title: Disease behavior in children with Crohn's disease: the effect of disease duration, ethnicity, genotype, and phenotype.
abstract: BACKGROUND
  Disease behavior in Crohn's disease (CD) may be modified by disease location and genotype. Disease behavior may change over time, and thus analysis requires follow-up. To date, there have been few pediatric studies that have evaluated the association between disease behavior and genotype with prolonged follow-up. The aim of our study was to evaluate the effect of genotype, phenotype, and ethnicity on disease behavior in pediatric CD.
  
  
  METHODS
  Evaluation of 128 pediatric CD was followed by analysis of 232 pediatric and adult-onset CD patients. Inclusion required at least 2 years of follow-up. Phenotype, ethnicity, and disease duration were recorded. Patients were genotyped for polymorphisms in the NOD2/CARD15 gene.
  
  
  RESULTS
  Colonic involvement was more frequent in younger patients. Pediatric disease at end of follow-up was classified as inflammatory (78%), penetrating (7%), and stricturing (17%). Duration of follow-up (mean 4.9 pediatric and 6.4 years mixed) was associated with more stricturing and penetrating disease. There was no association between mean age of onset and NOD2/CARD15, or either of these with disease behavior. These observations were replicated in the mixed cohort. Sephardic Jewish origin was inversely correlated with inflammatory behavior (P = 0.006), independent of NOD2/CARD15 genotype.
  
  
  CONCLUSIONS
  Duration of disease and ethnicity, irrespective of NOD2/CARD15 genotype and age of onset, were the only predictors for penetrating or stricturing disease.
authors.affiliation: Pediatric Day Care Unit, Department of Pediatrics, Bnai Zion Medical Center, 47 Golomb St., POB 4940, Haifa, 31048, Israel. shaoul_r@012.net.il
authors.forename: Ron
authors.initials: R
authors.lastname: Shaoul
authors.forename: Amir
authors.initials: A
authors.lastname: Karban
authors.forename: Shimon
authors.initials: S
authors.lastname: Reif
authors.forename: Batia
authors.initials: B
authors.lastname: Weiss
authors.forename: Raanan
authors.initials: R
authors.lastname: Shamir
authors.forename: Ada
authors.initials: A
authors.lastname: Tamir
authors.forename: Ofir
authors.initials: O
authors.lastname: Davidovich
authors.forename: Jonathan
authors.initials: J
authors.lastname: Halevi
authors.forename: Esther Leshinsky
authors.initials: EL
authors.lastname: Silver
authors.forename: Arie
authors.initials: A
authors.lastname: Levine
mesh_terms: D000293:Adolescent; D002648:Child; D015331:Cohort Studies; D003251:Constriction, Pathologic / Q000208:ethnology / Q000235:genetics / Q000503:physiopathology; D003424:Crohn Disease / Q000208:ethnology / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D006801:Humans; D007082:Ileum / Q000503:physiopathology; D007249:Inflammation / Q000208:ethnology / Q000235:genetics / Q000503:physiopathology; D007557:Israel; D008297:Male; D009154:Mutation / Q000235:genetics; D053473:Nod2 Signaling Adaptor Protein / Q000235:genetics; D010641:Phenotype; D013997:Time Factors
chemical_list: C429018:NOD2 protein, human; D053473:Nod2 Signaling Adaptor Protein