Surveillance and management of colorectal dysplasia and cancer in inflammatory bowel disease: Current practice and future perspectives

Abstract

Patients with inflammatory bowel disease (IBD) are at increased risk of developing colorectal cancer (CRC). Current guidelines recommend frequent surveillance colonoscopies for patients with at least left-sided ulcerative colitis, or Crohn's disease involving more than 30% of the colon. Surveillance allows for early detection and treatment of colorectal dysplasia and cancer. The first colonoscopy should be performed 8 to 10 years after onset of disease symptoms. European and British guidelines employ a risk-stratification algorithm that assigns patients to surveillance intervals of one, three or five years, whereas American guidelines recommend to perform surveillance every 1 to 3 years based on the (combined) presence of risk factors. Patients with concomitant primary sclerosing cholangitis are at an additionally increased risk, and should undergo annual surveillance starting immediately after the diagnosis. The current practice of surveillance is based on limited evidence, is resource intensive and cannot preclude the occurrence of interval carcinomas. Fortunately, advances in endoscopic techniques for mucosal visualisation, along with better control of inflammation, have resulted in a declining incidence of CRC in patients with IBD. Furthermore, advanced endoscopic resection techniques can be expected to result in a shift from surgical to endoscopic management of dysplastic lesions. In this review, we provide an up-to-date overview of colitis-associated CRC pathophysiology, epidemiology, surveillance practices, and management of dysplasia.

The Role of Diet and Lifestyle in Early-Onset Colorectal Cancer: A Systematic Review

“…The risk factors discussed so far are modifiable, but others are not. Well-established non-modifiable risk factors include age, family history, race, and hereditary gastrointestinal syndromes [ 120 , 121 , 122 , 123 , 124 , 125 , 126 , 127 ]. The combination of a congenital (un-modifiable) predisposition with the exposure to environmental (modifiable) risk factors, especially at a young age [ 128 ], can increase the risk of CRC to a greater extent than each factor alone through various mechanisms, including epigenetic changes and intestinal dysbiosis.…”

“…The interplay between genetic and environmental factors remains elusive. Most hereditary CRC syndromes display a consistent variability in terms of penetrance and expressivity [ 121 , 122 , 123 , 124 , 125 , 126 , 127 ]. Some have suggested that diet could explain, at least in part, this degree of variability [ 201 , 202 , 203 ].…”

Colorectal Cancer Surveillance in Patients with Inflammatory Bowel Diseases: Chromoendoscopy or Non-Chromoendoscopy, That Is the Question

“…The turning point that probably narrowed the gap of the detection yield between DCE and WLE is the introduction of HD system [64]. Indeed, the advent of HD colonoscopy raised questions about the redundancy of DCE due the fact that the majority of dysplasia is visible with HD [27,73]. DCE also displays the limits of a longer examination time, the need for supplementary training, and may be considered impractical by the physicians [73].…”

Stemness, Inflammation and Epithelial–Mesenchymal Transition in Colorectal Carcinoma: The Intricate Network

“…Inflammation has a well-known role in tumour pathogenesis. Regarding colorectal carcinoma, long-standing inflammatory bowel disease, including both Crohn’s disease and ulcerative colitis, is associated with a 1.4- to 2.2-fold increased risk of colorectal carcinoma [ 15 ]. In an already established tumour, the intensity or cellular composition of inflammation can have prognostic importance, and inflammation is also involved in generation of pre-metastatic niches [ 16 , 17 ].…”