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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