Toward an Integrated Clinical, Molecular and Serological Classification of Inflammatory Bowel Disease: Report of a Working Party of the 2005 Montreal World Congress of Gastroenterology

Silverberg, Mark S.; Satsangi, Jack; Ahmad, Tariq; Arnott, Ian; Bernstein, Çharles N.; Brant, Steven R.; Caprilli, R.; Colombel, Jean–Frédéric; Gasché, Christoph; Geboes, Karel; Jewell, D P; Karban, Amir; Loftus, Edward V.; Peña, Amado Salvador; Riddell, Robert H.; Sachar, David B.; Schreiber, Stefan; Steinhart, A. Hillary; Targan, Stephan R.; Vermeire, Séverine; Warren, Bryan F.

doi:10.1155/2005/269076

Cited by 2,978 publications

(2,087 citation statements)

References 47 publications

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“…Disease in each confirmed UC and CD patient was classified according to age of diagnosis, disease location and behaviour using the Montreal Classification system. 16 The control sample set comprised unrelated New Zealand Caucasians, aged over 17 years, who had no history of inflammatory disorders. 17 wild-type NOD2 genotype (all P-values 40.10).…”

Section: Resultsmentioning

confidence: 99%

Evidence of interaction of CARD8 rs2043211 with NALP3 rs35829419 in Crohn's disease

et al. 2010

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The location of CARD8 within an inflammatory bowel disease (IBD) locus and its role in the NALP3 inflammasome and as a nuclear factor (NF)kB inhibitor make it an attractive candidate risk gene for IBD. However, studies testing for the association of the CARD8 loss-of-function single-nucleotide polymorphism (SNP) rs2043211 with IBD have yielded mixed results. A recent study provided evidence that this discordance may result from an interaction of rs2043211 with loss-offunction variants in nucleotide-binding oligomerization domain protein 2 (NOD2) and a gain-of-function SNP (rs35829419) in NALP3. To confirm this interaction, we conducted a replication in an independent IBD sample set (n ¼ 1009 patients, n ¼ 517 controls). We found that the presence of the minor allele of rs2043211 with the major allele of rs35829419 conferred a protective effect against Crohn's disease (and vice versa), which intensified in the absence of NOD2 mutations (P 1,2/1,1 ¼ 0.009, odds ratio (OR) ¼ 0.66, 95% confidence interval (CI) (0.48-0.90); P 1,1/1,2 ¼ 0.015, OR ¼ 0.35, 95% CI (0.15-0.82)). We propose that these genotype combinations protect against gut inflammation by preventing the NALP3 inflammasome from producing excessive interleukin-1b.

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Section: Resultsmentioning

confidence: 99%

Evidence of interaction of CARD8 rs2043211 with NALP3 rs35829419 in Crohn's disease

et al. 2010

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“…A major problem in comparing these studies is the heterogeneity of phenotypic classifications presented, especially with regard to penetrating behavior. Some classification schemes, according to the Vienna classification, include perianal fistulas in fistulizing behavior, whereas others, following the Montreal classification, regard anal involvement as a different entity, separate from intra-abdominal penetrating disease [25,26,[30][31][32][33][34][35][36][37][38].…”

Section: Discussionmentioning

confidence: 99%

CARD15 Mutations and Perianal Fistulating Crohn’s Disease: Correlation and Predictive Value of Antibiotic Response

et al. 2010

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Background CARD15 mutations alter bowel immunity and increase susceptibility to Crohn 0 s disease (CD). However, the relation between these mutations and Crohn 0 s perianal fistulas has not been fully clarified. Aims To assess whether CARD15 mutations are associated with risk of developing Crohn's perianal fistulas and whether these mutations are predictors of the response of perianal fistulas to antibiotics. Methods CARD15 mutations were investigated in 203 consecutive CD patients. Presence/absence of history of perianal fistula was recorded. Patients with history of perianal fistula were divided into two groups (with/without CARD15 mutations), and response to antibiotics was evaluated in both groups. Results Of the 203 patients, 60 (29.6%) showed at least one CARD15 mutation and 55 (27.1%) had history of perianal fistula. History of perianal fistula was identified in 13 (21.7%) patients with mutations and in 42 (29.4%) patients without mutations (P = 0.260). Mean age at diagnosis of first perianal fistula was similar in patients with/without CARD15 mutations (28.7 ± 9.8 versus 29.7 ± 10.1 years, P = 0.758). Average time between disease onset and diagnosis of first perianal fistula was also similar in the two groups (4.6 ± 5.1 versus 5.0 ± 5.9 years, P = 0.816). Response of perianal fistulas to antibiotics (metronidazole alone or combined with ciprofloxacin) was significantly higher in patients without CARD15 mutations (7.7% versus 40.5%, P = 0.041). Conclusions In CD, CARD15 mutations are not associated with risk of developing perianal fistulas or with time of their outbreak. Nevertheless, patients with perianal fistulas and CARD15 mutations showed worse response to antibiotics.

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“…Eligible patients included men and women at least 18 years of age with an established diagnosis of UC according to standard criteria [24]. All patients were classified according to the "Montreal Classification" [25] and had to have active disease, defined as a partial Mayo score ≥2 points [4,26], despite concomitant treatment. ADA induction and maintenance regimen, the need for dose escalation and timing of treatment discontinuation were left to the investigators' judgement, as well as concomitant medications including oral and topical aminosalicylates, steroids and immunosuppressants.…”

Section: Methodsmentioning

confidence: 99%

Adalimumab in active ulcerative colitis: A “real-life” observational study

Armuzzi¹,

Biancone²,

Daperno³

et al. 2013

Digestive and Liver Disease

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a b s t r a c tBackground and aims: The effectiveness of adalimumab in the treatment of ulcerative colitis is under debate. Although controlled trials have shown that adalimumab is significantly better than placebo, the absolute clinical benefit is modest. We report data on the effectiveness of adalimumab in a cohort of ulcerative colitis patients treated in 22 Italian centres. Methods: All patients with active disease treated with adalimumab were retrospectively reviewed. Coprimary endpoints were clinical remission at weeks 4, 12, 24 and 54. Secondary endpoints were sustained clinical remission, steroid discontinuation, endoscopic remission and need for colectomy. Results: Eighty-eight patients were included. Most patients had received previous infliximab treatment. Clinical remission rates were 17%, 28.4%, 36.4% and 43.2% at 4, 12, 24 and 54 weeks respectively. Twentytwo patients required colectomy. Clinical remission and low C-reactive protein at week 12 predicted clinical remission at week 54 (OR 4.17, 95% CI 2.36-19.44; OR 2.63, 95% CI 2.32-14.94, respectively). Previous immunosuppressant use was associated with a lower probability of clinical remission at week 54 (OR 0.67, and with a higher rate of colectomy (HR 9.7, 95% CI 1.46-9.07). Conclusion: In this large "real-life" experience adalimumab appears effective in patients with otherwise medically refractory ulcerative colitis. Patients achieving early remission can expect a better long-term outcome.

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Toward an Integrated Clinical, Molecular and Serological Classification of Inflammatory Bowel Disease: Report of a Working Party of the 2005 Montreal World Congress of Gastroenterology

Cited by 2,978 publications

References 47 publications

Evidence of interaction of CARD8 rs2043211 with NALP3 rs35829419 in Crohn's disease

Evidence of interaction of CARD8 rs2043211 with NALP3 rs35829419 in Crohn's disease

CARD15 Mutations and Perianal Fistulating Crohn’s Disease: Correlation and Predictive Value of Antibiotic Response

Adalimumab in active ulcerative colitis: A “real-life” observational study

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