2024
Pathogenesis of euglycemic ketoacidosis associated with SGLT2 inhibitors
ŠITINA, Michal a Vladimír ŠRÁMEKZákladní údaje
Originální název
Pathogenesis of euglycemic ketoacidosis associated with SGLT2 inhibitors
Autoři
ŠITINA, Michal (203 Česká republika, domácí) a Vladimír ŠRÁMEK (203 Česká republika)
Vydání
Anesteziologie a intenzivní medicína, Praha, Česká lékařská společnost J.E. Purkyně, 2024, 1214-2158
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
30223 Anaesthesiology
Stát vydavatele
Česká republika
Utajení
není předmětem státního či obchodního tajemství
Odkazy
Impakt faktor
Impact factor: 0.100 v roce 2022
Organizační jednotka
Lékařská fakulta
UT WoS
001284895400003
Klíčová slova anglicky
gliflozins; SGLT2 inhibitors; euglycemic ketoacidosis; hyperchloremic acidosis; diabetes mellitus
Příznaky
Mezinárodní význam, Recenzováno
Změněno: 21. 8. 2024 12:10, Mgr. Tereza Miškechová
Anotace
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.