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异丙肾上腺素诱导1型糖尿病患者胰岛素抵抗并导致糖尿病酮症酸中毒

Isoproterenol Induced Insulin Resistance Leading to Diabetic Ketoacidosis in Type 1 Diabetes Mellitus.

作者信息

Hoff Ryan, Koh Chung-Kay

机构信息

Advocate Lutheran General Hospital, Park Ridge, IL, USA.

出版信息

Case Rep Endocrinol. 2018 Dec 17;2018:4328954. doi: 10.1155/2018/4328954. eCollection 2018.

DOI:10.1155/2018/4328954
PMID:30647979
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6311779/
Abstract

Isoproterenol is known to cause insulin resistance and is often used to treat bradyarrhythmias from atrioventricular block. We report a case of isoproterenol induced diabetic ketoacidosis in a 77-year-old female patient treated with isoproterenol for atrioventricular block prior to insertion of permanent pacemaker. Diabetic ketoacidosis (DKA) developed within hours of starting an isoproterenol drip, and there were no other precipitating factors at that time. DKA resolved quickly after discontinuing isoproterenol and starting insulin drip. DKA is a common complication of diabetes mellitus, with about 140,000 hospital admissions for DKA in 2009. While the rate of DKA has increased by nearly 50% between 1988 and 2009, the rate of mortality has decreased. There are many causes of diabetic ketoacidosis, such as medication noncompliance, infection, pancreatitis, stroke, myocardial infarction, and many others. Isoproterenol may lead to diabetic ketoacidosis by increasing insulin resistance.

摘要

已知异丙肾上腺素会导致胰岛素抵抗,常用于治疗房室传导阻滞引起的缓慢性心律失常。我们报告一例77岁女性患者,在植入永久性起搏器前因房室传导阻滞接受异丙肾上腺素治疗,发生了异丙肾上腺素诱发的糖尿病酮症酸中毒。在开始静脉滴注异丙肾上腺素数小时内即出现糖尿病酮症酸中毒(DKA),当时无其他诱发因素。停用异丙肾上腺素并开始静脉滴注胰岛素后,DKA迅速缓解。DKA是糖尿病的常见并发症,2009年约有14万例因DKA住院。虽然1988年至2009年间DKA的发生率增加了近50%,但死亡率有所下降。糖尿病酮症酸中毒有许多病因,如药物治疗依从性差、感染、胰腺炎、中风、心肌梗死等。异丙肾上腺素可能通过增加胰岛素抵抗导致糖尿病酮症酸中毒。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9d4/6311779/3cb168f9bd7e/CRIE2018-4328954.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9d4/6311779/3cb168f9bd7e/CRIE2018-4328954.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9d4/6311779/3cb168f9bd7e/CRIE2018-4328954.001.jpg

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BMJ Open. 2017 Aug 1;7(7):e016587. doi: 10.1136/bmjopen-2017-016587.
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