28 June 2013

Emmanuel Tiret, Saint-Antoine Hospital, Paris Colorectal Disease lecture, presented at ACPGBI Liverpool 2013, 2 July

After 10 years or more of evolution, patients with ulcerative colitis and Crohn’s colitis are at increased risk of developing colorectal cancer (CCR) that is estimated to be 2-5 times greater than the general population. The most important risk factors are the duration and the extent of the disease. The longer the duration of colitis and the more extensive the colonic involvement is, the greater the risk. Other factors which have been showed to be associated at a lesser extent with risk of colorectal cancer in IBD are primary sclerosing cholangitis, young age of disease onset, and family history of colorectal cancer. Preceding CCR, dysplasia is defined as an unequivocal neoplastic change that is intraepithelial and within the confinement of the glandular basement membrane. According to Riddell, several stages can be individualized: no dysplasia, indefinite for dysplasia, low grade dysplasia, high grade dysplasia and colorectal cancer. There are several macroscopic aspects:

1. Flat dysplasia which is detected from random biopsies from unremarkable mucosa in colitis area. Detection can be magnified by chromoendoscopy. It is recommended to perform 2 to 4 biopsies every 10cm in addition to macroscopically atypical lesions, and 33 and 64 biopsies are required to detect dysplasia with a 90% and 95% probability.
2. Raised dysplasia in endoscopically visible lesions, either DALM (dysplasia associated lesion mass) or ALM (associated lesion mass). DALM can be single or multiple polyps, bumps, plaques or velvety patches (image) which are usually unresectable endoscopically. Importantly, they are surrounded by flat dysplasia. DALM is highly associated with the presence of colorectal cancer and is a clear indication for colectomy irrespective of the grade of dysplasia in preoperative biopsies ALM is a well circumscribed polyp, located in diseased mucosa but not surrounded by flat dysplasia. Endoscopic resection should be performed if it is technically feasible, with biopsies of surrounding flat mucosa. If these biopsies do not show any dysplasia, surveillance is a good option. If biopsies in flat surrounding mucosa show some dysplasia, it should be considered as DALM with indication for surgery.
3. Sporadic adenoma, not located in diseased mucosa, not related to development of colitis, should be treated by polypectomy and surveillance.

One of the most difficult questions concerns the management of flat dysplasia, which must be confirmed by two expert pathologists. When flat high grade dysplasia is present, the risk of synchronous colorectal cancer is over 40%, and the risk of progression to CCR is 32%. So, high grade dysplasia confirmed by two different pathologists is an indication for surgery. When biopsies show only flat low grade dysplasia, the risk of synchronous CCR or progression to CRC or high grade dysplasia is 16-34%. In this situation, inter-observer variation is important. So, the choice between surveillance and surgery is difficult. Furthermore, the course of patients developing CCR following initial detection of flat low-grade dysplasia is highly variable in time and severity. Indication of surgery depends on multifocality and repeated low-grade dysplasia on consecutives colonoscopies.

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