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Pathogenesis of euglycemic ketoacidosis associated with SGLT2 inhibitors
Autoři | |
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Rok publikování | 2024 |
Druh | Článek v odborném periodiku |
Časopis / Zdroj | Anesteziologie a intenzivní medicína |
Fakulta / Pracoviště MU | |
Citace | |
www | https://www.aimjournal.cz/en/artkey/aim-202402-0002_pathogenesis-of-euglycemic-ketoacidosis-associated-with-sglt2-inhibitors.php?l=en |
Doi | http://dx.doi.org/10.36290/aim.2024.018 |
Klíčová slova | gliflozins; SGLT2 inhibitors; euglycemic ketoacidosis; hyperchloremic acidosis; diabetes mellitus |
Popis | 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. |