Laurent Beaugerie1, Magali Svrcek2, Philippe Seksik3, Anne-Marie Bouvier4, Tabassome Simon5, Matthieu Allez6, Hedia Brixi7, Jean-Marc Gornet6, Romain Altwegg8, Philippe Beau9, Bernard Duclos10, Arnaud Bourreille11, Jean Faivre4, Laurent Peyrin-Biroulet12, Jean-François Fléjou2, Fabrice Carrat13. 1. Department of Gastroenterology, AP-HP, Hôpital Saint-Antoine F-75012 and UPMC Univ Paris 06 F-75005, Paris, France. Electronic address: laurent.beaugerie@sat.aphp.fr. 2. Department of Pathology, AP-HP, Hôpital Saint-Antoine F-75012 and UPMC Univ Paris 06 F-75005, Paris, France. 3. Department of Gastroenterology, AP-HP, Hôpital Saint-Antoine F-75012 and UPMC Univ Paris 06 F-75005, Paris, France. 4. Registre Bourguignon des Cancers Digestifs F-21079, INSERM U866, CHRU Dijon, Université de Bourgogne, Bourgogne, France. 5. Clinical Pharmacology Unit, Unité de Recherche Clinique de l'Est Parisien, Assistance Publique-Hôpitaux de Paris, Hôpital Saint Antoine, F-75012, UPMC Univ Paris 06, Paris, France. 6. Department of Gastroenterology, AP-HP, Hôpital Saint-Louis F-75010 and University Paris Diderot F-75010, Paris, France. 7. Department of Gastroenterology and Digestive Oncology, Hôpital Robert-Debré, CHU de Reims, Reims Cedex, France. 8. Department of Hepatogastroenterology, University Hospital St Eloi, Montpellier, France. 9. Department of Hepatogastroenterology, Hôpital Jean Bernard, CHU 86021, Poitiers, France. 10. Department of Gastroenterology, Hôpitaux Universitaires de Strasbourg, Hôpital de Hautepierre F-67098, Universite de Strasbourg F-67000, INSERM U 682 F-67200, Strasbourg France. 11. Institut des Maladies de l'Appareil Digestif (IMAD), Gastroenterology Department, CHU-University Hospital, Nantes, France. 12. INSERM U954 and Department of Hepato-Gastroenterology, University Hospital of Nancy, Université Henri Poincaré 1, Vandoeuvre-lès-Nancy, France. 13. Department of Public Health, Hôpital Saint-Antoine, AP-HP, F-75012 and UMR-S 707, INSERM and UPMC Univ Paris 06 F-75012, Paris, France.
Abstract
BACKGROUND & AIMS: There is an unclear risk of colonic high-grade dysplasia (HGD) and colorectal cancer (CRC) among patients with inflammatory bowel disease (IBD) treated with immunosuppressants. We analyzed data on CRC development among patients with IBD enrolled in the observational cohort Cancers et Surrisque Associé aux Maladies Inflammatoires Intestinales En France (CESAME). METHODS: We followed and collected data from 19,486 patients with IBD (60.3% with Crohn's disease, 30.1% receiving thiopurine therapy) enrolled in CESAME from May 2004 and June 2005, and followed them until December 2007. When the study began, 2841 patients (14.6%) were characterized as having long-standing extensive colitis (ie, >10 years and involving ≥50% of the colon). Early lesions (HGD and CRC) were defined as those diagnosed within 10 years after diagnosis of IBD. RESULTS: Thirty-seven patients developed CRC during the follow-up period, and 20 developed colorectal HGD. The standardized incidence ratios of CRC were 2.2 for all IBD patients (95% confidence interval [CI]: 1.5-3.0; P < .0001), 7.0 for patients with long-standing extensive colitis (95% CI: 4.4-10.5; P < .001), and 1.1 for patients without long-standing extensive colitis (95% CI: 0.6-1.8; P = .84). Among patients with long-standing extensive colitis, the multivariate adjusted hazard ratio for colorectal HGD and cancer was 0.28 for those who received thiopurines compared with those who never received thiopurine therapy (95% CI: 0.1-0.9; P = .03). Twenty-two patients developed early lesions; 7 of these were related to IBD, based on histologic analysis. CONCLUSIONS: Patients with IBD and long-standing extensive colitis are at increased risk for CRC, although the risk is lower among patients receiving thiopurine therapy. Patients without long-standing extensive colitis have a risk for CRC similar to that of the general population, but they can develop IBD-related lesions within 10 years after diagnosis of IBD.
BACKGROUND & AIMS: There is an unclear risk of colonic high-grade dysplasia (HGD) and colorectal cancer (CRC) among patients with inflammatory bowel disease (IBD) treated with immunosuppressants. We analyzed data on CRC development among patients with IBD enrolled in the observational cohort Cancers et Surrisque Associé aux Maladies Inflammatoires Intestinales En France (CESAME). METHODS: We followed and collected data from 19,486 patients with IBD (60.3% with Crohn's disease, 30.1% receiving thiopurine therapy) enrolled in CESAME from May 2004 and June 2005, and followed them until December 2007. When the study began, 2841 patients (14.6%) were characterized as having long-standing extensive colitis (ie, >10 years and involving ≥50% of the colon). Early lesions (HGD and CRC) were defined as those diagnosed within 10 years after diagnosis of IBD. RESULTS: Thirty-seven patients developed CRC during the follow-up period, and 20 developed colorectal HGD. The standardized incidence ratios of CRC were 2.2 for all IBD patients (95% confidence interval [CI]: 1.5-3.0; P < .0001), 7.0 for patients with long-standing extensive colitis (95% CI: 4.4-10.5; P < .001), and 1.1 for patients without long-standing extensive colitis (95% CI: 0.6-1.8; P = .84). Among patients with long-standing extensive colitis, the multivariate adjusted hazard ratio for colorectal HGD and cancer was 0.28 for those who received thiopurines compared with those who never received thiopurine therapy (95% CI: 0.1-0.9; P = .03). Twenty-two patients developed early lesions; 7 of these were related to IBD, based on histologic analysis. CONCLUSIONS:Patients with IBD and long-standing extensive colitis are at increased risk for CRC, although the risk is lower among patients receiving thiopurine therapy. Patients without long-standing extensive colitis have a risk for CRC similar to that of the general population, but they can develop IBD-related lesions within 10 years after diagnosis of IBD.
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