Chai JT, Li XH, Jiang ZS. Euglycemic diabetic ketoacidosis associated with etogliflozin in post-pancreatitis diabetes: A case report. World J Clin Cases 2025; 13(27): 108550 [DOI: 10.12998/wjcc.v13.i27.108550]
Corresponding Author of This Article
Zhao-Shun Jiang, Academic Editor, Chief Physician, Professor, Department of Endocrinology, 960th Hospital of PLA, No. 25 Shifan Road, Tianqiao District, Jinan 250014, Shandong Province, China. jzs012@163.com
Research Domain of This Article
Endocrinology & Metabolism
Article-Type of This Article
Case Report
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 Clin Cases. Sep 26, 2025; 13(27): 108550 Published online Sep 26, 2025. doi: 10.12998/wjcc.v13.i27.108550
Euglycemic diabetic ketoacidosis associated with etogliflozin in post-pancreatitis diabetes: A case report
Jiang-Tao Chai, Xin-Hui Li, Zhao-Shun Jiang
Jiang-Tao Chai, Xin-Hui Li, Zhao-Shun Jiang, Department of Endocrinology, 960th Hospital of PLA, Jinan 250014, Shandong Province, China
Author contributions: Chai JT contributed to the conception, research, and drafting of the work, and approved the final version to be published; Li XH contributed to the research, and drafting of the work, and approved the final version to be published; Jiang ZS contributed to the conception, drafting, and critical revision of the work, and approved the final version to be published; They agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.
Informed consent statement: Informed written consent was obtained from the patient for publication of this report and any accompanying images.
Conflict-of-interest statement: The authors declare that they have no conflict of interest related to this report.
CARE Checklist (2016) statement: The authors have read the CARE Checklist (2016), and the manuscript was prepared and revised according to the CARE Checklist (2016).
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: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Zhao-Shun Jiang, Academic Editor, Chief Physician, Professor, Department of Endocrinology, 960th Hospital of PLA, No. 25 Shifan Road, Tianqiao District, Jinan 250014, Shandong Province, China. jzs012@163.com
Received: April 17, 2025 Revised: May 18, 2025 Accepted: June 24, 2025 Published online: September 26, 2025 Processing time: 110 Days and 18.9 Hours
Abstract
BACKGROUND
Sodium-glucose cotransporter-2 (SGLT-2) inhibitors improve cardiovascular and renal outcomes in diabetes but may induce euglycemic diabetic ketoacidosis (euDKA) via insulin-independent mechanisms. Post-pancreatitis diabetes mellitus (PPDM) patients with impaired β-cell function face undefined risks with these agents.
CASE SUMMARY
A 29-year-old man with PPDM developed euDKA 1 week after initiating etogliflozin (5 mg/day). On admission, laboratory tests revealed blood ketones > 4.5 mmol/L, pH 7.1, and glucose 10.78 mmol/L. Discontinuation of SGLT-2 inhibitor, insulin pump therapy (basal 12 U/day, premeal bolus 4 U), aggressive hydration (6000 mL first 2 days), and nutritional support normalized ketosis and acidosis within 24 hours.
CONCLUSION
Caution is warranted with SGLT-2 inhibitors in PPDM. Insulin therapy is preferred to prevent euDKA.
Core Tip: This is a first report of etogliflozin-induced euglycemic diabetic ketoacidosis (euDKA) in post-pancreatitis diabetes, which highlights risks of sodium-glucose cotransporter-2 (SGLT-2) inhibitors in β-cell compromised patients. Mechanistic analysis suggests that insulin replacement therapy should be prioritized over SGLT-2 inhibitors in post-pancreatitis diabetes mellitus to mitigate euDKA risk.
