Yim C, Mansell K, Hussein N, Arnason T. Current cancer therapies and their influence on glucose control. World J Diabetes 2021; 12(7): 1010-1025 [PMID: 34326951 DOI: 10.4239/wjd.v12.i7.1010]
Corresponding Author of This Article
Terra Arnason, FRCPC, MD, Academic Research, Doctor, Professor, Departments of Anatomy and Cell Biology and Medicine, Division of Endocrinology, University of Saskatchewan, Room 3654 Royal University Hospital 103 Hospital Drive, Saskatoon S7N 0W8, Saskatchewan, Canada. terra.arnason@usask.ca
Research Domain of This Article
Endocrinology & Metabolism
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Diabetes. Jul 15, 2021; 12(7): 1010-1025 Published online Jul 15, 2021. doi: 10.4239/wjd.v12.i7.1010
Current cancer therapies and their influence on glucose control
Carly Yim, Kerry Mansell, Nassrein Hussein, Terra Arnason
Carly Yim, Department of Medicine, University of Saskatchewan, Saskatoon S7N 0W8, Saskatchewan, Canada
Kerry Mansell, College of Pharmacy and Nutrition, University of Saskatchewan, Saskatoon S7N 5E5, Saskatchewan, Canada
Nassrein Hussein, Department of Medicine, Division of Endocrinology, University of Saskatchewan, Saskatoon S7N 0W8, Saskatchewan, Canada
Terra Arnason, Departments of Anatomy and Cell Biology and Medicine, Division of Endocrinology, University of Saskatchewan, Saskatoon S7N 0W8, Saskatchewan, Canada
Author contributions: Yim C, Mansell K, Hussein N and Arnason T contributed to the research and writing of distinct sections of the paper; Arnason T and Mansell K edited the manuscript.
Conflict-of-interest statement: Authors declare no conflict of interests for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Terra Arnason, FRCPC, MD, Academic Research, Doctor, Professor, Departments of Anatomy and Cell Biology and Medicine, Division of Endocrinology, University of Saskatchewan, Room 3654 Royal University Hospital 103 Hospital Drive, Saskatoon S7N 0W8, Saskatchewan, Canada. terra.arnason@usask.ca
Received: February 7, 2021 Peer-review started: February 7, 2021 First decision: March 16, 2021 Revised: April 11, 2021 Accepted: June 25, 2021 Article in press: June 25, 2021 Published online: July 15, 2021 Processing time: 154 Days and 10.4 Hours
Core Tip
Core Tip: Immune checkpoint inhibitors (ICI) rarely cause hyperglycemia, but glucose monitoring from their initiation is critical as rapid diabetic ketoacidosis can develop from underlying immune-mediated pancreatic beta-cell destruction. Therapy with mammalian target of rapamycin (mTOR) inhibitors, 5-fluorouracil (5-FU)-analogs and glucocorticoids have higher rates of hyperglycemia early in therapy that is not generally severe, but needs to be recognized and treated to optimize patient outcomes. The hyperglycemia occurring from the 5-FU and ICI classes is not reversible. The diabetes from ICIs arises from an absolute insulin deficiency vs the partial deficiency from the 5-FU class. Glucocorticoids and mTOR inhibitors predominantly cause insulin resistance.
