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Dig Dis Sci ; 54(1): 142-50, 2009 Jan.
Article in English | MEDLINE | ID: mdl-18594982

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.


Subject(s)
Crohn Disease , Phenotype , Adolescent , Child , Cohort Studies , Constriction, Pathologic/ethnology , Constriction, Pathologic/genetics , Constriction, Pathologic/physiopathology , Crohn Disease/ethnology , Crohn Disease/genetics , Crohn Disease/pathology , Crohn Disease/physiopathology , Disease Progression , Female , Follow-Up Studies , Genotype , Humans , Ileum/physiopathology , Inflammation/ethnology , Inflammation/genetics , Inflammation/physiopathology , Israel , Male , Mutation/genetics , Nod2 Signaling Adaptor Protein/genetics , Time Factors
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