Stress-Induced Diabetic Ketoacidosis Due to Transient Beta Cell Stunning in a Youth with Type 2 Diabetes Mellitus: A Case Report

Abstract

Abstract A 15-year-old boy was admitted to the intensive care unit of our hospital with complaints of increased urination, extreme tiredness, and nausea for the past 15 days. He had also lost 6.5 kg of weight (almost 10% of total body weight) in 1 month. On admission, his plasma glucose was 780 mg/dL, glycated haemoglobin (HbA1c) 11.6%, serum ketones >10.0 mmol/L, osmolality 346 mosm/kg, arterial pH 7.28, and bicarbonate 9 mEq/L. The C-peptide report initially indicated poor pancreatic beta cell reserve (fasting: 0.41 pmol/mL and stimulated: 0.46 pmol/mL). He was diagnosed with diabetic ketoacidosis and responded well to treatment, after which time he was switched to subcutaneous insulin. Ten days later, in the outpatient clinic, his fasting blood glucose was 132 mg/dL, postprandial blood glucose was 183 mg/dL, and C-peptide had improved to fasting: 0.89 pmol/mL and stimulated: 1.42 pmol/mL. Considering the presence of acanthosis nigricans on the neck, a body mass index in the overweight range, a positive family history of diabetes, and negative tests for pancreatic autoantibodies, an early onset diagnosis of type 2 diabetes mellitus was considered. Insulin was gradually withdrawn, and he was switched to metformin. Sustained recovery of C-peptide in this case indicates that lack of insulin at admission was due to beta cell stunning, rather than a total and irreversible loss of beta cells as expected in type 1 diabetes mellitus. Beta cell stunning is often reversible, as shown in this case.