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Original research
Optimal glycaemic control and the reduced risk of colorectal adenoma and cancer in patients with diabetes: a population-based cohort study
  1. Xianhua Mao1,
  2. Ka Shing Cheung1,2,
  3. Jing-Tong Tan1,
  4. Lung-Yi Mak1,
  5. Chi-Ho Lee1,
  6. Chi-Leung Chiang3,
  7. Ho Ming Cheng1,
  8. Rex Wan-Hin Hui1,
  9. Man Fung Yuen1,
  10. Wai Keung Leung1,
  11. Wai-Kay Seto1,2
  1. 1Department of Medicine, The University of Hong Kong, Hong Kong, Hong Kong
  2. 2Department of Medicine, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China
  3. 3Department of Clinical Oncology, The University of Hong Kong, Hong Kong, Hong Kong
  1. Correspondence to Dr Ka Shing Cheung, Department of Medicine, The University of Hong Kong, Hong Kong 999077, Hong Kong; cks634{at}hku.hk; Prof Wai-Kay Seto; wkseto{at}hku.hk

Abstract

Objective Whether varying degrees of glycaemic control impact colonic neoplasm risk in patients with diabetes mellitus (DM) remains uncertain.

Design Patients with newly diagnosed DM were retrieved from 2005 to 2013. Optimal glycaemic control at baseline was defined as mean haemoglobin A1c (HbA1c)<7%. Outcomes of interest included colorectal cancer (CRC) and colonic adenoma development. We used propensity score (PS) matching with competing risk models to estimate subdistribution HRs (SHRs). We further analysed the combined effect of baseline and postbaseline glycaemic control based on time-weighted mean HbA1c during follow-up.

Results Of 88 468 PS-matched patients with DM (mean (SD) age: 61.5 (±11.7) years; male: 47 127 (53.3%)), 1229 (1.4%) patients developed CRC during a median follow-up of 7.2 (IQR: 5.5–9.4) years. Optimal glycaemic control was associated with lower CRC risk (SHR 0.72; 95% CI 0.65 to 0.81). The beneficial effect was limited to left-sided colon (SHR 0.71; 95% CI 0.59 to 0.85) and rectum (SHR 0.71; 95% CI 0.57 to 0.89), but not right-sided colon (SHR 0.86; 95% CI 0.67 to 1.10). Setting suboptimal glycaemic control at baseline/postbaseline as a reference, a decreased CRC risk was found in optimal control at postbaseline (SHR 0.79), baseline (SHR 0.71) and both time periods (SHR 0.61). Similar associations were demonstrated using glycaemic control as a time-varying covariate (HR 0.75). A stepwise greater risk of CRC was found (Ptrend<0.001) with increasing HbA1c (SHRs 1.34, 1.30, 1.44, 1.58 for HbA1c 7.0% to <7.5%, 7.5% to <8.0%, 8.0% to <8.5% and ≥8.5%, respectively). Optimal glycaemic control was associated with a lower risk of any, non-advanced and advanced colonic adenoma (SHRs 0.73–0.87).

Conclusion Glycaemic control in patients with DM was independently associated with the risk of colonic adenoma and CRC development with a biological gradient.

  • POLYP
  • DIABETES MELLITUS
  • COLORECTAL ADENOMAS
  • COLORECTAL CANCER

Data availability statement

Data may be obtained from a third party and are not publicly available.

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Data availability statement

Data may be obtained from a third party and are not publicly available.

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Footnotes

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  • Contributors Study concept and design: XM, KSC and W-KS. Data acquisition: XM, KSC and J-TT. Data analysis: XM, KSC and W-KS. Data interpretation: XM, C-LC, RW-H, WKL and W-KS. Manuscript draft: XM, KSC and W-KS. Data analysis plan and data management: XM. Critical revision of manuscript: KSC, C-HL, L-YM, WKL, MFY and W-KS. Overall study supervision: KSC and W-KS. All authors participated in the preparation of the manuscript and have seen and approved the final version.

  • Funding Bau Tsu Zung Bau Kwan Yeu Hing Research and Clinical Fellowship, The University of Hong Kong.

  • Competing interests C-LC received research funding from AstraZeneca, Merck KGaA and Taiho. L-YM is an advisory board member of Gilead Sciences. WKL received speaker’s fees from AbbVie, Ferring Pharmaceuticals and Janssen. MFY received research funding from Assembly Biosciences, Arrowhead Pharmaceuticals, Bristol Myer Squibb, Fujirebio Incorporation, Gilead Sciences, Merck Sharp and Dohme, Springbank Pharmaceuticals, Sysmex, Roche and is an advisory board member and/or received research funding from AbbVie, Aligos therarpeutics, Arbutus Biopharma, Bristol Myer Squibb, Dicerna Pharmaceuticals, Finch Therapeutics, GlaxoSmithKline, Gilead Sciences, Janssen, Merck Sharp and Dohme, Clear B Therapeutics, Springbank Pharmaceuticals, Roche. W-KS received speaker’s fees from AstraZeneca, is an advisory board member and received speaker’s fees of Abbott, received research funding from Alexion Pharmaceuticals, Boehringer Ingelheim, Pfizer and Ribo Life Science, and is an advisory board member, received speaker’s fees and researching funding from Gilead Sciences. The other authors have nothing to disclose.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

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

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