抄録
A 47-year-old male with type 2 diabetes presented to the internal medicine department with nausea. Laboratory findings
showed metabolic acidosis on blood gas analysis and ketone bodies on urinary tests; however, serum glucose
levels were normal. A review of his drug history showed that semaglutide had been prescribed one week before this
episode at a 0.25 mg weekly subcutaneous dose. Semaglutide interruption resulted in eliminating his symptoms and
metabolic acidosis on blood gas analysis. The GLP-1 receptor increases insulin secretion, decreases glucagon secretion,
and delays gastric emptying, all of which lower blood glucose, resulting in the development of euglycemic ketoacidosis.
