Abstract
Introduction: The Ketogenic “Keto” or “Carnivore” has come into mainstream focus for patients trying to lose weight. The aim is to induce “ketosis” by catabolizing fat into ketone bodies. Using these as fuel rather than carbohydrates. This shift can occur over the course of several days when carbohydrate intake is restricted to 20-50 g daily. This is effective for short-term weight loss but may lead to life-threatening euglycemic diabetic (eDKA) ketoacidosis in those with diabetes mellitus (DM) on SGLT2 inhibitors. Case 1: 71 year-old woman with controlled type 2 DM on sitagliptin, metformin and canagliflozin was admitted for eDKA after she presenting with worsening symptoms of shortness of breath for 3 days. Three days prior to admission, she had been experiencing shortness of breath and was started on prednisone for a presumed COPD exacerbation. On presentation, her anion gap was measured to be 31 with a serum bicarbonate level of <5 mmol/L. Beta hydroxybutyrate was critically elevated 118mg/dl (ref. 0.2-2.8). Serum glucose level is 265 mg/dl. She was also noted to have pre-renal acute kidney injury. Upon questioning, she recently started a “carnivore diet” in which she cut her carbohydrate intake to near zero. eDKA was treated with an IV insulin DKA protocol. She was discharged home on sitagliptin and metformin. Canagliflozin was discontinued and moderate carbohydrate intake was recommended with her diet. Upon follow up at our endocrinology clinic, her hemoglobin A1c remained stable at 7.1%. Case 2: 51 year-old woman with uncontrolled Type 1 DM on continuous subcutaneous insulin infusion treatment and dapagliflozin was admitted for eDKA. She also utilized a continuous glucose monitor. She had started a Keto diet 4 months prior, restricting her carb intake to 30 g daily. She progressively became fatigued, anorexic with short of breath. Upon evaluation at an urgent care, she was found to be dyspneic with a blood glucose of 276 mg/dl and anion gap of 32 and serum bicarbonate of <5 mmol/L, beta hydroxybutyrate was found to be 138 mg/dl. Her hemoglobin A1c on admission to ICU was 8.1%. She was treated as per DKA treatment protocol. She responded well and discharged with increase in her basal doses. Conclusions: These cases demonstrate serious negative consequences that can occur with carbohydrate restriction with SGLT2 inhibitor use. Prior to this, one case has been reported of eDKA associated with Dapagliflozin[1], as well as two other a cases of eDKA associated with T1DM.[2] We postulate the common thread of carbohydrate restriction was essential in tipping the balance to DKA without the cardinal feature of hyperglycemia seen in the classical presentations of DKA. Here, we present our case series in efforts to raise awareness regarding risk of low carbohydrate diets in patient’s prescribed SGLT2. A detailed history regarding patient’s dietary habits and appropriate discuss on risks of new therapy is necessary.
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