1/26/2024 0 Comments Ibd colonoscopy findings36 However, no specific organism has been shown to cause IBD. 35 In PIBD and adult IBD, an increased load of entero-invasive Escherichia coli strains has been observed. The microbiome in Crohn’s disease has an increased abundance of specific bacterial families and a decrease of others. 32 33 34 Environmental factors likely influence many steps of the pathophysiology, such as the effect of diet and antibiotic use on epithelial barrier function and microbial diversity. Thus, a dysregulated immune response to commensal intestinal bacteria due to an underlying genetic predisposition is thought to be the trigger for chronic inflammation. 31 These genes code for proteins involved in innate and adaptive immunity, autophagy, and mucosal barrier integrity and play a key role in immune homeostasis. Genome-wide association studies have identified more than 200 genetic loci associated with IBD. In recent years, the specifics of the interaction of innate and adaptive responses to the disease process are becoming clearer. 22 A higher prevalence with increasing latitudes has been noted for pediatric onset Crohn’s disease in Scotland and for ulcerative colitis in Finland, 22 29 and an east-west gradient in IBD incidence was noted in Europe. 28 The relative risk for developing pediatric onset Crohn’s disease was higher in affluent areas, but this was not the case for ulcerative colitis. 18 A population based study in Wisconsin found that the incidence of PIBD was similar in different ethnic groups, as well as in densely populated compared with sparsely populated counties. 27 In British Columbia, South Asians had a threefold higher incidence of PIBD than non-South Asians. Hispanic and Asian children developed ulcerative colitis more often than Crohn’s disease. 26 In a community based healthcare delivery system in northern California, the incidence of ulcerative colitis increased 2.7-fold over a period of 10 years. 25 Australasian data indicate increasing incidence of PIBD, predominantly in children of European ancestry, with lower rates in indigenous populations. 24 People immigrating from low to high prevalence regions are at increased risk for developing IBD, particularly among first generation children. 23 Scotland has seen a 76% increase in diagnosis of PIBD since the mid-1990s, and the diagnosis was made at a younger age. Ontario has one of the highest rates of childhood onset IBD, with an accelerated increase in incidence in younger children. 7Table 1 1 shows the incidence of PIBD worldwide. Rates of PIBD are increasing worldwide, but accurate estimates are lacking. 6 This review summarizes the evidence on disease presentation, diagnostic approach, and treatment options in children aged up to 18 with IBD. 5 The focus of management should be on controlling gut inflammation and optimizing nutrition, growth, and quality of life (QOL), while preventing disease related or treatment related complications. Shortening the time to diagnosis and adherence to diagnostic and therapeutic guidelines should lead to improved clinical outcomes. As the genotypic-phenotypic understanding of IBD advances, customized treatment for individual patients will be developed. 4 Before 2000 the mainstay of treatment was anti-inflammatory drugs and corticosteroids, but now the armamentarium has expanded to immunomodulators and biologics. 1 2 3 The mean delay from onset to diagnosis is 11 months in new onset pediatric IBD (PIBD). IBD that starts in childhood is associated with more extensive disease, higher disease activity, and a more complicated course than adult onset IBD. The incidence and prevalence of inflammatory bowel diseases (IBD) is increasing, and 20-30% of cases present before the age of 20 years. Crohn’s disease and ulcerative colitis are chronic relapsing conditions Crohn’s disease involves the entire gastrointestinal tract from mouth to anus, whereas ulcerative colitis affects only the colon.
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