This study compares surgical and oncological outcomes in patients with Crohn's disease (CD)-related colorectal cancer (CRC) to those with sporadic CRC.

Patients treated between 1983 and 2013 were matched by stage, age, gender, American Society of Anesthesiologists (ASA), cancer site, and adjuvant chemotherapy.

For stages I and II, 107 patients were matched (58.9% male, mean age 59 years, 59.8% with ASA score 3). Tumor sites included the right (17.7%), transverse (4.7%), left colon (15.9%), and rectum (61.7%). CD patients exhibited longer operative times, higher pT stages, and 2.60 times the odds of postoperative complications (p = 0.03). Overall and disease-free survival were similar. For stage III, 54 patients were matched (57.4% male, mean age 54 years, 46.3% with ASA score 3). The cancer site distribution was right (29.7%), transverse (3.7%), left colon (18.5%), and rectum (48.1%). CD patients had longer operative times, increased blood loss, more involved lymph nodes, higher pT- and pN-stages. The rates of postoperative complications were not different (p = 0.19). CD-related CRC patients had similar overall (p = 0.06), and local recurrence-free survival (p = 0.07).

Despite facing worse perioperative and pathological characteristics, survival differences in stages I-III CD-related CRC compared with sporadic CRC patients were not significantly different.

Surveillance colonoscopies for patients with ulcerative colitis (UC) are necessary to monitor for the development of cancer and its precursor, dysplasia. The management of dysplasia in the setting of UC has been evolving over the past two decades. This is in large part due to higher resolution colonoscopes and development of advanced endoscopic techniques, such as chromoendoscopy, endoscopic mucosal resection, and endoscopic submucosal dissection. Mucosal evaluation, as well as identification and removal of dysplastic tissue, has improved markedly, such that the majority of dysplasia is now considered visible. Whereas previously random biopsies were deemed necessary for surveillance, currently their value is uncertain. Surveillance with high-definition colonoscopes is recommended and consideration of chromoendoscopy is suggested. During colonoscopy, if visible dysplasia is identified and removed completely, continued surveillance is appropriate. If dysplasia is unresectable or there are other high-risk factors such as primary sclerosing cholangitis or multifocality, patients should undergo colectomy. If random biopsies are taken and high-grade dysplasia is identified, that is, invisible dysplasia, patients should similarly consider colectomy. Surgical options include total proctocolectomy with end ileostomy versus ileal pouch-anal anastomosis. Patients undergoing pouch surgery must continue surveillance for dysplasia of the rectal cuff and the pouch. Although surgical management remains an important option for dysplasia in the setting of UC, endoscopic surveillance and resection have improved tremendously, leading to a shift in the overall management strategies for these patients.

The association between inflammatory bowel disease (IBD) and colorectal cancer (CRC) has been widely shown. This association is responsible for 10% to 15% of deaths in patients with IBD, even if according to some studies, the risk of developing CRC seems to be decreased. An adequate surveillance of patients identified as at-risk patients, might improve the management of IBD-CRC risk. In this article we review the literature data related to IBD-CRC, analyze potential risk factors such as severity of inflammation, duration, and extent of IBD, age at diagnosis, sex, family history of sporadic CRC, and coexistent primary sclerosing cholangitis, and update epidemiology on the basis of new studies. Confirmed risk factors for IBD-CRC are severity, extent, and duration of colitis, the presence of coexistent primary sclerosing cholangitis, and a family history of CRC. Current evidence-based guidelines recommend surveillance colonoscopy for patients with colitis 8 to 10 years after diagnosis, further surveillance is decided on the basis of patient risk factors. The classic white light endoscopy, with random biopsies, is now considered unsatisfactory. The evolution of technology has led to the development of new techniques that promise to increase the effectiveness of the monitoring programs. Chromoendoscopy has already proved highly effective and several guidelines suggest its use with a target biopsy. Confocal endomicroscopy and autofluorescence imaging are currently being tested and for this reason they have not yet been considered as useful in surveillance programs.

Patients with long-standing inflammatory bowel disease (IBD) have an increased risk of colorectal cancer (CRC). The association between IBD and CRC is well supported, but reported risk estimates vary widely. Although recent evidence from population-based studies reports a decline in risk, CRC accounts for 10-15% of all deaths in IBD. The potential causes of recent epidemiological trends and the real magnitude of risk of CRC in IBD are subjects of debate. The molecular pathway leading to CRC differs from the classic adenoma-to-CRC sequence. Chronic inflammation contributes to the development of low- and high-grade dysplasia which may further convert into CRC. Patients with a young age at onset, long-standing and extensive colitis with severe inflammatory burden, a family history of sporadic CRC, and concomitant primary sclerosing cholangitis are at greatest risk. The CRC risk in patients with colonic Crohn's disease is similar to that of ulcerative colitis. IBD-associated CRC can frequently be detected at late stages and at a younger age. The long-term prognosis of CRC may be poorer in patients with IBD than in those with sporadic CRC. Regular surveillance colonoscopies may permit earlier detection of CRC, with a corresponding improved prognosis. The interval between surveillance colonoscopies is dependent on each patient's personal risk profile.

Neoplasia complicating ulcerative colitis (UC-neoplasia) is a problem that is poorly addressed by present surveillance techniques. The association of greater than 300 single nucleotide polymorphisms (SNPs) with inflammatory bowel disease (IBD) suggests the possibility that certain genetic polymorphisms might identify patients with UC destined for malignant degeneration. This present study tested the hypothesis that presently known IBD-associated SNPs may correlate with UC-neoplasia.

A total of 41 patients with UC-neoplasia (mean age 56 ± 2.1 years) were identified from our divisional IBD Biobank (low-grade dysplasia n = 13, high-grade dysplasia n = 8, colorectal cancer [CRC] n = 20). These patients were individually age, sex, and disease duration matched with UC patients without neoplasia. Primary sclerosing cholangitis and family history of CRC were recorded. Patients were genotyped for 314 of the most commonly IBD-associated SNPs by a custom SNP microarray. Logistic regression and Fischer exact test were used for statistical analysis.

After Bonferroni correction, none of the 314 IBD-associated SNPs correlated with UC-neoplasia when compared with matched UC controls. The incidence of primary sclerosing cholangitis was greater in the UC-neoplasia group (10/41, 24% vs 3/41, 7%; P = .03) compared with UC controls. The severity of neoplasia (low grade dysplasia versus high grade dysplasia versus CRC) correlated with disease duration (7.9 vs 13.4 vs 20.7 years, respectively).

The lack of correlation between well-known IBD-associated SNPs and UC-neoplasia demonstrated in this study suggests that the development of neoplasia in patients with UC is associated with genetic determinants other than those that predispose to inflammation or results from posttranslational modifications or epigenetic factors rather than germline polymorphisms.