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SAT-685 Euglycemic Diabetic Ketoacidosis in T1d: The Era of SGLT-2 Inhibitors and Keto-Diet

机译:T1D中SAT-685神般血糖糖尿病酮症病:SGLT-2抑制剂和酮饮的时代

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摘要

Introduction Euglycemic diabetic ketoacidosis (DKA) is a challenging diagnosis since near normal blood sugar levels can be misleading. In the present case, we describe a patient with Type 1 Diabetes (T1D) on SGLT2 who underwent a strict low carb diet. Case Report A 70-year-old female with past medical history of unspecified diabetes mellitus and primary hypothyroidism presented to emergency room complaining of nausea and dizziness of four days with decreased oral intake. She was alert and oriented, normal weight (52 kg, BMI 20 kg/m2) with stable vital signs, except for mild tachypnea (22/min). Initial labs showed serum glucose 136 mg/dL, bicarbonate 10 mmol/L (normal 20-31), anion gap of 27, venous blood gas pH 7.1, B-hydroxybutyrate 8.8 mmol/L (normal 0.02-0.27), glucosuria > 500 mg/dL, and moderate ketonuria. Screening for ethyl alcohol and ethylene glycol was negative. Lactic acid, cardiac enzymes, renal and liver function tests were normal. She was diagnosed with diabetes mellitus at age 37, on insulin since then. No alcohol use. Her new primary care physician found an A1C of 9.0% for which metformin 1000mg oral twice a day and empagliflozin 12.5 mg oral daily were added and aspart insulin was discontinued. Daily glargine remained at 20 units daily. She was advised to lose weight for which she started a keto-diet 4 weeks prior to this presentation. She had lost 15 pounds since then accompanied by polyuria and polydipsia. Upon admission, she received IV insulin and IV fluids. An endocrinology consultation was requested for euglycemic DKA secondary to SGLT2 complicated by starvation ketosis. Antibodies against glutamic acid decarboxylase were positive at 250 IU/mL (normal < 5). She was discharged on glargine, aspart insulins and oral medications were discontinued. Conclusion This case shows the importance of identifying the specific type of diabetes for appropriate individualization of therapy. Following a keto-diet in unrecognized T1D can trigger ketoacidosis in the setting of SGLT2 inhibitors leading to euglycemic diabetes ketoacidosis.
机译:引入正常血糖糖尿病酮症酸中毒(DKA)是因为接近正常的血糖水平,可以误导挑战诊断。在本案中,我们描述了在SGLT2 1型糖尿病(T1D)谁接受了严格的低碳水化合物饮食的患者。病例报告一名70岁的女性,未指定的糖尿病和原发性甲状腺功能减退的既往病史呈现给急诊室恶心的四天减少误服头晕的抱怨。她生命体征平稳警报和定向,正常体重(52千克,BMI为20kg /平方米),除了轻度呼吸急促(22 /分钟)。初始实验室表明血清葡萄糖136毫克/分升,碳酸氢钠10毫摩尔/ L(正常20-31),27阴离子间隙,静脉血气pH值7.1,B羟基丁酸酯8.8毫摩尔/ L(正常0.02-0.27),糖尿> 500毫克/分升,和中等酮尿。筛选乙醇和乙二醇为阴性。乳酸,心肌酶,肾和肝功能检查均正常。从那时起,她在37岁时被诊断为糖尿病,胰岛素。无酒精的使用。她的新的初级保健医生发现,9.0%的A1C针对二甲双胍1000毫克口服,每日两次和恩格列净12.5毫克口服,每天添加和门冬胰岛素已经停产了。每日甘精胰岛素,每天保持在20个单位。她被告知要为她前4周此演示文稿开始酮饮食减肥。她失去了15磅,自那时以来伴随着尿和烦渴。入院时,她收到IV胰岛素和静脉输液。被要求为正常血糖DKA继发SGLT2饥饿性酮症复杂的内分泌科咨询。对谷氨酸脱羧酶抗体是阳性的,在250 IU /毫升(通常<5)。她对甘精胰岛素出院,门冬胰岛素和口服药物被中止。结论该情况下示出了识别糖尿病的特定类型治疗的适当的个性化的重要性。继无法识别T1D酮饮食可以SGLT2抑制剂导致血糖正常的糖尿病酮症酸中毒的设置引发酮症酸中毒。

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