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Re: Cumulative burden of inflammation predicts colorectal neoplasia risk in ulcerative colitis: a large single-centre study
  1. Yoshinaga Okugawa1,2,3,
  2. Yuji Toiyama1,2,3,
  3. Masato Kusunoki3,
  4. Ajay Goel1,2
  1. 1Center for Gastrointestinal Research, Center for Translational Genomics and Oncology, Baylor Scott & White Research Institute, Baylor University Medical Center, Dallas, Texas, USA
  2. 2Charles A Sammons Cancer Center, Baylor Research Institute, Baylor University Medical Center, Dallas, Texas, USA
  3. 3Division of Reparative Medicine, Department of Gastrointestinal and Pediatric Surgery, Institute of Life Sciences, Graduate School of Medicine, Mie University, Mie, Japan
  1. Correspondence to Professor Ajay Goel, Center for Gastrointestinal Research, Center for Translational Genomics and Oncology, Baylor Scott & White Research Institute and Charles A Sammons Cancer, Baylor University Medical Center, Dallas, TX 75246, USA; ajay.goel{at}baylorhealth.edu

https://doi.org/10.1136/gutjnl-2018-316205

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    In a recent issue of the journal, Choi1 and colleagues have assessed cumulative inflammatory burden (CIB) using endoscopic and histological findings from surveillance colonoscopy, and for the first time have revealed that CIB was significantly associated with the development of colorectal neoplasia (CRN) in patients with UC. This study is an elegant article and very meaningful from a clinical standpoint because the mean severity of microscopic inflammation derived from all surveillance procedures performed in the last decade has suggested it to be an important predictive biomarker for risk stratification of CRN in patients with UC. However, we would like to draw attention to a few important issues related to this very interesting article.

    First, the authors evaluated endoscopic and histological inflammatory scores from the most extreme degree …

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    Footnotes

    • YO and YT contributed equally.

    • Contributors All authors contributed towards writing of this article.

    • Funding The present work was supported by CA72851, CA181572, CA184792, CA187956 and CA202797 grants from the National Cancer Institute, National Institute of Health; RP140784 from the Cancer Prevention Research Institute of Texas; grants from the Sammons Cancer Center and Baylor Foundation; as well as funds from the Baylor Scott & White Research Institute, Dallas, Texas, USA, awarded to AG.

    • Competing interests None declared.

    • Patient consent Not required.

    • Provenance and peer review Not commissioned; internally peer reviewed.

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