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• W2037693817 abstract "Pediatric gastroenterology, hepatology, and nutrition are vital components of our clinical practices, in the education and training of future leaders, and in bringing discoveries from the laboratory to influence the manner in which we provide clinical care. As patients with congenital disorders and early-onset diseases are living longer, the interface between pediatric and adult gastroenterology is increasing at a rapid pace. With these considerations in mind, it is opportune for us to project what lies ahead in pediatric gastroenterology, hepatology, and nutrition. We hope the readership finds this summary by distinguished leaders in the field helpful. This is a very exciting time for pediatric gastroenterology, because new clinical and basic research techniques have allowed us to begin to identify cellular/molecular mechanisms of disease and the associations of single nucleotide polymorphisms with disease expression and outcome and as potential biomarkers to predict the phenotypic expression of diseases. As a result of the research approaches to the prevention of disease, we can theoretically identify individuals at risk for expression of disease (eg, NOD2/CARD15 single nucleotide polymorphisms and Crohn’s disease) and therefore potentially lessen the phenotypic expression of disease by instituting preventative measures earlier. Because prevention of chronic disease expression is cost-effective with regard to medical care, this research approach should be of clinical relevance to gastroenterologists. In addition, a large amount of research literature has accumulated with regard to hypotheses suggesting that intrauterine or perinatal insults may result in delayed expression of disease during adulthood. We refer to the so-called “Barker intrauterine programming hypothesis,” which suggests that inappropriate intrauterine nutrition may result in the expression of diabetes, hypertension, cardiovascular disease, and so on during middle adult life. In addition, the so-called “hygiene hypothesis” suggests that inadequate initial colonization of the newborn gut or a lack of exposure to neonatal infectious agents may result in an increased expression of allergic and autoimmune disease during late childhood and adulthood due to an inadequate development of mucosal immune system (eg, lack of oral tolerance). We will attempt to review these and other topics of importance to pediatric gastroenterology in the subsequent paragraphs. In 1987, David Barker and his epidemiology group in the United Kingdom proposed that intrauterine malnutrition (small for gestational age newborn) and poor weight gain in the first year of life were associated with an increased incidence of cardiovascular disease (particularly in adults older than 50 years of age), hypertension, and glucose intolerance during adulthood. This retrospective report was confirmed with several prospective publications on The Netherlands famine during World War II, which affected women during early, mid, and late stages of gestation. Because of the health care system in the Netherlands, these patients were followed up over a long period and were shown to have an associated increased risk of cardiovascular-, pulmonary-, and nutrition- (obesity) related diseases. Subsequently, animal and prospective human studies have suggested that either undernutrition or overnutrition in utero can be associated with epigenetic changes as well as intrauterine adverse programming of organ function. More recently, evidence of single nucleotide polymorphisms in choline, folic acid, and copper metabolism has been associated with birth defects, mental retardation, and other neurologic deficits. These observations may lead to a subsequent amniotic fluid or cord blood tests for genetic predisposition to disease and active approaches to the prevention of adult expression of gastrointestinal diseases. A very interesting area of gastrointestinal research over the past decade has been regarding microbial-epithelial “crosstalk,” initially involving pathogen-gut interaction as the basis for the pathogenesis of infectious gastroenteritis and more recently the interaction of commensal bacteria with gut epithelium and lymphoid cells. This research was stimulated by the discovery that a family of receptors, toll-like receptors, was expressed on lymphoid, dendritic, and endothelial and epithelial cells, which provided the cellular basis for communication between microorganism molecular patterns and eukaryotic cells as the basis for innate immune responses. More recently, basic science studies performed with germ-free animals have suggested that microbial-epithelial/lymphoid interaction must occur in the neonatal-immature gut phase to develop important immunologic processes such as oral tolerance, an important immune function needed to prevent the expression of allergy and autoimmune diseases. In the Walker laboratory using human immature enterocyte models (fetal small intestinal cell lines, fetal intestinal xenografts, and organ culture), it has been shown that immature intestinal epithelium reacts to microbial stimulation by an increased inflammatory response (interleukin-8) due to underexpression of negative regulators (Tollip, IRAK-M, A20, and so on) of nuclear factor κβ–stimulated inflammatory cytokine transcription. These underexpressed genes are stimulated to express and thereby down-regulate excessive inflammation by trophic factors (cortisone, transforming growth factor β, and so on) in amniotic fluid and early breast milk. We believe this maturational step helps in the prevention of necrotizing enterocolitis. Several recent publications have underscored the importance of the hygiene hypothesis as an explanation for increased expression of immune-mediated diseases over the past several decades. In addition, recent basic publications have suggested that early interaction of colonizing bacteria with the neonatal gut can orchestrate development of the mucosal immune system. Finally, some seminal reports have appeared in reviews by pediatric gastrointestinal physicians/scientists over the past few years that provide insight into the combined role of genetic predisposition and environmental stimuli in the expression of a variety of gastrointestinal, liver, and nutritional conditions. These reports underscore the importance of understanding the pathogenesis of disease at the cellular/molecular level. By examining a potential chronic gastrointestinal condition during the pediatric period, before complications of the condition affect definition of its pathogenesis, studies can better approach prevention or modification of phenotypic expression. Examples over the past few years are listed in the references.1Simmons R. Developmental origins of adult metabolic disease: concepts and controversies.Trends Endocrinol Metab. 2005; 16: 390-394Abstract Full Text Full Text PDF PubMed Scopus (88) Google Scholar, 2Hoffman P.L. Regan F. Cutfield W.S. Prematurity—another example of perinatal metabolic programming.Horm Res. 2006; 66: 33-39Crossref PubMed Scopus (45) Google Scholar, 3Gillman M.W. Epidemiological challenges in studying the fetal origins of adult chronic disease.Int J Epidemiol. 2002; 31: 294-299Crossref PubMed Google Scholar, 4Painter R.C. de Rooij S.R. Bossuyt P.M. Simmers T.A. Osmond C. Barker D.J. Bleker O.P. Roseboom T.J. Early onset of coronary artery disease after prenatal exposure to the Dutch famine.Am J Clin Nutr. 2006; 84: 322-327PubMed Google Scholar, 5Baker D.J.P. Fetal origins of coronary heart disease.Br Med J. 1995; 311: 171-174Crossref PubMed Scopus (2534) Google Scholar, 6Park C.S. Role of compensatory mammary growth in epigenetic control of gene expression.FASEB J. 2005; 19: 1586-1591Crossref PubMed Scopus (30) Google Scholar, 7Gluckman P.D. Hanson M.A. Living with the past: evolution, development and patterns of disease.Science. 2004; 305: 1733-1736Crossref PubMed Scopus (1395) Google Scholar, 8Eder W. Klimecki W. Yu L. von Mutius E. Riedler J. Braun-Fahrlander C. Nowak D. Martinez F.D. ALEX Study TeamToll-like receptor 2 as a major gene for asthma in children of European farmers.J Allergy Clin Immunol. 2004; 113: 482-488Abstract Full Text Full Text PDF PubMed Scopus (415) Google Scholar, 9Guarner F. Bourdet-Sicard R. Brandtzaeg P. Gill H.S. McGuirk P. van Eden W. Versalovic J. Weinstock J.V. Rook G.A. Mechanisms of disease: the hygiene hypothesis revisited.Nat Clin Pract Gastroenterol Hepatol. 2006; 3: 275-284Crossref PubMed Scopus (230) Google Scholar, 10Bach J.-F. The effect of infections on susceptibility to autoimmune and allergic disease.N Engl J Med. 2002; 347: 911-920Crossref PubMed Scopus (2036) Google Scholar, 11Wills-Karp M. Santeliz J. Karp C.L. The germless theory of allergic disease: revisiting the hygiene hypothesis.Nat Rev Immunol. 2001; 1: 69-75Crossref PubMed Scopus (655) Google Scholar, 12Green C. Elliott L. Beaudoin C. Bernstein C.N. A population-based ecologic study of inflammatory bowel disease: searching for etiologic clues.Am J Epidemiol. 2006; 164 (discussion 624–628): 615-623Crossref PubMed Scopus (116) Google Scholar, 13Hooper L.V. Wong M.H. Thelin A. Hansson L. Falk P.G. Gordon J.I. Molecular analysis of commensal host-microbial relationships in the intestine.Science. 2001; 291: 881-884Crossref PubMed Scopus (1678) Google Scholar, 14Han X. Sosnowska D. Bonkowski E.L. Denson L.A. Growth hormone inhibits signal transducer and activator of transcription 3 activation and reduces disease activity in murine colitis.Gastroenterology. 2005; 129: 185-203Abstract Full Text Full Text PDF PubMed Scopus (64) Google Scholar, 15Vesikari T. Matson D.O. Dennehy P. Van Damme P. Santosham M. Rodriguez Z. Dallas M.J. Heyse J.F. Goveia M.G. Black S.B. Shinefield H.R. Christie C.D. Ylitalo S. Itzler R.F. Coia M.L. Onorato M.T. Adeyi B.A. Marshall G.S. Gothefors L. Campens D. Karvonen A. Watt J.P. O’Brien K.L. DiNubile M.J. Clark H.F. Boslego J.W. Offit P.A. Heaton P.M. Rotavirus Efficacy and Safety Trial (REST) Study TeamSafety and efficacy of a pentavalent human-bovine (WC3) reassortant rotavirus vaccine.N Engl J Med. 2006; 354: 23-33Crossref PubMed Scopus (1574) Google Scholar, 16Ruiz-Palacios G.M. Perez-Schael I. Velazquez F.R. Abate H. Breuer T. Clemens S.C. Cheuvart B. Espinoza F. Gillard P. Innis B.L. Cervantes Y. Linhares A.C. Lopez P. Macias-Parra M. Ortega-Barria E. Richardson V. Rivera-Medina D.M. Rivera L. Salinas B. Pavia-Ruz N. Salmeron J. Ruttimann R. Tinoco J.C. Rubio P. Nunez E. Guerrero M.L. Yarzabal J.P. Damaso S. Tornieporth N. Saez-Llorens X. Vergara R.F. Vesikari T. Bouckenooghe A. Clemens R. De Vos B. O’Ryan M. Human Rotavirus Vaccine Study GroupSafety and efficacy of an attenuated vaccine against severe rotavirus gastroenteritis.N Engl J Med. 2006; 354: 11-22Crossref PubMed Scopus (1546) Google Scholar, 17Bacchetta R. Passerini L. Gambineri E. Dai M. Allan S.E. Perroni L. Dagna-Bricarelli F. Sartirana C. Matthes-Martin S. Lawitschka A. Azzari C. Ziegler S.F. Levings M.K. Roncarolo M.G. Defective regulatory and effector T cell functions in patients with FOX3 mutations.J Clin Invest. 2006; 116: 1713-1722Crossref PubMed Scopus (418) Google Scholar, 18Sperling M.A. ATP-sensitive potassium channels—neonatal diabetes mellitus and beyond.N Engl J Med. 2006; 355: 507-510Crossref PubMed Scopus (62) Google Scholar, 19Babenko A.P. Polak M. Cave H. Busiah K. Czernichow P. Scharfmann R. Bryan J. Aguilar-Bryan L. Vaxillaire M. Froguel P. Activating mutations in the ABCC8 gene in neonatal diabetes mellitus.N Engl J Med. 2006; 355: 456-466Crossref PubMed Scopus (546) Google Scholar, 20Pearson E.R. Flechtner I. Njolstad P.R. Malecki M.T. Flanagan S.E. Larkin B. Ashcroft F.M. Klimes I. Codner E. Iotova V. Slingerland A.S. Shield J. Robert J.J. Holst J.J. Clark P.M. Ellard S. Sovik O. Polak M. Hattersley A.T. Neonatal Diabetes International Collaborative GroupSwitching from insulin to oral sulfonylureas in patients with diabetes due to Kir6.2 mutations.N Engl J Med. 2006; 355: 467-477Crossref PubMed Scopus (785) Google Scholar, 21Wang J. Cortina G. Wu S.V. Tran R. Cho J.H. Tsai M.J. Bailey T.J. Jamrich M. Ament M.E. Treem W.R. Hill I.D. Vargas J.H. Gershman G. Farmer D.G. Reyen L. Martin M.G. Mutant neurognin-3 in congenital malabsorptive diarrhea.N Engl J Med. 2006; 355: 270-280Crossref PubMed Scopus (239) Google Scholar, 22Liu C. Aronow B.J. Jegga A.G. Wang N. Miethke A. Mourya R. Bezerra J.A. Novel resequencing chip customized to diagnose mutations in patients with inherited syndromes of intrahepatic cholestasis.Gastroenterology. 2007; 131 (xx-xx)Google Scholar, 23Konikoff M.R. Noel R.J. Blanchard C. Kirby C. Jameson S.C. Buckmeier B. Akers R. Cohen M.B. Collins M.H. Assa’ad A.H. Aceves S.S. Putnam P.E. Rothenberg M.E. A randomized double-blind placebo-controlled trial of fluticasone propionate for pediatric eosinophilic esophagitis.Gastroenterology. 2006; 131: 1381-1391Abstract Full Text Full Text PDF PubMed Scopus (516) Google Scholar This is a “snapshot” of investigations in pediatric gastroenterology today. We envision, as research approaches become more sophisticated, that further genetic-based pediatric diseases manifesting in adulthood will be uncovered and the genetic profiles of infants from amniotic fluid cells will be used to predict the potential for gastrointestinal disease presentation and allow for early preventative measures that can be started to prevent or minimize genetic expression. As part of the future of pediatric gastroenterology, we envision use of gene replacement to prevent disease (eg, microvillus inclusion disease, α-antitrypsin disease, and so on)." @default.
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• W2037693817 title "State of Pediatric Gastroenterology, Hepatology, and Nutrition: 2006 and Beyond" @default.
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