Gajjar Kushani, Luthra Pooja
Internal Medicine, University of Connecticut Health Center, Farmington, USA.
Cureus. 2019 Apr 4;11(4):e4384. doi: 10.7759/cureus.4384.
We describe the case report of a patient with euglycemic diabetic ketoacidosis (euDKA), in the setting of sodium-glucose cotransporter-2 (SGLT2) inhibitor use, complicated by hypertriglyceridemia (HTG). A 28-year-old female with a history of gestational diabetes mellitus and subsequent type 2 diabetes mellitus (T2DM) on dapagliflozin and metformin presented with a one-week history of polyuria, poor appetite, and vomiting. On admission, serum glucose was 111 mg/dl, bicarbonate 18 mmol/l, anion gap 20, triglycerides 508 mg/dL, and venous pH 7.27. Serum ketone levels could not be assessed, as blood samples kept hemolyzing due to significant lipemia. The patient was initially admitted for starvation ketosis. However, serum chemistry obtained six hours after presentation revealed no change in the anion gap and a rise in triglycerides. She was treated with an insulin drip for euDKA and HTG with the resolution of the clinical picture. We performed a literature review of this topic and discuss the pathophysiology, diagnosis, management, and prevention of SGLT2-inhibitor-induced euDKA.
我们报告了一例在使用钠-葡萄糖协同转运蛋白2(SGLT2)抑制剂的情况下发生正常血糖性糖尿病酮症酸中毒(euDKA)并伴有高甘油三酯血症(HTG)的病例。一名28岁女性,有妊娠期糖尿病病史,后续诊断为2型糖尿病(T2DM),正在使用达格列净和二甲双胍治疗,出现多尿、食欲减退和呕吐一周。入院时,血清葡萄糖为111mg/dl,碳酸氢盐为18mmol/l,阴离子间隙为20,甘油三酯为508mg/dL,静脉血pH值为7.27。由于严重脂血导致血样持续溶血,无法评估血清酮水平。患者最初因饥饿性酮症入院。然而,就诊六小时后检测的血清化学指标显示阴离子间隙无变化,甘油三酯升高。她接受了胰岛素静脉滴注治疗,euDKA和HTG得到缓解,临床症状消失。我们对该主题进行了文献综述,并讨论了SGLT2抑制剂诱导的euDKA的病理生理学、诊断、管理和预防。