J 2024

Pathogenesis of euglycemic ketoacidosis associated with SGLT2 inhibitors

ŠITINA, Michal a Vladimír ŠRÁMEK

Základní 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

Štítky

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.