Division of Endocrinology and Metabolism, Department of Internal Medicine, Taiwan Adventist Hospital, Taiwan.
J Formos Med Assoc. 2018 Sep;117(9):849-854. doi: 10.1016/j.jfma.2018.02.004. Epub 2018 Feb 21.
Sodium-glucose cotransporter-2 (SGLT-2) inhibitors are the newest class of oral antidiabetic drugs (OADs), approved to be a second-line OAD for type 2 diabetes in Taiwan since 2016. The U.S. Food and Drug Administration (FDA) and the European Medicines Agency (EMA) had both released statements associating the use of SGLT-2 inhibitors may increase the risk of eu-glycemic diabetic ketoacidosis (euDKA). This review reveals the possible pathophysiology with a chain of metabolic adaptions to decrease plasma glucose and increase plasma ketone bodies through pancreas, kidney, liver and adipose tissue. Moreover, euDKA is a potential and rare complication of treatment with SGLT-2 inhibitors when coexisting with triggering factors. It is an emerging challenge for clinical physicians and patients treated with SGLT-2 inhibitors. Therefore, first report of SGLT-2 inhibitor induced euDKA in a T2D Taiwanese and literature review of possible pathophysiology and contributing factors are presented in order to make more attentions in public.
钠-葡萄糖共转运蛋白 2（SGLT-2）抑制剂是最新一类口服抗糖尿病药物（OADs），自 2016 年以来，在台湾被批准作为 2 型糖尿病的二线 OAD。美国食品和药物管理局（FDA）和欧洲药品管理局（EMA）都发布声明称，使用 SGLT-2 抑制剂可能会增加血糖正常的糖尿病酮症酸中毒（euDKA）的风险。本综述揭示了可能的病理生理学机制，包括一系列代谢适应，通过胰腺、肾脏、肝脏和脂肪组织降低血糖并增加血浆酮体。此外，当存在触发因素时，euDKA 是 SGLT-2 抑制剂治疗的潜在且罕见的并发症。因此，本文报道了一名台湾 2 型糖尿病患者使用 SGLT-2 抑制剂引起的 euDKA，并对可能的病理生理学和促成因素进行了文献回顾，以便引起公众更多关注。
