Epidemiology and the natural course of inflammatory bowel disease. Gastroenterol Clin North Am 28(vii):255-281
Ulcerative colitis and Crohn's disease are inflammatory disorders of the gastrointestinal tract that are distributed unevenly within populations and throughout the world. Although the exact causes of inflammatory bowel disease (IBD) remain unknown, study of the epidemiology of IBD has provided insight into pathogenesis. This article examines the geographic, ethnic, and other trends of IBD; risk factors (including genetic and environmental); and the natural history of IBD.
Available from: Mohammad Adil
- "Inflammatory bowel disease (IBD) encompasses an array of conditions including chronic inflammation of the mucosal and sub-mucosal layers of the large intestine and rectum        . Intra rectal-administration of acetic acid produces a reproducible laboratory animal model for preclinical evaluation of potential drug candidates for inflammatory bowel disease [8-11] . "
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ABSTRACT: The aim of this study was to evaluate the effect of naringin on experimentally induced inflammatory bowel disease in rats. Naringin (20, 40 and 80 mg/kg) was given orally for 7 days to Wistar rats before induction of colitis by intrarectal instillation of 2 mL of 4% (v/v) acetic acid solution. The degree of colonic mucosal damage was analyzed by examining mucosal damage, ulcer area, ulcer index and stool consistency. Intrarectal administration of 4% acetic acid resulted in significant modulation of serum alkaline phosphatase, lactate dehydrogenase, superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA) and myeloperoxidase (MPO) content along with colonic nitric oxide (NO), xanthine oxidase (XO) level and protein carbonyl content in the colonic tissue as well as in blood. Naringin (40 and 80 mg/kg) exerted a dose dependent (P < 0.05) ameliorative effect, as it significantly increased hematological parameter as well as colonic SOD and GSH. There was a significant (P < 0.05) and dose dependant inhibition of macroscopical score, ulcer area along with colonic MDA, MPO activity by the 7 days of pretreatment of naringin (40 and 80 mg/kg). Biochemical studies revealed a significant (P < 0.05) dose dependant inhibition in serum alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) levels by pretreatment of naringin. Increased levels of colonic NO, XO, protein carbonyl content and DNA damage were also significantly decreased by naringin pretreatment. The findings of the present investigation propose that naringin has an anti-inflammatory, anti-oxidant and anti-apoptotic potential effect at colorectal sites as it modulates the production and expression of oxidative mediators such as MDA, MPO, NO and XO, thus reducing DNA damage.
Available from: Zeljko Krznarić
- "Inflammatory bowel disease (IBD) encompasses Crohn's disease (CD) and ulcerative colitis (UC). Both CD and UC are chronic inflammatory disorders of the gastrointestinal tract with a combined incidence of 2–20 per 100,000 in the developed world . In recent years, considerable progress in the field of IBD genetics has led to identification of a number of genetic factors involved in the pathogenesis of the disease. "
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Inflammatory bowel diseases (IBD) are chronic diseases of unknown etiology and pathogenesis in which genetic factors contribute to development of disease. MDR1/ABCB1 is an interesting candidate gene for IBD. The role of two single nucleotide polymorphisms, C3435T and G2677T remains unclear due to contradictory results of current studies. Thus, the aims of this research were to investigate the association of MDR1 polymorphisms, C3435T and G2677T, and IBD.
A total of 310 IBD patients, 199 Crohn's disease (CD) patients and 109 ulcerative colitis (UC) patients, and 120 healthy controls were included in the study. All subjects were genotyped for G2677T/A and C3435T polymorphism using RT-PCR. In IBD patients, review of medical records was performed and patients were phenotyped according to the Montreal classification.
Significantly higher frequency of 2677T allele (p = 0.05; OR 1.46, 95% CI (1.0-2.14)) and of the 3435TT genotype was observed among UC patients compared to controls (p = 0.02; OR 2.12; 95% CI (1.11-4.03). Heterozygous carriers for C3435T were significantly less likely to have CD (p = 0.02; OR 0.58, 95% CI (0.36-0.91)). Haplotype analysis revealed that carriers of 3435T/2677T haplotype had a significantly higher risk of having UC (p = 0.02; OR 1.55; 95% CI (1.06-2.28)).
MDR1 polymorphisms are associated with both CD and UC with a stronger association with UC.
Available from: Suzanne Devkota
- "Inflammatory bowel diseases, both Crohn’s Disease (CD) and Ulcerative Colitis (UC) are complex immune disorders that clearly exhibit a genetic basis [6, 7]. Genome-wide association studies (GWAS) have shown that many genes correlate with the development of CD and UC, however, not every individual presenting with genetic abnormalities will develop disease. "
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ABSTRACT: The incidence of inflammatory bowel diseases (IBD), as well as other inflammatory conditions, has dramatically increased over the past half century. While many studies have shown that IBD exhibits a genetic component via genome-wide association studies, genetic drift alone cannot account for this increase, and other factors, such as those found in the environment must play a role, suggesting a "multiple hit" phenomenon that precipitates disease. One major environmental factor, dietary intake, has shifted to a high fat, high carbohydrate Western-type diet in developing nations, nearly in direct correlation with the increasing incidence of IBD. Recent evidence suggests that specific changes in dietary intake have led to a shift in the composite human gut microbiota, resulting in the emergence of pathobionts that can thrive under specific conditions. In the genetically susceptible host, the emerging pathobionts can lead to increasing incidence and severity of IBD and other inflammatory disorders. Since the gut microbiota is plastic and responds to dietary modulations, the use of probiotics, prebiotics, and/or dietary alterations are all intriguing complementary therapeutic approaches to alleviate IBD symptoms. However, the interactions are complex and it is unlikely that a one-size-fits all approach can be utilized across all populations affected by IBD. Exploration into and thoroughly understanding the interactions between host and microbes, primarily in the genetically susceptible host, will help define strategies that can be tailored to an individual as we move towards an era of personalized medicine to treat IBD.
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