Inflammatory polyps occur more frequently in inflammatory bowel disease than other colitis patients

Abstract

Background Colitis is generally considered a risk factor for colon neoplasia. However, not all types of colitis seem to have equal neoplastic transformation potential. Aim To determine the prevalence of colorectal polyps in a predominantly African American population with inflammatory bowel disease (IBD) and Non-IBD/Non-Infectious Colitis (NIC). Methods We retrospectively evaluated medical records of 1060 patients previously identified with colitis at Howard University Hospital, based on ICD-10 code. Among these, 485 patients were included in the study: 70 IBD and 415 NIC based on a thorough review of colonoscopy, pathology and clinical reports. Logistic regression analysis was applied to estimate the risk of polyps in patients with IBD compared to those with NIC after adjusting for age and sex. A subgroup analysis within the IBD group was performed. Results Of the 485 patients, 415 were NIC and 70 were IBD. Seventy-three percent of the NIC patients and 81% of the IBD patients were African Americans. Forty six percent of IBD and 41% of NIC cases were male. IBD patients were younger than NIC patients (median age of 38 years vs. 50, P < 0.001). The prevalence of all types of polyps was 15.7 and 8.2% in the IBD and NIC groups, respectively (P = 0.045). Among patients with polyps, the prevalence of inflammatory polyps was higher in the IBD group (55%) compared to the NIC group (12%). After adjusting for age, sex and race, odds ratio of inflammatory polyps in IBD patients was 6.0 (P = 0.016). Adenoma prevalence was 4.3% (3/70) in IBD patients and 3.9% (16/415) in the NIC patients (p = 0.75). The anatomic distribution of lesions and colitis shows that polyps occur predominantly in the colitis field regardless of colitis type. More polyps were present in the ulcerative colitis patients when compared to Crohn’s disease patients (27% vs. 5%, P < 0.001) within the IBD group. Conclusion Our study shows that inflammatory polyps are more common in IBD patients when compared to NIC patients. Most polyps were in the same location as the colitis.

Association between Endometrial Polyps and Chronic Endometritis: Is It Time for a Paradigm Shift in the Pathophysiology of Endometrial Polyps in Pre-Menopausal Women? Results of a Systematic Review and Meta-Analysis

“…Chronic inflammation has been identified as a causative factor in the development of polyps in different mucosal tissues across the human body (i.e., urinary tract, upper respiratory tract and lower gastrointestinal tract) [ 47 , 48 , 49 ]. With regard to EPs, a potential inflammation-driven pathogenesis has been long neglected by the scientific community.…”

Formation of benign tumors by stem cell deregulation

“…Such benign tumors would originate from deregulated intestinal SCs, while these deregulated intestinal SCs would show increased proliferation relative to homeostatically-regulated intestinal SCs, and would thus have increased chances of gaining new genetic and epigenetic changes, and of further evolving towards cancer. In support of this view, it was proposed that intestinal cancers originate from intestinal SCs that, through acquiring changes, escaped from normal regulation [ 96 ], while patients inflicted with inflammatory bowel diseases have a greater risk of developing polyps [ 97 ], and colon cancers [ 98 ]. This idea of a progression from a normal intestinal SC to a benign tumor (adenoma) generating intestinal SC finds a strong support in lineage tracing studies performed in the mouse intestine and human colon [ 2 , 99 ].…”

Research progress on the carcinogenesis mechanism of inflammation in ulcerative colitis: a narrative review

“…Patients with UC are prone to colorectal cancer and dysplastic polyps, as well as sporadic adenomas (7). Previous studies have assessed the incidence of dysplastic lesions in UC patients and found that the incidence of adenomatous polyps in IBD is extremely low, only about 2% (19,20). This may be due to the beneficial protection of chemical drugs in UC and the inhibition of the inflammatory process of UC in adenoma development (21).…”