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Fasting blood glucose was linearly associated with colorectal cancer risk in the population without self-reported diabetes mellitus history

Fasting plasma glucose level was linearly associated with colorectal cancer (CRC) risk. However, the dose–response relationship between fasting blood glucose (FBG) and CRC risk was still uncertain. A total of 11,632 patients without self-reported diabetes mellitus and colorectal polyps’ history were...

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Autores principales: Wu, Jingjing, He, Huimin, Zhang, Qi, Zhang, Yan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Lippincott Williams & Wilkins 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8389900/
https://www.ncbi.nlm.nih.gov/pubmed/34449465
http://dx.doi.org/10.1097/MD.0000000000026974
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author Wu, Jingjing
He, Huimin
Zhang, Qi
Zhang, Yan
author_facet Wu, Jingjing
He, Huimin
Zhang, Qi
Zhang, Yan
author_sort Wu, Jingjing
collection PubMed
description Fasting plasma glucose level was linearly associated with colorectal cancer (CRC) risk. However, the dose–response relationship between fasting blood glucose (FBG) and CRC risk was still uncertain. A total of 11,632 patients without self-reported diabetes mellitus and colorectal polyps’ history were identified in the Korean Multicenter Cancer Cohort (1993–2005). The nonlinear relationship was estimated through a restricted cubic spline regression, and a two-piece-wise Cox proportional hazards model was further performed to calculate the threshold effect. Multiple imputation was used to control the bias from missing data. Overall, 1.1% (n = 132) of participants were diagnosed with CRC in the follow-up duration. With a median follow-up duration of 12.0 years, participants with FBG ≥126 mg/dL were associated with higher CRC risk (adjusted hazard ratio [HR], 1.67; 95% confidence interval [CI]: 1.01, 2.76). Landmark analyses limited to long-term survivors demonstrated increased CRC risk with FBG ≥ 126 mg/dL in all subsets (≥3years: HR,1.93 (95% CI: 1.13–3.29); ≥5years: HR, 2.04 (95% CI: 1.–3.63); ≥10years: HR, 2.50 (95% CI: 1.19–5.25)). With FBG smoothly increasing before, the latter increased dramatically after the turning point (P for nonlinearity = 0.283). When FBG was increasing per mmol/L, HR was 1.07(95% CI: 0.90, 1.29) for FBG < 126 mg/dL and 1.27 (95% CI: 1.06, 1.53) for FBG ≥ 126 mg/dL. Besides, HR was 1.09 (95% CI: 1.02, 1.16) for the CRC risk. In the population without self-reported diabetes mellitus and colorectal polyps’ history. FBG was linearly associated with CRC risk, especially for FBG over 126 mg/dL.
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spelling pubmed-83899002021-09-02 Fasting blood glucose was linearly associated with colorectal cancer risk in the population without self-reported diabetes mellitus history Wu, Jingjing He, Huimin Zhang, Qi Zhang, Yan Medicine (Baltimore) 4500 Fasting plasma glucose level was linearly associated with colorectal cancer (CRC) risk. However, the dose–response relationship between fasting blood glucose (FBG) and CRC risk was still uncertain. A total of 11,632 patients without self-reported diabetes mellitus and colorectal polyps’ history were identified in the Korean Multicenter Cancer Cohort (1993–2005). The nonlinear relationship was estimated through a restricted cubic spline regression, and a two-piece-wise Cox proportional hazards model was further performed to calculate the threshold effect. Multiple imputation was used to control the bias from missing data. Overall, 1.1% (n = 132) of participants were diagnosed with CRC in the follow-up duration. With a median follow-up duration of 12.0 years, participants with FBG ≥126 mg/dL were associated with higher CRC risk (adjusted hazard ratio [HR], 1.67; 95% confidence interval [CI]: 1.01, 2.76). Landmark analyses limited to long-term survivors demonstrated increased CRC risk with FBG ≥ 126 mg/dL in all subsets (≥3years: HR,1.93 (95% CI: 1.13–3.29); ≥5years: HR, 2.04 (95% CI: 1.–3.63); ≥10years: HR, 2.50 (95% CI: 1.19–5.25)). With FBG smoothly increasing before, the latter increased dramatically after the turning point (P for nonlinearity = 0.283). When FBG was increasing per mmol/L, HR was 1.07(95% CI: 0.90, 1.29) for FBG < 126 mg/dL and 1.27 (95% CI: 1.06, 1.53) for FBG ≥ 126 mg/dL. Besides, HR was 1.09 (95% CI: 1.02, 1.16) for the CRC risk. In the population without self-reported diabetes mellitus and colorectal polyps’ history. FBG was linearly associated with CRC risk, especially for FBG over 126 mg/dL. Lippincott Williams & Wilkins 2021-08-27 /pmc/articles/PMC8389900/ /pubmed/34449465 http://dx.doi.org/10.1097/MD.0000000000026974 Text en Copyright © 2021 the Author(s). Published by Wolters Kluwer Health, Inc. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/4.0 (https://creativecommons.org/licenses/by/4.0/)
spellingShingle 4500
Wu, Jingjing
He, Huimin
Zhang, Qi
Zhang, Yan
Fasting blood glucose was linearly associated with colorectal cancer risk in the population without self-reported diabetes mellitus history
title Fasting blood glucose was linearly associated with colorectal cancer risk in the population without self-reported diabetes mellitus history
title_full Fasting blood glucose was linearly associated with colorectal cancer risk in the population without self-reported diabetes mellitus history
title_fullStr Fasting blood glucose was linearly associated with colorectal cancer risk in the population without self-reported diabetes mellitus history
title_full_unstemmed Fasting blood glucose was linearly associated with colorectal cancer risk in the population without self-reported diabetes mellitus history
title_short Fasting blood glucose was linearly associated with colorectal cancer risk in the population without self-reported diabetes mellitus history
title_sort fasting blood glucose was linearly associated with colorectal cancer risk in the population without self-reported diabetes mellitus history
topic 4500
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8389900/
https://www.ncbi.nlm.nih.gov/pubmed/34449465
http://dx.doi.org/10.1097/MD.0000000000026974
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