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Richard K. Russell

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     Edinburgh Research Explorer                                      Upper Gastrointestinal Involvement in Pediatric Crohn's DiseaseReplyCitation for published version:Van Limbergen, J, Wilson, DC, Russell, RK, Drummond, HE & Satsangi, J 2009, 'Upper GastrointestinalInvolvement in Pediatric Crohn's Disease Reply' Gastroenterology, vol 136, no. 7, pp. 2409-2410.,10.1053/j.gastro.2009.04.044Digital Object Identifier (DOI):10.1053/j.gastro.2009.04.044Link:Link to publication record in Edinburgh Research ExplorerDocument Version:Publisher final version (usually the publisher pdf)Published In:GastroenterologyPublisher Rights Statement:© 2009 AGA InstituteGeneral rightsCopyright for the publications made accessible via the Edinburgh Research Explorer is retained by the author(s)and / or other copyright owners and it is a condition of accessing these publications that users recognise andabide by the legal requirements associated with these rights.Take down policyThe University of Edinburgh has made every reasonable effort to ensure that Edinburgh Research Explorercontent complies with UK legislation. If you believe that the public display of this file breaches copyright pleasecontact openaccess@ed.ac.uk providing details, and we will remove access to the work immediately andinvestigate your claim.Download date: 20. Feb. 20152. IBD working group of the European Society for the Pediatric Gas-troenterology HaN. Inflammatory bowel disease in children andadolescents: recommendations for diagnosis- the Porto criteria.J Pediatr Gastroenterol Nutr 2005;41:1–7.3. Lennards-Jones JE. Classification of inflammatory bowel disease.Scan J Gastroenterol 1989;24(Suppl 170):2–6.4. North American Society of Pediatric Gastroenterology HaN, ColitisFoundation of America, Bousvarous A, Antonioli DA, Colletti AB, etal. Differentiating ulcerative colitis from Crohn disease in childrenand young adults: report of a working group of the North AmericanSociety of Gastroenterology, Hepatology and Nutrition and theCrohn’s and Colitis Foundation of America. J Pediatr GastroenterolNutr 2007;44:653–674.5. Grill BB, Lang R, Markowitz R, et al. Delayed gastric emptying inchildren with Crohn’s disease. J Clin Gastroenterol 1985;7:216–226.6. Lenaerts C, Roy CC, Vaillancourt M, et al. High incidence of uppergastrointestinal tract in children with Crohn disease. Pediatric1989;83:777–781.7. Kugathasan S, Judd RH, Hoffman RG, et al. Epidemiologic andclinical characteristics of children with newly diagnosed inflamma-tory bowel disease in Wisconsin: a statewide population-basedstudy. J Pediatr 2003;143:525–531.8. Gupta N, Bostrom AG, Kirschner BS, et al. Gender differences inpresentation and course of disease in pediatric patients withCrohn disease. Pediatrics 2007;120:e1418–e1425.doi:10.1053/j.gastro.2008.12.077Reply. In his comment on our recent paper describingthe phenotype of childhood-onset inflammatory boweldisease (IBD), Dr Matary highlights several importantissues pertaining to the investigation and classification ofinvolvement of the upper gastrointestinal (GI) tract inpediatric Crohn’s disease (CD).1,2 To enable a comparisonof the pediatric phenotype with adult-onset disease, weused the Montreal classification of IBD rather than amore detailed, anatomic classification of disease extentwhich we have previously used in the genotype–pheno-type analysis of NOD2/CARD15 variants.3 Our investi-gation protocol based on the ESPGHAN Porto-criteria,adhered to by the pediatric gastroenterologists at the 3recruiting centers, states that biopsies are taken routinelyfrom the upper GI tract during the investigation ofpediatric IBD.4 Involvement of any anatomic locationwas defined as either macroscopic, microscopic, or both.Macroscopically, the minimum criteria for involvementof a disease location were ulceration or the presence of anaphthous lesion. Erythema and/or edema did not sufficeto score a site as affected by CD. Microscopically, non-specific inflammation or inflammatory changes thatcould be otherwise explained (eg, reflux esophagitis orHelicobacter pylori gastritis) were not classified as CD.Interobserver variability was addressed by the qualitycontrol of phenotypic data by a dedicated database man-ager (HED) after review of the case notes (includingendoscopy, pathology, and radiology reports).The application of the recent Montreal classification,which has addressed some of the difficulties of previoussystems in classifying pediatric IBD (specifically the in-volvement of the upper GI tract, which precluded classi-fication of lower GI disease in the Vienna classification),makes comparisons with historical datasets trouble-some.5,6 In these older datasets, as for example that de-scribed in the study by Lenaerts et al,7 the upper GI tractwas typically not investigated in the absence of clear upperGI-related symptoms, as acknowledged in their manuscript.In the absence of clear upper GI symptoms, esophagogas-troduodenoscopy is also rarely performed in the investiga-tion of adult-onset CD.8 However, involvement of the upperGI tract has been reported to be as high as 75% in prospec-tive adult CD studies where esophagogastroduodenoscopywas routinely performed.9,10 Furthermore, in the Montrealclassification, jejunal disease is scored as upper GI disease(the L1 category is limited to ileal disease), which furthercompromises comparison with older classification systems,dividing the GI tract into the upper, small bowel, and colon.Our finding that60% of children affected by Crohn’sdisease display involvement of the upper GI tract is,therefore, comparable with contemporary prospectivestudies in adult onset CD and further highlights theimportance of a comprehensive assessment of our pedi-atric CD patients.JOHAN VAN LIMBERGENDAVID C. WILSONDepartment of Pediatric Gastroenterology andNutrition andRoyal Hospital for Sick Children Edinburgh, UnitedKingdomChild Life and Health, University of EdinburghEdinburgh, United KingdomRICHARD K. RUSSELLDepartment of Pediatric GastroenterologyYorkhill HospitalGlasgow, United KingdomHAZEL E. DRUMMONDJACK SATSANGIGastrointestinal UnitMolecular Medicine CentreWestern General HospitalUniversity of EdinburghEdinburgh, United Kingdom1. El-Matary W. Upper gastrointestinal involvement in pediatricCrohn’s disease. Gastroenterology. In press.2. Van Limbergen J, Russell RK, Drummond HE, et al. Definition ofphenotypic characteristics of childhood-onset inflammatory boweldisease. Gastroenterology 2008;135:1114–1122.3. Russell RK, Drummond HE, Nimmo ER, et al. Genotype-phenotypeanalysis in childhood-onset Crohn’s disease: NOD2/CARD15 vari-ants consistently predict phenotypic characteristics of severe dis-ease. Inflamm Bowel Dis 2005;11:955–964.4. IBD Working Group of the European Society for Paediatric Gas-troenterology HaN. Inflammatory bowel disease in children andadolescents: recommendations for diagnosis—the Porto criteria.J Pediatr Gastroenterol Nutr 2005;41:1–7.5. Silverberg MS, Satsangi J, Ahmad T, et al. Toward an integratedclinical, molecular and serological classification of inflammatorybowel disease: Report of a Working Party of the 2005 MontrealJune 2009 CORRESPONDENCE 2409World Congress of Gastroenterology. Can J Gastroenterol 2005;19:5A–36A.6. Gupta N, Bostrom AG, Kirschner BS, et al. Gender differences inpresentation and course of disease in pediatric patients withCrohn disease. Pediatrics 2007;120:e1418–e1425.7. Lenaerts C, Roy CC, Vaillancourt M, et al. High incidence of uppergastrointestinal tract involvement in children with Crohn’s dis-ease. Pediatrics 1989;83:777–781.8. Nikolaus S, Schreiber S. Diagnostics of inflammatory bowel dis-ease. Gastroenterology 2007;133:1670–1689.9. Hommes DW, van Deventer SJ. Endoscopy in inflammatory boweldiseases. Gastroenterology 2004;126:1561–1573.10. Witte AMC, Veenendaal RA, van Hogezand RA, et al. Crohn’sDisease of the Upper gastrointestinal tract: the value of endo-scopic examination. Scand J Gastroenterol 1998;33:100–105.Conﬂicts of interestThe authors disclose no conﬂicts.FundingJohan Van Limbergen was funded by a Research TrainingFellowship from Action Medical Research, The Gay-Ramsay-Steel-Maitland or Stafford Trust and the Hazel M. Wood Charitable Trust.Jack Satsangi was the holder of by a Wellcome Trust ProgrammeGrant (072789/Z/03/Z). David C. Wilson is the holder of a MedicalResearch Council Project Grant (G0800675).Financial assistance was also provided by Schering-Plough and theGI/Nutrition Research Fund, Child Life and Health, University ofEdinburgh.doi:10.1053/j.gastro.2009.04.044In the January 2009 issue of GASTROENTEROLOGY, the Comment Fromthe Editor described 8 cohorts of patients with acute Hepatitis C inNorth America in an effort to heighten awareness of this interestingpatient population. The following letters highlight additional uniqueand valuable acute hepatitis C cohorts in North America and furtheremphasize the important window of opportunity to identify at-riskpopulations within correctional facilities. Collectively, these cohortsprovide important opportunities to better understand the epidemiol-ogy, natural history, and effective therapeutic approaches of acutehepatitis C in North America, as well as the early pathogenetic mech-anisms.Acute Hepatitis C Infection inCorrectional SettingsDear Sir:We greatly appreciated the recent spotlight on theimportant epidemiologic, immunologic, and virologic re-search that is ongoing in US cohorts of acute hepatitis Cinfection.1 We would like to take this opportunity tohighlight an additional aspect of acute hepatitis C that isevidenced in our work within the Massachusetts correc-tional system, where we have initiated screening pro-grams for acute hepatitis C virus (HCV) infection duringthe medical intake examination for recently incarceratedinmates. More than 3200 inmates have been screenedwith a short questionnaire eliciting information regard-ing high-risk behaviors. Through the help of medicalproviders based in the correctional system, we have iden-tified 140 subjects at high risk of infection; surpris-ingly, 37 cases of acute HCV infection were subsequentlydiagnosed over a 15-month period (manuscript in prep-aration). These results demonstrate that, beyond the well-known epidemic of chronic HCV in the correctionalsystem, there is also a high rate of acute HCV infection,mainly among recently incarcerated new drug users.2The Centers for Disease Control and Prevention man-dated in 2003 that primary and secondary HCV preven-tion efforts should be focused on injection drug usersand specifically cited prison facilities as an ideal settingfor such efforts.3 However, the feasibility and the accept-ability of such interventions were unknown. Since 2006,we have found widespread acceptance of our interven-tions, including HIV testing and immunizations againsthepatitis A and B infection. We are examining the utilityof new algorithms of expanded diagnostic criteria foracute HCV infection in new-onset injection drug users,who often have no prior record of serologic testing. Wehave also shown that treatment of acute HCV infectionin the prisons is feasible, safe, and effective. As noted inour pilot project,4 we have found that the burden of mostnew HCV infections is occurring in Caucasian subjects,although there is wide representation of Hispanics andblacks within our prison population. Furthermore, studyof these interesting trends is being planned.Despite some exemplary exceptions,1 the diagnosis andtreatment of acute HCV in injection drugs users has beengenerally low. However, our concentrated efforts withinthe structured environment of the correctional settingdemonstrate that this avenue of intervention has highyield among a largely underserved patient population.Because more than half of US inmates are incarceratedowing to new drug use offenses, there is indeed a “win-dow of opportunity” to make a difference.5BARBARA MCGOVERNAssociate ProfessorTufts University School of MedicineLemuel Shattuck HospitalJamaica Plain, MassachusettsARTHUR KIMClinical Instructor in MedicineHarvard Medical SchoolMassachusetts General HospitalBoston, MassachusettsGEORG LAUERHarvard Medical SchoolMassachusetts General HospitalBoston, Massachusetts1. Cox A, Page K, Bruneau J, et al. Rare birds in North America: acutehepatitis C cohorts. Gastroenterology 2009;136:26–39.2. Baillargeon J, Wu H, Kelley MJ. Hepatitis C seroprevalence amongnewly incarcerated inmates in the Texas correctional system. Pub-lic Health 2003;117:43–48.3. Weinbaum C, Lyerla R, Margolis H. Prevention and control ofinfections with hepatitis viruses in correctional settings. MMWRRecomm Rep 2003;52:1–36.4. McGovern B, Wurcel A, Kim A, et al. Acute hepatitis C virusinfection in incarcerated injection drug users. Clin Infect Dis 2006;42:1663–1670.2410 CORRESPONDENCE GASTROENTEROLOGY Vol. 136, No. 7

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