Detailed Information on Publication Record
2024
Pathogenesis of euglycemic ketoacidosis associated with SGLT2 inhibitors
ŠITINA, Michal and Vladimír ŠRÁMEKBasic 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
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
30223 Anaesthesiology
Country of publisher
Czech Republic
Confidentiality degree
není předmětem státního či obchodního tajemství
References:
Impact factor
Impact factor: 0.100 in 2022
Organization unit
Faculty of Medicine
UT WoS
001284895400003
Keywords in English
gliflozins; SGLT2 inhibitors; euglycemic ketoacidosis; hyperchloremic acidosis; diabetes mellitus
Tags
International impact, Reviewed
Změněno: 21/8/2024 12:10, Mgr. Tereza Miškechová
Abstract
V originále
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.