ŠITINA, Michal and Vladimír ŠRÁMEK. Pathogenesis of euglycemic ketoacidosis associated with SGLT2 inhibitors. Anesteziologie a intenzivní medicína. Praha: Česká lékařská společnost J.E. Purkyně, 2024, vol. 35, No 2, p. 98-103. ISSN 1214-2158. Available from: https://dx.doi.org/10.36290/aim.2024.018.
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Basic information
Original name Pathogenesis of euglycemic ketoacidosis associated with SGLT2 inhibitors
Authors ŠITINA, Michal (203 Czech Republic, belonging to the institution) and Vladimír ŠRÁMEK (203 Czech Republic).
Edition Anesteziologie a intenzivní medicína, Praha, Česká lékařská společnost J.E. Purkyně, 2024, 1214-2158.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 30223 Anaesthesiology
Country of publisher Czech Republic
Confidentiality degree is not subject to a state or trade secret
WWW URL
Impact factor Impact factor: 0.100 in 2022
Organization unit Faculty of Medicine
Doi http://dx.doi.org/10.36290/aim.2024.018
UT WoS 001284895400003
Keywords in English gliflozins; SGLT2 inhibitors; euglycemic ketoacidosis; hyperchloremic acidosis; diabetes mellitus
Tags 14110518, rivok
Tags International impact, Reviewed
Changed by Changed by: Mgr. Tereza Miškechová, učo 341652. Changed: 21/8/2024 12:10.
Abstract
Euglycemic ketoacidosis associated with SGLT2 inhibitors, also referred to as gliflozins, is a rare but potentially fatal clinical entity characterized by metabolic acidosis with normal or only mildly elevated glycemia, predominantly in patients with type 2 diabetes mellitus. In addition to ketoacidosis, hyperchloremic acidosis may also contribute significantly to metabolic acidosis. Relative hypoglycemia induced by gliflozins and concomitant stress condition lead to decreased insulin level and increased glucagon, cortisol, and catecholamines, which stimulates ketogenesis. At the same time, gliflozins induce complex renal metabolic dysfunction, in particular impaired renal elimination of acids and renal ammoniogenesis, resulting in hyperchloremic acidosis. In patients treated with gliflozins, acid-base balance and ketonemia should be checked in a timely manner when their condition worsens. Treatment of acidosis consists of discontinuation of gliflozin and administration of insulin at a dose sufficient to suppress ketogenesis. Because of the risk of acidosis, gliflozins should be discontinued at least 3 days before elective surgery and resumed only after stabilization and reliable restoration of oral intake. Similarly, gliflozins should be discontinued in most hospitalized nonsurgical patients with risk factors for the development of acidosis, such as in patients with acute infection, acute heart disease, stroke, fasting before examination, or alcohol abuse.
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