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Background: Patients with Crohn's disease can develop intestinal strictures, containing various degrees of inflammation and fibrosis. Differentiation of the main component of a stricturing lesion is the key for defining the therapeutic management., Aims: We assessed for the first time the accuracy of magnetic resonance elastography in detecting intestinal fibrosis and predicting clinical course in patients with Crohn's disease., Methods: This was a prospective study of adult patients with Crohn's disease and magnetic resonance imaging examination, including magnetic resonance elastography, between April 2019 and February 2020. The association between the bowel stiffness value and the degree of fibrosis was evaluated. The relationship between the stiffness value and the occurrence of clinical events was also investigated., Results: A total of 69 patients were included. The stiffness value measured by magnetic resonance elastography was correlated with the degree of fibrosis (p < 0.001). A bowel stiffness ≥ 3.57 kPa predicted the occurrence of clinical events with an area under the curve of 0.82 (95% CI 0.71-0.93). Bowel stiffness ≥ 3.57 kPa was associated with an increased risk of clinical events (p < 0.0001)., Conclusion: In Crohn's disease, magnetic resonance elastography is a reliable tool for detecting intestinal fibrosis and predicting a worse disease outcome., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Patients with inflammatory bowel disease are at increased risk of colorectal cancer, which has worse prognosis than sporadic colorectal cancer. Until recently, understanding of pathogenesis in inflammatory bowel disease-associated colorectal cancer was restricted to the demonstration of chromosomic/microsatellite instabilities and aneuploidy. The advance of high-throughput sequencing technologies has highlighted the complexity of the pathobiology and revealed recurrently mutated genes involved in the RTK/RAS, PI3K, WNT, and TGFβ pathways, leading to potentially new targetable mutations. Moreover, alterations of mitochondrial DNA and the dysregulation of non-coding sequences have also been described, as well as several epigenetic modifications. Although recent studies have brought new insights into pathobiology and raised the prospect of innovative therapeutic approaches, the understanding of colorectal carcinogenesis in inflammatory bowel disease and how it differs from sporadic colorectal cancer remains not fully elucidated. Further studies are required to better understand the pathogenesis and molecular alterations leading to human inflammatory bowel disease-associated colorectal cancer.