N Jewel Samadder1, John F Valentine2, Stephen Guthery3, Harminder Singh4, Charles N Bernstein4, Jonathan A Leighton5, Yuan Wan6, Jathine Wong6, Kenneth Boucher7, Lisa Pappas8, Kerry Rowe9, Randall W Burt10, Karen Curtin11, Ken R Smith12. 1. Division of Gastroenterology and Hepatology, Department of Medicine, Mayo Clinic, Phoenix, Arizona; Department of Medicine (Gastroenterology), University of Utah, Salt Lake City, Utah. Electronic address: Samadder.jewel@mayo.edu. 2. Department of Medicine (Gastroenterology), University of Utah, Salt Lake City, Utah. 3. Department of Pediatrics (Gastroenterology), University of Utah, Salt Lake City, Utah. 4. University of Manitoba IBD Clinical and Research Centre, Division of Gastroenterology, Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada. 5. Division of Gastroenterology and Hepatology, Department of Medicine, Mayo Clinic, Phoenix, Arizona. 6. Department of Pedigree and Population Resource, University of Utah, Salt Lake City, Utah; Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah. 7. Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah; Department of Medicine (Epidemiology), University of Utah, Salt Lake City, Utah. 8. Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah. 9. Department of Bioinformatics, Intermountain Healthcare, Salt Lake City, Utah. 10. Department of Medicine (Gastroenterology), University of Utah, Salt Lake City, Utah; Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah; Department of Oncological Sciences, University of Utah, Salt Lake City, Utah. 11. Department of Pedigree and Population Resource, University of Utah, Salt Lake City, Utah; Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah; Department of Medicine (Genetic Epidemiology), University of Utah, Salt Lake City, Utah. 12. Department of Pedigree and Population Resource, University of Utah, Salt Lake City, Utah; Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah; Department of Family and Consumer Studies, University of Utah, Salt Lake City, Utah.
Abstract
BACKGROUND & AIMS: Individuals with inflammatory bowel diseases (IBDs) have an increased risk of developing colorectal cancer (CRC). Although family history of CRC is a well-established risk factor in healthy individuals, its role in patients with IBD is less clear. We aimed to estimate the risk of CRC in a cohort of patients with IBD from Utah and the significance of family history of CRC in a first-degree relative (FDR). METHODS: We identified Utah residents with IBD, using the Intermountain Healthcare and University of Utah Health Sciences databases, from January 1, 1996, through December 31, 2011. CRCs were identified using the Utah Cancer Registry and linked to pedigrees from the Utah Population Database. CRC incidence was compared with that of the state population by standardized incidence ratios (SIRs). RESULTS: A cohort of 9505 individuals with IBD was identified and 101 developed CRC during the study period. The SIR for CRC in patients with Crohn's disease was 3.4 (95% CI, 2.3-4.4), and in patients with ulcerative colitis was 5.2 (95% CI, 3.9-6.6). Patients with IBD and a concurrent diagnosis of primary sclerosing cholangitis had the greatest risk of CRC (SIR, 14.8; 95% CI, 8.3-21.2). A history of CRC in a FDR was associated with a nearly 8-fold increase in risk of CRC in patients with IBD (SIR, 7.9; 95% CI, 1.6-14.3), compared with the state population. CONCLUSIONS: Patients with IBD have a 3- to 5-fold increase in risk of CRC, and those with CRC in a FDR have an almost 8-fold increase in risk. Family history may act as a simple measure to identify individuals with IBD at highest risk for CRC and indicates the need for enhanced surveillance in this population.
BACKGROUND & AIMS: Individuals with inflammatory bowel diseases (IBDs) have an increased risk of developing colorectal cancer (CRC). Although family history of CRC is a well-established risk factor in healthy individuals, its role in patients with IBD is less clear. We aimed to estimate the risk of CRC in a cohort of patients with IBD from Utah and the significance of family history of CRC in a first-degree relative (FDR). METHODS: We identified Utah residents with IBD, using the Intermountain Healthcare and University of Utah Health Sciences databases, from January 1, 1996, through December 31, 2011. CRCs were identified using the Utah Cancer Registry and linked to pedigrees from the Utah Population Database. CRC incidence was compared with that of the state population by standardized incidence ratios (SIRs). RESULTS: A cohort of 9505 individuals with IBD was identified and 101 developed CRC during the study period. The SIR for CRC in patients with Crohn's disease was 3.4 (95% CI, 2.3-4.4), and in patients with ulcerative colitis was 5.2 (95% CI, 3.9-6.6). Patients with IBD and a concurrent diagnosis of primary sclerosing cholangitis had the greatest risk of CRC (SIR, 14.8; 95% CI, 8.3-21.2). A history of CRC in a FDR was associated with a nearly 8-fold increase in risk of CRC in patients with IBD (SIR, 7.9; 95% CI, 1.6-14.3), compared with the state population. CONCLUSIONS:Patients with IBD have a 3- to 5-fold increase in risk of CRC, and those with CRC in a FDR have an almost 8-fold increase in risk. Family history may act as a simple measure to identify individuals with IBD at highest risk for CRC and indicates the need for enhanced surveillance in this population.