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Euglycemic Ketoacidosis in Two Patients Without Diabetes After Introduction of Sodium-Glucose Cotransporter 2 Inhibitor for Heart Failure With Reduced Ejection Fraction.
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- Author(s): Umapathysivam MM;Umapathysivam MM;Umapathysivam MM;Umapathysivam MM;Umapathysivam MM; Gunton J; Gunton J; Gunton J; Stranks SN; Stranks SN; Stranks SN; Jesudason D; Jesudason D; Jesudason D; Jesudason D
- Source:
Diabetes care [Diabetes Care] 2024 Jan 01; Vol. 47 (1), pp. 140-143.- Publication Type:
Case Reports; Journal Article- Language:
English - Source:
- Additional Information
- Source: Publisher: American Diabetes Association Country of Publication: United States NLM ID: 7805975 Publication Model: Print Cited Medium: Internet ISSN: 1935-5548 (Electronic) Linking ISSN: 01495992 NLM ISO Abbreviation: Diabetes Care Subsets: MEDLINE
- Publication Information: Publication: Alexandria Va : American Diabetes Association
Original Publication: New York, American Diabetes Assn. - Subject Terms: Diabetes Mellitus, Type 2*/complications ; Diabetes Mellitus, Type 2*/drug therapy ; Diabetic Ketoacidosis*/chemically induced ; Sodium-Glucose Transporter 2 Inhibitors*/adverse effects ; Ketosis* ; Heart Failure*/drug therapy ; Heart Failure*/complications; Humans ; Hypoglycemic Agents/adverse effects ; Stroke Volume ; Insulin/adverse effects ; Glucose/therapeutic use ; Sodium/adverse effects
- Abstract: Objective: Ketoacidosis induced by sodium-glucose cotransporter 2 inhibitor (SGLT2i) treatment has been consistently observed in clinical practice in patients with type 2 diabetes despite minimal indication from the landmark cardiovascular outcome trials. It has been postulated that individuals without diabetes will not develop this complication due to an adequate insulin secretory capacity, which will protect against significant ketone formation. Cardiovascular outcome trials examining SGLT2i use in individuals with heart failure but not diabetes have not reported ketoacidosis.
Research Design and Methods: We describe the first two case reports of severe nondiabetic ketoacidosis after initiation of an SGLT2i for the treatment of heart failure with reduced ejection fraction, and we describe the management strategies employed and implication for the pathophysiology of SGLT2i-associated ketoacidosis.
Results: Each individual presented with ketoacidosis triggered by reduced oral nutrition intake. For both individuals, ketoacidosis resolved with intravenous glucose administration, encouragement of consumption of oral glucose-containing fluid, and minimal insulin administration.
Conclusions: These two cases demonstrate that SGLT2i-associated ketoacidosis is possible in individuals without diabetes.
(© 2023 by the American Diabetes Association.) - Comments: Comment in: MMW Fortschr Med. 2024 Jun;166(10):26-27. (PMID: 38806910)
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Clin Endocrinol (Oxf). 2023 Mar;98(3):449-451. (PMID: 35234304)
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N Engl J Med. 2020 Oct 8;383(15):1413-1424. (PMID: 32865377)
N Engl J Med. 2017 Jun 8;376(23):2300-2302. (PMID: 28591538) - Accession Number: 0 (Hypoglycemic Agents)
0 (Sodium-Glucose Transporter 2 Inhibitors)
0 (Insulin)
IY9XDZ35W2 (Glucose)
9NEZ333N27 (Sodium) - Publication Date: Date Created: 20231121 Date Completed: 20231222 Latest Revision: 20240529
- Publication Date: 20240529
- Accession Number: PMC10733652
- Accession Number: 10.2337/dc23-1163
- Accession Number: 37988720
- Source:
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