Inflammatory bowel disease in children 5 years of age and younger

Mamula, Petar; Telega, Grzegorz; Markowitz, Jonathan E.; Brown, Kenneth N.; Russo, Pierre; Piccoli, David A.; Baldassano, Robert N.

doi:10.1111/j.1572-0241.2002.05915.x

Cited by 188 publications

(106 citation statements)

References 35 publications

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“…We have shown that involvement of the ileum is age dependent: children Ͻ8 years old at the time of diagnosis had significantly less involvement of the ileum and more isolated colonic disease than children Ͼ8 years at diagnosis, confirming previous studies. 7,8,25 In a large study of nearly 1400 North American early-onset patients, Heyman et al 7 demonstrated by multifactorial analysis that a colonic predominant phenotype exists in IBD diagnosed under the age of 8 years. Paul et al 8 studied 413 pediatric IBD patients and also demonstrated a greater tendency for very young patients to present with colonic disease.…”

Section: Discussionmentioning

confidence: 99%

Definition of Phenotypic Characteristics of Childhood-Onset Inflammatory Bowel Disease

et al. 2008

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See Dubinsky MC et al on page 1105 in CGH;See editorial on page 1038. Background & Aims:Childhood-onset inflammatory bowel disease (IBD) might be etiologically different from adult-onset IBD. We analyzed disease phenotypes and progression of childhood-onset disease and compared them with characteristics of adult-onset disease in patients in Scotland. ; 43% vs 3%; P < .0001; OR, 23.36; 95% CI, 13.45-40.59) with less isolated ileal (L1; 2% vs 31%; P < .0001; OR, 0.06; 95% CI, 0.03-0.12) or colonic disease (L2; 15% vs 36%; P < .0001; OR, 0.31; 95% CI, 0.21-0.46). UC was extensive in 82% of the children at diagnosis, versus 48% of adults (P < .0001; OR, 5.08; 95% CI, 2.73-9.45); 46% of the children progressed to develop extensive colitis during followup. Forty-six percent of children with CD and 35% with UC required immunomodulatory therapy within 12 months of diagnosis. The median time to first surgery was longer in childhood-onset than adult-onset patients with CD (13.7 vs 7.8 years; P < .001); the reverse was true

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Section: Discussionmentioning

confidence: 99%

Definition of Phenotypic Characteristics of Childhood-Onset Inflammatory Bowel Disease

et al. 2008

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“…The disease can affect both children and adults. Early presentation of the disease in the first decades of life carries significant morbidity and mortality (5)(6)(7). A high risk for complications associated with early onset of the disease is thought to reflect longer lifetime duration of disease and medication use, effects of the disease during periods of growth and development, and possibly a more severe phenotype of the disease as a result of a specific genotype-causing predisposition to early onset of the disease.…”

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confidence: 99%

Is Age of Onset of Crohn's Disease Governed by Mutations in NOD2/Caspase Recruitment Domains 15 and Toll-Like Receptor 4? Evaluation of a Pediatric Cohort

et al. 2005

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Crohn's disease (CD) is caused by a combination of environmental and genetic factors. It is not clear at present whether age of onset (AOO) is a random event or dictated by genotype or environmental factors. Mutations in the NOD2/caspase recruitment domains 15 (CARD15) and in the Toll-like receptor 4 (TLR4) gene have been associated with increased susceptibility for CD. We sought to determine whether single or multiple mutations in these genes are linked to earlier susceptibility for CD. A cohort of 189 patients with CD (82 pediatric onset, 107 adult onset) were genotyped for three disease-associated singlenucleotide polymorphisms (SNPs), one haplotype association (JW1-SNP5), and one background polymorphism (P268S) of the NOD2/CARD15 gene and for two SNPs of TLR4. Analysis of heterozygosity, homozygosity, alleles, and haplotypes of cohort on age or pediatric onset was performed. AOO ranged from 8 mo to 68 y. The presence of the three NOD2/CARD15 and two TLR4 mutations, the NOD2/CARD15 JW haplotype, compound heterozygosity, and homozygosity were not associated with AOO. Presence of P268S in the absence of known NOD2/ CARD15 mutations was correlated with increasing age and adult onset of CD, whereas pediatric-onset disease was associated with male gender and the wild-type NOD2/CARD15 haplotype. Mutations in NOD2/CARD15 and TLR4 are not significantly associated with AOO in our population. Mutations that are not in linkage disequilibrium with the background mutation P268S of the NOD2/CARD15 gene probably play a more significant role in pediatric-onset disease. Crohn's disease (CD) is thought to result from combined effects of environmental agents and a genetically susceptible host. A central role for the innate immune responses to discrete antigens has been postulated. A perturbation in the immune response to luminal bacteria leads to inflammation in the gastrointestinal tract (1-4). The disease can affect both children and adults. Early presentation of the disease in the first decades of life carries significant morbidity and mortality (5-7). A high risk for complications associated with early onset of the disease is thought to reflect longer lifetime duration of disease and medication use, effects of the disease during periods of growth and development, and possibly a more severe phenotype of the disease as a result of a specific genotype-causing predisposition to early onset of the disease.

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“…Laboratuvar olarak lökositoz, sola kayma, anemi, trombositoz ve hipoproteinemi, hipoalbüminemi görülebilir. Toksik megakolon akut fulminan kolitin en ciddi formudur (32,39,40,41,42).…”

Section: üLseratif Kolit (üK)unclassified

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Çokuğraş¹

2011

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Inflammatory bowel disease in children 5 years of age and younger

Cited by 188 publications

References 35 publications

Definition of Phenotypic Characteristics of Childhood-Onset Inflammatory Bowel Disease

Definition of Phenotypic Characteristics of Childhood-Onset Inflammatory Bowel Disease

Is Age of Onset of Crohn's Disease Governed by Mutations in NOD2/Caspase Recruitment Domains 15 and Toll-Like Receptor 4? Evaluation of a Pediatric Cohort

Kronik enflamatuar barsak hastalıkları

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