P0121 Pp Environmental Risk Factors in Inflammatory Bowel Disease (Ibd): A Pediatric Population-Based Case-Control Study

Baron, S.; Gower, C.; Merle, V.; Leplat, Christophe; Marti, Raymond; Yzet, Thierry; Lerebours, Éric; Dupas, Jean Louis; Debeugny, Stéphane; Salomez, Jean‐Louis; Cortot, A.; Colombel, J.-F.; Turck, Dominique

doi:10.1097/00005176-200406001-00245

Cited by 8 publications

(10 citation statements)

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“…However, this analysis was restricted to children who had no older siblings, although no association was found between those with older siblings as opposed to younger siblings. In contrast, having older, and not younger, siblings for UC was associated with a higher risk for developing the disease [84]. Unfortunately, this study suffered from weak analysis, and data on the effects of having brothers and sisters or having older siblings were not presented, which makes it difficult to assess the role of birth rank.…”

Section: Prenatal and Childhood Factorsmentioning

confidence: 94%

“…Out of a total of 17 published studies, only four studies of CD and four of UC were of high methodological quality [83]. In most cases, the odds ratios did not demonstrate statistical significance, and these studies often suffer from potential recall bias [78,84]. Whether breastfeeding protects against the development of IBD due to its role for priming immunological responses remains unclear.…”

Section: Prenatal and Childhood Factorsmentioning

confidence: 99%

“…CD was more common in those who lived in houses with a hot-water tap during childhood [86], whereas bedroom sharing was a risk factor for UC. Breastfeeding and bacillus Calmette-Guerin vaccination were significant risk factors for CD, but drinking tap water was a protective factor [84]. The role of measles infection or vaccination with mycobacterium infection on risk of IBD remains controversial [78].…”

Section: Prenatal and Childhood Factorsmentioning

confidence: 99%

“…The last two decades have seen tremendous efforts to identify cause, mechanisms and potential cures for the disease. Although few successes have been accomplished, major elements in the intricate pathways leading to the disease remain unclear, and deciphering them presents numerous challenges [78][79][80][81][82][83][84].…”

Section: Decreased Induction/secretion Of Gstsmentioning

confidence: 99%

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Role of genes, the environment and their interactions in the etiology of inflammatory bowel diseases

Ahmed¹

2006

Expert Review of Molecular Diagnostics

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Few of the studied genes demonstrate association with inflammatory bowel disease (IBD). Three mutations in the nucleotide-binding oligomerization domain 2 gene have consistently shown to be independent risk factors for Crohn's disease, but none of the alleles exhibited high sensitivity or specificity for IBD. Linkage analysis implicated several loci on various chromosomes, and epistasis has been demonstrated. The etiopathogenesis of IBD remains unknown, and environmental contribution to their pathogenesis is evident from genetic studies that demonstrated incomplete monozygotic twins concordandance rate for both Crohn's and ulcerative colitis. Smoking has shown an opposite effect on disease phenotype, with an adverse effect on disease course for Crohn's disease, but a slight beneficial effect in ulcerative colitis. The contribution of infectious agents to susceptibility to IBD appears to be strong. However, the role of nutrition on the etiology and therapy of IBD is not clear. Inconsistencies in environmental risk factors could be due to gene-environment interactions, making it essential to study the role of genetics and environmental contribution to the etiopathology of IBD. Transgenic or knockout mice, such as interleukin-10(-/-), T-cell receptor alpha(-/-), Galphai(2) (-/-) and N-cadherin(-/-), develop colitis-like inflammation similar to humans. Therefore, animal models must be further studied to explore mechanistic interactions.

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Section: Prenatal and Childhood Factorsmentioning

confidence: 94%

Section: Prenatal and Childhood Factorsmentioning

confidence: 99%

Section: Prenatal and Childhood Factorsmentioning

confidence: 99%

Section: Decreased Induction/secretion Of Gstsmentioning

confidence: 99%

See 2 more Smart Citations

Role of genes, the environment and their interactions in the etiology of inflammatory bowel diseases

Ahmed¹

2006

Expert Review of Molecular Diagnostics

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“…Baron et al identified breast feeding as being an independent risk factor for the development of paediatric CD. 33 This may work in a number of ways, one of which is to provide the infant with blocking antibody to an array of dietary and microbial antigens and thus reduce both oral tolerance and pathogen exposure at a critical stage of immunological development. Secondly, analysis of the mucosa associated bacteria of patients with active IBD and controls suggests that patients have a reduction in the diversity of intestinal bacteria compared with the control group.…”

Section: Widening the Concept Of Pathogen Exposure In Ibdmentioning

confidence: 99%

Resistance to lamivudine therapy: is there more than meets the eye?

Dusheiko

Bertoletti²

2005

Gut

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Evolving Experimental Platforms to Evaluate Ulcerative Colitis

et al. 2022

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tissue thus altering tissue integrity, anatomy, and physiology subsequently affecting the overall health-related quality of life (HRQoL) of afflicted individuals. [1][2][3] It is estimated that the lifetime financial loss associated with the typical UC patient can be greater than $1 million/patient to cover direct and indirect medical expenses including treatment, hospitalizations, and general medical care. [3][4][5][6][7] As an example, vedolizumab and adalimumab treatment for UC had total direct medical costs of $100 022 and $151 133, respectively, per patient. [8] This number varies greatly depending upon the severity of the disease with a greater expense attributed to those exhibiting a poor clinical disposition. At the domestic level, the total cost to treat UC is estimated to be between $4-14 billion per year which seems to rise on an annual basis. [3,6,7] The specific etiological basis regarding the initiation and progression of UC is currently unknown. Physical manifestations of severe UC take the form of ulcerations affecting the mucosal lining, specifically along the length of the affected large intestine and rectum as depicted in Figure 1. These lesions contain an overabundant accumulation of innate and adaptive immune cells, including T cells, that promote an inflammatory environment Ulcerative colitis (UC) is a multifactorial disease defined by chronic intestinal inflammation with idiopathic origins. It has a predilection to affect the mucosal lining of the large intestines and rectum. Management of UC depends upon numerous factors that include disease pathogenesis and severity that are maintained via medical or surgical means. Chronic inflammation that is left untreated or managed poorly from a clinical stance can result in intestinal ulceration accompanied by resulting physiological dysfunction. End-stage UC is mediated by surgical intervention with the resection of diseased tissue. This can lead to numerous health-related quality of life issues but is considered a curative approach. Regimens to treat UC are ever evolving and find their basis within various platforms to evaluate and treat UC. Numerous modeling systems have been examined to delineate potential mechanisms of action. However, UC is a heterogenous disease spanning unknown genetic origins coupled with environmental factors that can influence disease outcomes and related treatment procedures. Unfortunately, there is no one-size-fits-all model to fully assess all facets of UC. Within the context of this review article, the utility of various approaches that have been employed to gain insight into different aspects of UC will be investigated.

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P0121 Pp Environmental Risk Factors in Inflammatory Bowel Disease (Ibd): A Pediatric Population-Based Case-Control Study

Cited by 8 publications

References 0 publications

Role of genes, the environment and their interactions in the etiology of inflammatory bowel diseases

Role of genes, the environment and their interactions in the etiology of inflammatory bowel diseases

Resistance to lamivudine therapy: is there more than meets the eye?

Evolving Experimental Platforms to Evaluate Ulcerative Colitis

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