Diagnosis and Treatment > Medication

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Mohammed Faraz Rafey Galway University Hospitals, Galway, Ireland
HRB Clinical Research Facility, National University of Ireland Galway, Galway, Ireland

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Arslan Butt Galway University Hospitals, Galway, Ireland

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Barry Coffey Galway University Hospitals, Galway, Ireland

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Lisa Reddington Galway University Hospitals, Galway, Ireland

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Aiden Devitt Galway University Hospitals, Galway, Ireland

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David Lappin Galway University Hospitals, Galway, Ireland

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Francis M Finucane Galway University Hospitals, Galway, Ireland
HRB Clinical Research Facility, National University of Ireland Galway, Galway, Ireland

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Summary

We describe two cases of SGLT2i-induced euglycaemic diabetic ketoacidosis, which took longer than we anticipated to treat despite initiation of our DKA protocol. Both patients had an unequivocal diagnosis of type 2 diabetes, had poor glycaemic control with a history of metformin intolerance and presented with relatively vague symptoms post-operatively. Neither patient had stopped their SGLT2i pre-operatively, but ought to have by current treatment guidelines.

Learning points:

  • SGLT2i-induced EDKA is a more protracted and prolonged metabolic derangement and takes approximately twice as long to treat as hyperglycaemic ketoacidosis.

  • Surgical patients ought to stop SGLT2i medications routinely pre-operatively and only resume them after they have made a full recovery from the operation.

  • While the mechanistic basis for EDKA remains unclear, our observation of marked ketonuria in both patients suggests that impaired ketone excretion may not be the predominant metabolic lesion in every case.

  • Measurement of insulin, C-Peptide, blood and urine ketones as well as glucagon and renal function at the time of initial presentation with EDKA may help to establish why this problem occurs in specific patients.

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Senhong Lee of Endocrinology, Monash Health, Clayton, Victoria, Australia

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Aparna Morgan of Endocrinology, Monash Health, Clayton, Victoria, Australia

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Sonali Shah of Endocrinology, Monash Health, Clayton, Victoria, Australia

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Peter R Ebeling of Endocrinology, Monash Health, Clayton, Victoria, Australia
Department of Medicine, School of Clinical Sciences, Monash University, Clayton, Victoria, Australia

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Summary

We report a case of a 67-year-old man with type 2 diabetes presented with diabetic ketoacidosis, two weeks after his first dose of nivolumab therapy for non–small-cell lung carcinoma. He was started on empagliflozin two days prior in the setting of hyperglycaemia after the initiation of nivolumab therapy. Laboratory evaluation revealed an undetectable C-peptide and a positive anti-glutamic acid decarboxylase (GAD) antibody. He was treated with intravenous fluids and insulin infusion and was subsequently transitioned to subcutaneous insulin and discharged home. He subsequently has developed likely autoimmune thyroiditis and autoimmune encephalitis.

Learning points:

  • Glycemic surveillance in patients receiving immune checkpoint inhibitors is recommended.

  • Early glycemic surveillance after commencement of anti-programmed cell death-1 (PD-1) inhibitors may be indicated in selected populations, including patients with underlying type 2 diabetes mellitus and positive anti-glutamic acid decarboxylase (GAD) antibody.

  • Sodium-glucose co transporter-2 (SGLT2) inhibitors should be used with caution in patients on immunotherapy.

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