Tags

Type your tag names separated by a space and hit enter

Inflammatory bowel disease in children: a pediatrician's perspective.

Abstract

Crohn's disease (CD) and ulcerative colitis (UC) are common and heterogeneous chronic inflammatory bowel disorders of childhood that account for up to 25% of all patients with inflammatory bowel disease (IBD). In CD, the familial pattern of disease concordance would suggest that genetics contribute to disease etiology. Children are more likely to have proximal small bowel disease complicated by stricture formation, fistulization and the need for surgical intervention. The predisposition for small bowel disease has been associated with mutations of the nucleotide oligomerization domain 2 (NOD2)/Caspase activation and recruitment domain 15 (CARD15) gene on chromosome 16 in 1/3 of patients with CD. Homozygous patients also show an early age at disease onset and a relatively high relative risk for isolated stricturing distal ileal disease. The potential clinical role for NOD2 testing in either the diagnosis or the therapeutic management of patients with CD has yet to be determined. The precise age of onset of CD and UC can be difficult in children. Subclinical phases of disease can be identified through a decrease in weight and height velocity, and a delay in pubertal development. However, a confident distinction between CD and UC also remains a taxonomic dilemma in 25% of pediatric patients with IBD, despite recent technological advances in diagnostic techniques, including gadolinium enhanced magnetic resonance imaging (MRI) and capsule endoscopy, and serological testing. The early introduction of immunomodulators, including azathioprine and 6-mercaptopurine have proven efficacy in maintaining long-term remission without concurrent corticosteroids. The pharmacogenomic of 6-MP metabolism has been shown to be useful in predicting susceptibility to antimetabolite induced toxicity, and possibly allowing physician's to individualize drug therapy to improve clinical response. Novel treatment strategies, including infliximab are being developed in Pediatrics with the aim at improving overall treatment efficacy and potentially avoid surgery.

Authors+Show Affiliations

Division of Pediatric Gastroenterology, The Johns Hopkins School of Medicine, Baltimore, MD 21287, USA. ccuffari@jhmi.edu

Source

Minerva pediatrica 58:2 2006 Apr pg 139-57

MeSH

Anti-Inflammatory Agents, Non-Steroidal
Antimetabolites
Child
Colitis, Ulcerative
Environment
Genetic Predisposition to Disease
Humans
Ileus
Immunoglobulin A
Immunoglobulin G
Inflammatory Bowel Diseases
Intracellular Signaling Peptides and Proteins
Mass Screening
Mercaptopurine
Mesalamine
Nod2 Signaling Adaptor Protein
Risk Factors

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

16835574

Citation

Cuffari, C. "Inflammatory Bowel Disease in Children: a Pediatrician's Perspective." Minerva Pediatrica, vol. 58, no. 2, 2006, pp. 139-57.
Cuffari C. Inflammatory bowel disease in children: a pediatrician's perspective. Minerva Pediatr. 2006;58(2):139-57.
Cuffari, C. (2006). Inflammatory bowel disease in children: a pediatrician's perspective. Minerva Pediatrica, 58(2), pp. 139-57.
Cuffari C. Inflammatory Bowel Disease in Children: a Pediatrician's Perspective. Minerva Pediatr. 2006;58(2):139-57. PubMed PMID: 16835574.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inflammatory bowel disease in children: a pediatrician's perspective. A1 - Cuffari,C, PY - 2006/7/13/pubmed PY - 2006/8/25/medline PY - 2006/7/13/entrez SP - 139 EP - 57 JF - Minerva pediatrica JO - Minerva Pediatr. VL - 58 IS - 2 N2 - Crohn's disease (CD) and ulcerative colitis (UC) are common and heterogeneous chronic inflammatory bowel disorders of childhood that account for up to 25% of all patients with inflammatory bowel disease (IBD). In CD, the familial pattern of disease concordance would suggest that genetics contribute to disease etiology. Children are more likely to have proximal small bowel disease complicated by stricture formation, fistulization and the need for surgical intervention. The predisposition for small bowel disease has been associated with mutations of the nucleotide oligomerization domain 2 (NOD2)/Caspase activation and recruitment domain 15 (CARD15) gene on chromosome 16 in 1/3 of patients with CD. Homozygous patients also show an early age at disease onset and a relatively high relative risk for isolated stricturing distal ileal disease. The potential clinical role for NOD2 testing in either the diagnosis or the therapeutic management of patients with CD has yet to be determined. The precise age of onset of CD and UC can be difficult in children. Subclinical phases of disease can be identified through a decrease in weight and height velocity, and a delay in pubertal development. However, a confident distinction between CD and UC also remains a taxonomic dilemma in 25% of pediatric patients with IBD, despite recent technological advances in diagnostic techniques, including gadolinium enhanced magnetic resonance imaging (MRI) and capsule endoscopy, and serological testing. The early introduction of immunomodulators, including azathioprine and 6-mercaptopurine have proven efficacy in maintaining long-term remission without concurrent corticosteroids. The pharmacogenomic of 6-MP metabolism has been shown to be useful in predicting susceptibility to antimetabolite induced toxicity, and possibly allowing physician's to individualize drug therapy to improve clinical response. Novel treatment strategies, including infliximab are being developed in Pediatrics with the aim at improving overall treatment efficacy and potentially avoid surgery. SN - 0026-4946 UR - https://www.unboundmedicine.com/medline/citation/16835574/Inflammatory_bowel_disease_in_children:_a_pediatrician's_perspective_ DB - PRIME DP - Unbound Medicine ER -