Background and study aims: Despite ample research on the dysplasia to carcinoma risk in ulcerative colitis, there are scant data on the prevalence of adenomatous polyps in this population.
Methods: The number and histology of all polyps detected at colonoscopies of ulcerative colitis patients aged > 50 during 2006 – 2012 were compared with similarly aged controls undergoing screening colonoscopy.
Results: There were 206 patients with ulcerative colitis and 624 controls included in the study (mean age 61.7 ± 8.7 vs. 60.8 ± 6.1, respectively; P = 0.15). Adenomatous polyps were detected in only 13/206 colonoscopies for ulcerative colitis compared with 162 /624 controls (6.3 % vs. 25.9 %, respectively; odds ratio [OR] 0.19, 95 % confidence interval [CI] 0.1 – 0.34; P < 0.0001). When also considering all prior colonoscopies performed over 7.7 ± 4.6 years of follow-up (mean 4.1 ± 2.9 colonoscopies/patient, range 1 – 15, total 832 colonoscopies), the risk of ever finding an adenoma in ulcerative colitis patients was still significantly lower compared with controls (14.1 % vs. 25.9 %, respectively; OR 0.47, 95 %CI 0.3 – 0.72; P = 0.0005). On multivariable analysis, adenomas were positively associated with advanced age (OR 1.07/year, 95 %CI 1.03 – 1.1; P < 0.0001) and with increasing body mass index (BMI; OR 1.06/kg/m2, 95 %CI 1.01 – 1.1; P = 0.01) and negatively associated with having ulcerative colitis (OR 0.15, 95 %CI 0.09 – 0.44; P = 0.0005). Among 115 Crohn’s disease patients aged > 50 years, the rate of ever-adenomas in small-bowel Crohn’s disease was similar to the controls (P = 0.8) and not influenced by 5-aminosalicylic acid use, whereas patients with colonic Crohn’s disease had a significantly lower rate of adenomas compared with the controls (3.9 % vs. 25.9 %; P = 0.002).
Conclusion: Unlike patients with small-bowel Crohn’s disease, patients with ulcerative colitis or with colonic Crohn’s disease seldom develop sporadic adenomatous polyps. These data may provide novel clues to a possible role for colonic immune activation in restricting the adenoma to carcinoma sequence while propagating the dysplasia to carcinoma pathway.
