Endocrine Abstracts

Case history: We present the case of a 51-year-old female of South-East Asian origin presenting with a four-day history of feeling progressively unwell with vomiting, reduced oral intake and urinary symptoms. Her past medical history was T2D (HbA1c 98 mmol/mol March 2018). Drug history on admission was Metformin 500 mg twice daily, Gliclazide 160 mg twice daily, Ramipril 1.25 mg once daily and Dapagliflozin 10 mg once daily. The initiation date of Dapagliflozin and Ramipril coincided with the start of her symptoms.

Investigations: Blood tests (biochemistry, haematology), blood cultures, urine culture.

Results and treatment: The patient was septic on admission with a metabolic acidosis (pH 7.28, lactate 1.7 mmol/L, HCO3 14.8 mmol/L, glucose 21.5 mmol/L, base excess −10.8 mmol/L) with blood ketones 5.6 mmol/L. Anti-GAD antibody negative with a random paired insulin C-peptide 350 pmol/L and glucose 5.3 mmol/L. She was started on a fixed rate insulin infusion 5.8 units/hour and the Dapagliflozin stopped. Blood and urine cultures were positive for Escherichia coli fully sensitive to co-amoxiclav (treatment started).

Conclusions and points for discussion: Dapagliflozin is a sodium glucose cotransporter 2 inhibitor (SGLT-2i). SGLT-2i’s improve glycaemic control and weight loss through increased urinary excretion of glucose. The association with DKA has been reported in insulin dependent T2D. Our patients elevated HbA1C and poor compliance should raise suspicion for likely insulin deficiency. This coupled with the use of an SGLT-2i increased her risk of developing DKA. Her urinary tract infection further compounded her stress response and progression into DKA. In patients with poor glycaemic control and a long duration of diabetes, consideration should be given to initiating insulin before an SGLT-2i.