Razok A, Ata F, Ahmed SMI, Al Mohanadi DHSH. Sodium-glucose co-transporter 2 inhibitors induced euglycemic diabetic ketoacidosis within four days of initiation. World J Diabetes 2022; 13(3): 272-274 [PMID: 35432760 DOI: 10.4239/wjd.v13.i3.272]
Corresponding Author of This Article
Fateen Ata, BSc, MBBS, MD, Doctor, Department of Internal Medicine, Hamad Medical Corporation, Al Rayyan Street, Bin Omran Area, Al Rayyan, Doha 3050, Qatar. docfateenata@gmail.com
Research Domain of This Article
Endocrinology & Metabolism
Article-Type of This Article
Letter to the Editor
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. Mar 15, 2022; 13(3): 272-274 Published online Mar 15, 2022. doi: 10.4239/wjd.v13.i3.272
Sodium-glucose co-transporter 2 inhibitors induced euglycemic diabetic ketoacidosis within four days of initiation
Almurtada Razok, Fateen Ata, Sara Mohamed Ibrahim Ahmed, Dabia Hamad S H Al Mohanadi
Almurtada Razok, Fateen Ata, Sara Mohamed Ibrahim Ahmed, Dabia Hamad S H Al Mohanadi, Department of Internal Medicine, Hamad Medical Corporation, Doha 3050, Qatar
Dabia Hamad S H Al Mohanadi, Department of Endocrinology, Hamad Medical Corporation, Doha 3050, Qatar
Author contributions: Razok A, Ata F, and Ahmed SMI wrote the letter; Al Mohanadi DHSH revised the letter.
Conflict-of-interest statement: The authors have no actual or potential conflict of interest to declare.
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: Fateen Ata, BSc, MBBS, MD, Doctor, Department of Internal Medicine, Hamad Medical Corporation, Al Rayyan Street, Bin Omran Area, Al Rayyan, Doha 3050, Qatar. docfateenata@gmail.com
Received: September 6, 2021 Peer-review started: September 6, 2021 First decision: December 4, 2021 Revised: December 5, 2021 Accepted: February 10, 2022 Article in press: February 10, 2022 Published online: March 15, 2022 Processing time: 189 Days and 20.7 Hours
Abstract
Euglycemic diabetic ketoacidosis (EDKA) is a well-known complication of sodium-glucose co-transporter 2 inhibitors, and many cases with variable onset following the initiation of these agents are reported before, with a median onset of approximately 2 wk. This letter discusses a 45-year-old lady who initially presented with ischemic stroke but developed EDKA 4 d after starting empagliflozin, a rare occurrence. The patient had severe metabolic acidosis that necessitated admission into the intensive care unit. Prompt discontinuation of empagliflozin and DKA management resulted in clinical recovery.
Core Tip: With a steady surge in the prescription of sodium-glucose co-transporter 2 inhibitors (SGLT2-i) in medical conditions including type 2 diabetes mellitus (DM), type 1 DM, and heart failure, there are increasingly reported cases of euglycemic diabetic ketoacidosis (EDKA) with their use. EDKA in the context of SGLT2-i use is reported in various patients with different precipitating factors, some even with no inciting event. One of the rarely reported inciting events is stroke. Another aspect of SGLT2-i induced EDKA which remains relatively less understood is the time of initiation of the drug to the development of EDKA. In our patient, severe EDKA developed within 4 d of empagliflozin initiation, necessitating intensive care and discontinuation of empagliflozin, resulting in complete recovery regarding the EDKA.
