Sodium-Glucose Cotransporter 2 (SGLT2) Inhibitor Induced Ketoacidosis in a Patient Misdiagnosed As a Type 2 Diabetic

Presentation Number: SAT 604
Date of Presentation: April 1st, 2017

Jenan Gabi* and Ayman Hussein Elkadry
Marshall University School of Medicine

Abstract

Introduction:

SGLT2 inhibitors are a newer class of anti-diabetic medications approved in 2013 for use in diabetes mellitus (DM) type II, but used off label in type 1. Multiple reports of diabetic ketoacidosis (DKA) in both types of diabetes resulted in the FDA issuing a warning in May 2015 about the possibility of DKA from SGLT2 inhibitor use.

Case report:

A 29 year-old female with a BMI of 30 and Hashimotos thyroiditis was diagnosed with DM II when she was 24. Blood glucose remained high on 3 oral medications so she ended up on insulin within the first year of diagnosis. Because she was uncontrolled with 40 units of Lantus and Aspart sliding scale insulin (SSI), her primary care physician switched her to Toujeo but at 20 units daily, Aspart 10 units with meals and added dapagliflozin 10 mg daily. Two months later she presented to the ER with shortness of breath, cough and vomiting. Her lab work was significant for a pH of 7.08, bicarbonate 7 mmol/dL, anion gap 24 mmol/L, moderate ketones on dipstick, elevated acetone 0.05%, hemoglobin A1c 12.2%, but, her serum glucose was only 213 mg/dL. Beta-HCG was negative. She was admitted to the ICU and treated for DKA with IV insulin and fluids, then switched to a regimen of Lantus and Lispro. GAD-65 came back elevated 63.7 U/ml and C-peptide checked 4 weeks later was low 0.3 ng/mL. She was diagnosed with Latent autoimmune diabetes of adults (LADA) and plans were made for insulin pump.

Discussion:

SGLT2 inhibitors work by decreasing reabsorption of glucose in the proximal renal tubules, which results in the desired lower blood glucose concentration. This same mechanism leads to lower insulin levels which in turn, and in the perfect setting, ultimately leads to DKA with minimally elevated or even normal glucose (euglycemic DKA). Those at higher risk are patients with DM I, LADA or long standing DM II with little beta-cell reserve. Precipitating events have been linked to decreasing the dose of insulin, as in our case, or carbohydrate restriction like in illness, fasting, surgery or strict diets. Other risk factors are pancreas disease or alcohol intake. Pregnancy was ruled out as it is a known cause of euglycemic DKA. Many patients are misdiagnosed as having DM II due to their weight or age, which places them at risk for SGLT2 inhibitor induced DKA. Our patient was young, progressed to insulin fast and had another autoimmune disease which, despite her weight, should have raised suspicion of DM I or LADA.

Conclusion:

SGLT2 inhibitors are helpful medications when given to the right patient. Candidates should be chosen carefully; Type 2 diabetics with good Beta cell reserve. They should be warned about the possible complications, including DKA. It is crucial to realize that many patients are misdiagnosed as DM type II when they actually have type I or LADA. Workup to differentiate should be considered before starting an SGLT2 inhibitor if there are any suspicious features from the patients’ history.

 

Nothing to Disclose: JG, AHE