Canagliflozin

Canagliflozin Reactions 1704, p75 - 2 Jun 2018 Euglycaemic diabetic ketoacidosis and Fanconi syndrome: case report A 54-year-old woman developed euglycaemic diabetic ketoacidosis and Fanconi syndrome during treatment with canagliflozin for type 2 diabetes mellitus [route and durations of treatment to reactions onsets not stated; not all outcomes stated]. The woman, who had type 2 diabetes mellitus, presented with chest pain. She was noted to have euglycaemic diabetic ketoacidosis. She had a blood glucose level of 175 mg/dL. She also had anion gap metabolic acidosis with an increased beta hydroxybutyrate level, reduced serum bicarbonate and a normal serum lactate level. Her ongoing medications included canagliflozin 300mg daily for type 2 diabetes mellitus, lisinopril and atorvastatin. The woman started receiving treatment with insulin till the anion gap disappeared. She was then switched to oral medications. Subsequently, she developed hypophophataemia and persistent non-anion gap metabolic acidosis. Urinalysis showed glycosuria, which was expected with canagliflozin use. She also had generalised aminoaciduria with predominant glycine excretion and phosphaturia with fractional phosphate excretion of 23% and serum phosphate level of 1.8 mg/dL. These findings indicated impaired renal tubular function and were consistent with Fanconi syndrome. Thereafter, her prior lab reports were reviewed, which showed a persistent non-anion gap metabolic acidosis for the previous two years. The non-anion gap metabolic acidosis was temporally related to her canagliflozin therapy. Subsequently, the canagliflozin therapy was discontinued, and she was started on insulin therapy. During this period, her renal function remained normal. Author comment: "Herein, we present the case of a diabetic patient on canagliflozin who presented with [euglycaemic diabetic ketoacidosis] and found to have proximal renal tubular acidosis with Fanconi syndrome that was attributable to the drug." Esprit DH, et al. Fanconi syndrome associated with SGLT2 inhibitor, canagliflozin. Nephrology 23: 493, No. 5, May 2018. Available from: URL: http:// doi.org/10.1111/nep.13094 - USA 803323134 0114-9954/18/1704-0001/$14.95 Adis © 2018 Springer International Publishing AG. All rights reserved Reactions 2 Jun 2018 No. 1704 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Reactions Weekly Springer Journals

Canagliflozin

Reactions Weekly , Volume 1704 (1) – Jun 2, 2018
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Publisher
Springer International Publishing
Copyright
Copyright © 2018 by Springer International Publishing AG, part of Springer Nature
Subject
Medicine & Public Health; Drug Safety and Pharmacovigilance; Pharmacology/Toxicology
ISSN
0114-9954
eISSN
1179-2051
D.O.I.
10.1007/s40278-018-46718-9
Publisher site
See Article on Publisher Site

Abstract

Reactions 1704, p75 - 2 Jun 2018 Euglycaemic diabetic ketoacidosis and Fanconi syndrome: case report A 54-year-old woman developed euglycaemic diabetic ketoacidosis and Fanconi syndrome during treatment with canagliflozin for type 2 diabetes mellitus [route and durations of treatment to reactions onsets not stated; not all outcomes stated]. The woman, who had type 2 diabetes mellitus, presented with chest pain. She was noted to have euglycaemic diabetic ketoacidosis. She had a blood glucose level of 175 mg/dL. She also had anion gap metabolic acidosis with an increased beta hydroxybutyrate level, reduced serum bicarbonate and a normal serum lactate level. Her ongoing medications included canagliflozin 300mg daily for type 2 diabetes mellitus, lisinopril and atorvastatin. The woman started receiving treatment with insulin till the anion gap disappeared. She was then switched to oral medications. Subsequently, she developed hypophophataemia and persistent non-anion gap metabolic acidosis. Urinalysis showed glycosuria, which was expected with canagliflozin use. She also had generalised aminoaciduria with predominant glycine excretion and phosphaturia with fractional phosphate excretion of 23% and serum phosphate level of 1.8 mg/dL. These findings indicated impaired renal tubular function and were consistent with Fanconi syndrome. Thereafter, her prior lab reports were reviewed, which showed a persistent non-anion gap metabolic acidosis for the previous two years. The non-anion gap metabolic acidosis was temporally related to her canagliflozin therapy. Subsequently, the canagliflozin therapy was discontinued, and she was started on insulin therapy. During this period, her renal function remained normal. Author comment: "Herein, we present the case of a diabetic patient on canagliflozin who presented with [euglycaemic diabetic ketoacidosis] and found to have proximal renal tubular acidosis with Fanconi syndrome that was attributable to the drug." Esprit DH, et al. Fanconi syndrome associated with SGLT2 inhibitor, canagliflozin. Nephrology 23: 493, No. 5, May 2018. Available from: URL: http:// doi.org/10.1111/nep.13094 - USA 803323134 0114-9954/18/1704-0001/$14.95 Adis © 2018 Springer International Publishing AG. All rights reserved Reactions 2 Jun 2018 No. 1704

Journal

Reactions WeeklySpringer Journals

Published: Jun 2, 2018

References

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