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经典糖尿病酮症酸中毒与正常血糖变异型:旧中有新。

Classic diabetic ketoacidosis and the euglycemic variant: Something old, something new.

作者信息

Mehta Adi E, Zimmerman Robert

机构信息

Department of Endocrinology, Diabetes, and Metabolism, Cleveland Clinic, Cleveland, OH; Clinical Assistant Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Department of Endocrinology, Diabetes, and Metabolism, Cleveland Clinic, Cleveland, OH; Clinical Assistant Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH.

出版信息

Cleve Clin J Med. 2025 Jan 2;92(1):33-39. doi: 10.3949/ccjm.92a.24075.

DOI:10.3949/ccjm.92a.24075
PMID:39746727
Abstract

Diabetic ketoacidosis (DKA) was historically considered a condition typical of type 1 diabetes. However, patients with type 2 diabetes may present with DKA, usually with higher blood glucose levels and milder ketoacidosis. With the increased use of sodium-glucose cotransporter 2 (SGLT-2) inhibitors, the variant euglycemic DKA has been described. SGLT-2 inhibitors cause a low level of ambient ketones; any additional ketone formation predisposes to ketoacidosis, while the agent's glycosuric effect limits hyperglycemia. The principles of DKA management are fluid administration, electrolyte control, and glucose control with insulin. In euglycemic DKA, the immediate use of a glucose-containing intravenous fluid induces endogenous insulin secretion and stops ketogenesis. Due to the half-life of SGLT-2 inhibitors, the duration of euglycemic DKA may be more prolonged.

摘要

糖尿病酮症酸中毒(DKA)在历史上被认为是1型糖尿病的典型病症。然而,2型糖尿病患者也可能出现DKA,通常血糖水平更高且酮症酸中毒程度较轻。随着钠-葡萄糖协同转运蛋白2(SGLT-2)抑制剂的使用增加,已出现了变异型正常血糖性DKA。SGLT-2抑制剂会导致体内酮体水平较低;任何额外的酮体生成都会引发酮症酸中毒,而该药物的糖尿作用则限制了高血糖。DKA的治疗原则是补液、控制电解质以及使用胰岛素控制血糖。在正常血糖性DKA中,立即使用含葡萄糖的静脉输液可诱导内源性胰岛素分泌并停止酮体生成。由于SGLT-2抑制剂的半衰期,正常血糖性DKA的持续时间可能会更长。

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