop a preventive HCV vaccine still is needed. The answer is almost certainly affirmative. Vaccines that protect against hepatitis A and B virus infections were first targeted to health care workers. The value of adding a vaccine to prevent accidental HCV infection in the workplace is clear.Will There Be a Vaccine to Protect Against the Hepatitis C Virus?Benoît Callendret, Christopher M. Walker10.1053/j.gastro.2012.02.010Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5Commentary13841387http://www.gastrojournal.org/article/PIIS0016508512002272/abstract?rss=yes Hepatitis E has been considered to be a travel-associated, acute, self-limiting liver disease that causes fulminant hepatic failure in specific high-risk groups only. However, hepatitis E virus (HEV) infection can also be acquired in industrialized countries—HEV genotype 3 infection is a zoonosis, with pigs and rodents serving as animal reservoirs. In recent years, cases of chronic HEV infection that were associated with progressive liver disease have been described in several cohorts of immunocompromised individuals, including recipients of organ transplants. The topic of hepatitis E is therefore re-emerging and has raised the following important questions: what is the risk for HEV infection in Western countries (eg, from eating uncooked meat)? How frequently does chronic hepatitis E develop among human immunodeficiency virus–infected patients and recipients of organ transplants? What are the treatment options? What is the current status of vaccine development? What do we know about the pathogenesis of HEV infection, and why does it have a more severe course in pregnant women? This review summarizes the current knowledge on the pathogenesis and treatment of HEV infection. Pathogenesis and Treatment of Hepatitis E Virus InfectionHeiner Wedemeyer, Sven Pischke, Michael P. Manns10.1053/j.gastro.2012.02.014Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5Review13881397.e1http://www.gastrojournal.org/article/PIIS0016508512004659/abstract?rss=yesEditorial Board10.1053/S0016-5085(12)00465-9Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5FrontmatterA2A2http://www.gastrojournal.org/article/PIIS0016508512004660/abstract?rss=yesTable of Contents10.1053/S0016-5085(12)00466-0Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5FrontmatterA7A8http://www.gastrojournal.org/article/PIIS0016508512004672/abstract?rss=yesGastroenterology is the premiere journal in the field of gastrointestinal disease and is led by an internationally renowned board of editors. As the official journal of the AGA Institute, Gastroenterology delivers up-to-date and authoritative coverage of both basic and clinical gastroenterology and hepatology. Regular features include research and perspectives by leading authorities, reports on the latest technologies for diagnosing and treating digestive diseases, images illustrating important clinical findings, reviews of scholarly media, medical news, meeting summaries, video abstracts, and monthly podcasts. Gastroenterology also bridges the gap between basic and clinical science by publishing comprehensive reviews on important topics such as pancreatitis and liver disease.Information for Authors and Readers10.1053/S0016-5085(12)00467-2Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5FrontmatterA10A11http://www.gastrojournal.org/article/PIIS0016508512004684/abstract?rss=yesCopyright Assignment. 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.)Copyright Assignment, Authorship Responsibility, NIH Funding, Financial Disclosure, Institutional Review Board/Animal Care Committee Approval, and Sponsorship10.1053/S0016-5085(12)00468-4Gastroenterology 142, 6 (2012)2012-05-01Gastroenterology2012-05-011426S0016-5085(11)X0018-5FrontmatterA16A16