The known colitis-dysplasia-carcinoma sequence allows for gastroenterologist-endoscopists to identify early neoplastic changes and perform maneuvers that will result in improved outcomes for patients. The key maneuvers that can lead to improved cancer-free survival are, firstly, endoscopic removal of dysplasia using standard polypectomy techniques; and, secondly, timely colectomy for patients with insufficiently resected dysplasia. Inadequately described molecular and genetic pathways allow for a more rapid progression of colitis to dysplasia than that described in noncolitis mucosa. Additionally, such progression, in the face of inflamed mucosa, can be difficult to detect and obfuscated to the eye of an endoscopist. As optics continue to improve and endoscopic adjuncts - principally chromoendoscopy with methylene blue or indigo carmine - have been developed, we have the ability to better identify and remove dysplastic lesions from patients with colitis. Thus, while we have the opportunity to change the natural history of low-grade dysplasia (LGD), we must proceed with caution in patients in whom an identifiable lesion is incompletely identified or resected. Patients in whom no specific lesion from which LGD is identified or resected harbor an approximate 20% risk of already having a cancer, and should be referred for colectomy. Patients in whom lesions are identified and removed may continue undergoing surveillance, but should be followed more closely with colonoscopic evaluation every 6 months using scopes and scope systems with the best available optics and chromoendoscopic techniques. This article reviews the available evidence supporting these recommendations.
|Original language||English (US)|
|Number of pages||6|
|Journal||Inflammatory Bowel Disease Monitor|
|State||Published - Dec 1 2010|
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