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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Akihiko Ando Division of Endocrinology and Metabolism, Department of Internal Medicine, Jichi Medical University, Tochigi, Japan

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Shoichiro Nagasaka Division of Endocrinology and Metabolism, Department of Internal Medicine, Jichi Medical University, Tochigi, Japan
Division of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine, Showa University Fujigaoka Hospital, Kanagawa Japan

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Shun Ishibashi Division of Endocrinology and Metabolism, Department of Internal Medicine, Jichi Medical University, Tochigi, Japan

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Summary

We report a case of a woman with diabetes mellitus caused by a genetic defect in ABCC8-coding sulfonylurea receptor 1 (SUR1), a subunit of the ATP-sensitive potassium (KATP) channel protein. She was diagnosed with diabetes at 7 days after birth. After intravenous insulin drip for 1 month, her hyperglycaemia remitted. At the age of 13 years, her diabetes relapsed, and after that she had been treated by intensive insulin therapy for 25 years with relatively poor glycaemic control. She was switched to oral sulfonylurea therapy and attained euglycaemia. In addition, her insulin secretory capacity was ameliorated gradually.

Learning points:

  • Genetic testing should be considered in any individuals or family with diabetes that occurred within the first year or so of life.

  • Sulfonylurea can achieve good glycaemic control in patients with KATP channel mutations by restoring endogenous insulin secretion, even if they were treated with insulin for decades.

  • Early screening and genetic testing are important to improve the prognosis of patients with neonatal diabetes mellitus arising from ABCC8 or KCNJ11 mutation.

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