Use of insulin degludec/aspart after resolution of euglycemic diabetic ketoacidosis associated with dapagliflozin in a female patient with newly diagnosed maturity onset diabetes of the young type 3

Abstract

Abstract Introduction Maturity-onset diabetes of the young (MODY) is a monogenic disorder characterized by beta cell dysfunction. MODY presents generally at a young onset, and usually does not prone to ketosis. MODY should be distinguished from type 1(T1D) or type 2 diabetes(T2D), because the treatment modalities may be different. In this case, we aimed to emphasize the successful use of insulin degludec/aspart (IDegAsp) after resolution euglycemic diabetic ketoacidosis (euDKA) in a patient latterly diagnosed with MODY. Clinical Case A 39-year-old female patient was referred to our clinic with severe hyperglycemia. SMBG results revealed that blood glucose levels were about 300–400 mg/dL indicating severe hyperglycemia. She has been followed up for T2D 15 years and had been taking oral antidiabetic regimen until 6 months ago. Insulin glargine was prescribed 6 months ago, but she gave up insulin and had been taking linagliptin 5 mg/day and dapagliflozin 10 mg/day. The previous history was remarkable for arrhythmia which was treated with ablation 15 years ago. Maternal history of T2D was present. On physical examination, heart rate was 100/min, and systemic examination findings were in normal range except for central obesity. Laboratory evaluation revealed that fasting blood glucose was 212 mg/dL, HbA1c 10.2%, creatinine 1.1 mg/dL, and ketone 3+ in urinalysis. Arterial blood gas analysis revealed mild acidosis (pH 7.25, HCO3 18 mmol/L). The patient was hospitalized with a diagnosis of euDKA. Intravenous hydration with 0.9% NaCL and regular insulin was administered, and oral antidiabetic medications were stopped. In the follow-up, intensive insulin regimen (preprandial insulin glulisine 3×5 unit and basal insulin glargine 1×15 unit) was given after the resolution of euDKA. Although dose adjustments, two attacks of near-hypoglycemia (71 and 77 mg/dL) were detected in the first week after resolution of euDKA. IDegAsp (premeal 2×12 unit) was substituted for glargine and glulisine. Due to the maintenance of glycemic regulation by oral antidiabetic regimen for a long period, and the existence of maternal history of T2D, genetic analysis was performed with a pre-diagnosis of MODY. To exclude T1D, we demonstrated that autoantibodies (islet cell antibody 5.01 U/mL, and Anti-GAD antibody 7.74 IU/mL) for T1D were negative. HNF1A heterozygous mutation was detected, and MODY type 3 was diagnosed. HbA1c level was gradually regressed to 8.8%, and then to 6.3%. By the diagnosis of MODY type 3, gliclazide treatment was considered. Basal fasting C-peptide level was measured as 1.22 ng/mL. The antidiabetic regimen was revised as linagliptin 5 mg/day and gliclazide 30 mg/day, and insulin was stopped. Conclusion Some types of MODY is associated with mild hyperglycemia, however some others necessitate insulin treatment. The number of reports regarding the use of IDegAsp in MODY is limited. We reached HbA1c target with IDegAsp in a patient with MODY type 3 after resolution of euDKA.