The risk of ketoacidosis from an SGLT2 inhibitor is exacerbated by a ketogenic diet, clinicians in Tasmania have warned.

A woman with type 2 diabetes who started on the Atkins diet while taking empagliflozin developed euglycaemic ketoacidosis and had to be hospitalised, according to a case report from Dr Shampa Sinha and colleagues from the Royal Hobart Hospital.

The risk of ketoacidosis may have been further worsened by diarrhoea she had experienced that would contribute to hypovolaemia and ketogenesis, they write in the MJA.

The 64-year-old woman presented to the emergency department with progressively reduced consciousness for three days, preceded by vomiting and diarrhoea.

She had been taking 10 mg empagliflozin and 5 mg linagliptin for a year and had been well until she started the Atkins diet  – high in fats and low in carbohydrates – about 2 months previously.

Her most recent glycated haemoglobin level was 58 mmol/mol and her initial blood tests demonstrated high anion gap metabolic acidosis, an initial blood sugar level of 10.3 mmol/L and a serum ketone level of 4.7 mmol/L.

She was diagnosed as having euglycaemic ketoacidosis secondary to using a sodium–glucose cotransporter type 2 (SGLT2) inhibitor (empagliflozin) and precipitated by her diarrhoeal illness and her Atkins diet.

The anion gap was normalised after a dextrose and insulin infusion, the patient became progressively more alert and was discharged two days later.

“This case highlights the risks of combining ketogenic diets such as the Atkins diet with SGLT2 inhibitors,” writes Dr Sinha.

She notes that hypovolaemia from the diuretic effect of the SGLT2 inhibitors will stimulates release of counter-regulatory hormones such as glucagon, cortisol and adrenaline, and thus further increase insulin resistance, lipolysis and ketogenesis.

“High protein, low carbohydrate ketogenic diets such as Atkins in isolation usually only result in a mild, temporary ketosis. In the setting of an SGLT2 inhibitor and infective illness, however, it increased our patient’s susceptibility to ketosis,” the authors note.