Can dysplasia surveillance be better targeted in ulcerative colitis by using faecal calprotectin?

Abstract

Background: In the inflammatory bowel diseases, chronic inflammation predisposes to dysplasia and colorectal carcinoma, leading to the need of surveillance colonoscopies. The most-used marker of colonic inflammation is faecal calprotectin. Its correlation with endoscopic and histological findings is well-documented. In this study, we evaluated the role of sequential faecal calprotectin measurements in predicting colorectal dysplasia, to identify patients with increased risk of dysplasia or colonic malignancy in ulcerative colitis.

Methods: We collected the faecal calprotectin measurements and colorectal histology reports of patients with ulcerative colitis treated in Helsinki University Hospital (Helsinki, Finland) between 2007 and 2017, with a focus on IBD-associated neoplasia, inflammatory activity, and sporadic adenomas. Using the time-weighted AUC of faecal calprotectin as a marker of inflammatory burden, we tested the performance of faecal calprotectin to predict the risk for colorectal neoplasia.

Results: In total, 982 patients with ulcerative colitis were included. Of them, 845 had pancolitis and 127 concomitant primary sclerosing cholangitis. Forty-one patients (4%) had IBD-associated colorectal dysplasia and seven (0.7%) developed adenocarcinoma. In patients with constantly elevated faecal calprotectin level (>500 µg/g), colorectal neoplasia was more frequent compared to those with low (<200 µg/g) calprotectin (13% and 4%, p < 0.05). Histological inflammatory activity was also related to more frequent dysplastic changes.

Conclusions: Colon dysplasia and adenocarcinoma are more common among ulcerative colitis patients with constantly elevated faecal calprotectin than in patients in remission. The role of inflammatory activity in inducing neoplastic changes in colon is further supported by histology, as histological inflammatory activity correlates with dysplasia.

Keywords:

• Inflammatory bowel disease
• colonoscopy
• dysplasia
• neoplasia
• surveillance
• calprotectin

Acknowledgements

No additional writing assistance was used for this manuscript. AMP and MF contributed to the design of the study. AMP, TV, JA, and AM collected data. AMP, SQ, SH, AM and SK analysed the data. AMP, SQ, KLK and MF drafted the manuscript. All authors critically revised the manuscript for important intellectual content. All authors approved the final version of this manuscript.

Disclosure statement

The authors report there are no competing interests to declare.

Data availability statement

The data underlying this article are available in the article.

Additional information

Funding

This work was supported by the Mary and George Ehrnrooth’s Foundation [grant number 202010018] and a grant from the Helsinki University Hospital Research Fund [TYH2015405].