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钠-葡萄糖共转运蛋白 2 抑制剂用于射血分数降低的心力衰竭后,两名非糖尿病患者出现血糖正常性酮症酸中毒。

Euglycemic Ketoacidosis in Two Patients Without Diabetes After Introduction of Sodium-Glucose Cotransporter 2 Inhibitor for Heart Failure With Reduced Ejection Fraction.

机构信息

Southern Adelaide Diabetes and Endocrine Services, Flinders Medical Centre, Adelaide, South Australia, Australia.

Endocrine Department, Queen Elizabeth Hospital, Woodville South, South Australia, Australia.

出版信息

Diabetes Care. 2024 Jan 1;47(1):140-143. doi: 10.2337/dc23-1163.

DOI:10.2337/dc23-1163
PMID:37988720
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10733652/
Abstract

OBJECTIVE

Ketoacidosis induced by sodium-glucose cotransporter 2 inhibitor (SGLT2i) treatment has been consistently observed in clinical practice in patients with type 2 diabetes despite minimal indication from the landmark cardiovascular outcome trials. It has been postulated that individuals without diabetes will not develop this complication due to an adequate insulin secretory capacity, which will protect against significant ketone formation. Cardiovascular outcome trials examining SGLT2i use in individuals with heart failure but not diabetes have not reported ketoacidosis.

RESEARCH DESIGN AND METHODS

We describe the first two case reports of severe nondiabetic ketoacidosis after initiation of an SGLT2i for the treatment of heart failure with reduced ejection fraction, and we describe the management strategies employed and implication for the pathophysiology of SGLT2i-associated ketoacidosis.

RESULTS

Each individual presented with ketoacidosis triggered by reduced oral nutrition intake. For both individuals, ketoacidosis resolved with intravenous glucose administration, encouragement of consumption of oral glucose-containing fluid, and minimal insulin administration.

CONCLUSIONS

These two cases demonstrate that SGLT2i-associated ketoacidosis is possible in individuals without diabetes.

摘要

目的

尽管标志性心血管结局试验的适应证很少,但在 2 型糖尿病患者的临床实践中,仍持续观察到钠-葡萄糖共转运蛋白 2 抑制剂(SGLT2i)治疗引起的酮症酸中毒。据推测,由于胰岛素分泌能力充足,没有糖尿病的个体不会发生这种并发症,这将防止大量酮体形成。检查 SGLT2i 在心力衰竭但无糖尿病个体中使用的心血管结局试验并未报告酮症酸中毒。

研究设计和方法

我们描述了首例因射血分数降低的心力衰竭开始使用 SGLT2i 治疗后发生严重非糖尿病酮症酸中毒的两例病例报告,并描述了所采用的管理策略及其对 SGLT2i 相关酮症酸中毒发病机制的影响。

结果

每个人的酮症酸中毒都是由减少口服营养摄入引发的。对于这两个人,酮症酸中毒通过静脉输注葡萄糖、鼓励摄入含有葡萄糖的口服液体以及最小剂量的胰岛素治疗得到解决。

结论

这两例病例表明,SGLT2i 相关的酮症酸中毒在无糖尿病的个体中是可能的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a88/10733652/aad1f35ada04/dc231163f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a88/10733652/32cdf2246d8f/dc231163F0GA.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a88/10733652/aad1f35ada04/dc231163f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a88/10733652/32cdf2246d8f/dc231163F0GA.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a88/10733652/aad1f35ada04/dc231163f1.jpg

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