Pathogenesis of euglycemic ketoacidosis associated with SGLT2 inhibitors
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F24%3A00081432" target="_blank" >RIV/00159816:_____/24:00081432 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/00216224:14110/24:00136887
Výsledek na webu
<a href="https://aimjournal.cz/artkey/aim-202402-0002_pathogenesis-of-euglycemic-ketoacidosis-associated-with-sglt2-inhibitors.php?back=%2Fsearch.php?query%3DPost-operative%2Bsleep-disordered%2Bbreathing%2Bwith%2Bdifferent%2Banesthesia%2Btechniques%253A%26sfrom%3D90%26spage%3D30" target="_blank" >https://aimjournal.cz/artkey/aim-202402-0002_pathogenesis-of-euglycemic-ketoacidosis-associated-with-sglt2-inhibitors.php?back=%2Fsearch.php?query%3DPost-operative%2Bsleep-disordered%2Bbreathing%2Bwith%2Bdifferent%2Banesthesia%2Btechniques%253A%26sfrom%3D90%26spage%3D30</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.36290/aim.2024.018" target="_blank" >10.36290/aim.2024.018</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Pathogenesis of euglycemic ketoacidosis associated with SGLT2 inhibitors
Popis výsledku v původním jazyce
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.
Název v anglickém jazyce
Pathogenesis of euglycemic ketoacidosis associated with SGLT2 inhibitors
Popis výsledku anglicky
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.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
30223 - Anaesthesiology
Návaznosti výsledku
Projekt
—
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2024
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Anesteziologie a intenzivní medicína
ISSN
1214-2158
e-ISSN
1805-4412
Svazek periodika
35
Číslo periodika v rámci svazku
2
Stát vydavatele periodika
CZ - Česká republika
Počet stran výsledku
6
Strana od-do
98-103
Kód UT WoS článku
001284895400003
EID výsledku v databázi Scopus
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