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SUN-LB030 Empagliflozin Causing Euglycemic Diabetic Ketoacidosis

Background: Empagliflozin is a sodium glucose co-transporter 2 (SGLT-2) inhibitor that works in the proximal renal tubules reducing resorption of glucose and increasing urinary glucose excretion. It effectively lowers glycated hemoglobin (HbA1C) values and reduces risks of adverse cardiovascular eve...

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Autores principales: Thomas, Mathew, Tran, Ly, White, Christopher, Deppe, John, Davidson, James
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Endocrine Society 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6552746/
http://dx.doi.org/10.1210/js.2019-SUN-LB030
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author Thomas, Mathew
Tran, Ly
White, Christopher
Deppe, John
Davidson, James
author_facet Thomas, Mathew
Tran, Ly
White, Christopher
Deppe, John
Davidson, James
author_sort Thomas, Mathew
collection PubMed
description Background: Empagliflozin is a sodium glucose co-transporter 2 (SGLT-2) inhibitor that works in the proximal renal tubules reducing resorption of glucose and increasing urinary glucose excretion. It effectively lowers glycated hemoglobin (HbA1C) values and reduces risks of adverse cardiovascular events compared to other antidiabetic medications. Common side effects include urinary frequency, genital mycotic infection, and urinary tract infection. A less common, but potentially life-threatening side effect, is euglycemic diabetic ketoacidosis (euDKA). Clinical Case: We present a 60-year-old woman with a history of poorly controlled Type 2 diabetes with a HbA1C of 10.7% on empagliflozin and glipizide, who presented with a nine day history of lethargy, fever, chills, myalgia, and nausea with poor oral intake. Two days prior, she was diagnosed with Influenza A. Initial laboratory results revealed evidence of a metabolic acidosis with a bicarbonate level of 6 (21-31 mmol/L), anion gap of 27 (3-15 mmol/L), and a blood glucose level of 189 (70-100 mg/dL). Urinalysis showed glycosuria and ketones. A venous blood gas was significant for a pH of 7.00 (7.31-7.41) and pCO2 of 22 (41-51 mmHg). Serum osmolality was 331 (289-309 mosm/kg) and a serum acetone level was high at 0.058% (0.0-0.010%). Serum ethanol, methanol, and isopropanol were negative thus ruling out possible ingestion as a source of osmolar gap. The patient was diagnosed with euDKA secondary to empagliflozin with precipitating factors being acute illness and decreased oral intake.Within 42 hours, treatment with normal saline and insulin infusion, the metabolic acidosis, anion gap, and osmolar gap normalized. Empagliflozin was discontinued upon discharge. Conclusion: A review of current literature suggests euDKA from empagliflozin is rare with only four cases reported to date. As SGLT-2 inhibitors continue to be increasingly prescribed, awareness of this potential complication in the setting of misleading blood glucose levels and an osmolar gap is integral for the early detection and treatment of euDKA. Patient counseling on this uncommon adverse event, especially during times of decreased oral intake and acute illness should be provided. Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. Abstracts presented at a news conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.
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spelling pubmed-65527462019-06-13 SUN-LB030 Empagliflozin Causing Euglycemic Diabetic Ketoacidosis Thomas, Mathew Tran, Ly White, Christopher Deppe, John Davidson, James J Endocr Soc Diabetes Mellitus and Glucose Metabolism Background: Empagliflozin is a sodium glucose co-transporter 2 (SGLT-2) inhibitor that works in the proximal renal tubules reducing resorption of glucose and increasing urinary glucose excretion. It effectively lowers glycated hemoglobin (HbA1C) values and reduces risks of adverse cardiovascular events compared to other antidiabetic medications. Common side effects include urinary frequency, genital mycotic infection, and urinary tract infection. A less common, but potentially life-threatening side effect, is euglycemic diabetic ketoacidosis (euDKA). Clinical Case: We present a 60-year-old woman with a history of poorly controlled Type 2 diabetes with a HbA1C of 10.7% on empagliflozin and glipizide, who presented with a nine day history of lethargy, fever, chills, myalgia, and nausea with poor oral intake. Two days prior, she was diagnosed with Influenza A. Initial laboratory results revealed evidence of a metabolic acidosis with a bicarbonate level of 6 (21-31 mmol/L), anion gap of 27 (3-15 mmol/L), and a blood glucose level of 189 (70-100 mg/dL). Urinalysis showed glycosuria and ketones. A venous blood gas was significant for a pH of 7.00 (7.31-7.41) and pCO2 of 22 (41-51 mmHg). Serum osmolality was 331 (289-309 mosm/kg) and a serum acetone level was high at 0.058% (0.0-0.010%). Serum ethanol, methanol, and isopropanol were negative thus ruling out possible ingestion as a source of osmolar gap. The patient was diagnosed with euDKA secondary to empagliflozin with precipitating factors being acute illness and decreased oral intake.Within 42 hours, treatment with normal saline and insulin infusion, the metabolic acidosis, anion gap, and osmolar gap normalized. Empagliflozin was discontinued upon discharge. Conclusion: A review of current literature suggests euDKA from empagliflozin is rare with only four cases reported to date. As SGLT-2 inhibitors continue to be increasingly prescribed, awareness of this potential complication in the setting of misleading blood glucose levels and an osmolar gap is integral for the early detection and treatment of euDKA. Patient counseling on this uncommon adverse event, especially during times of decreased oral intake and acute illness should be provided. Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. Abstracts presented at a news conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO. Endocrine Society 2019-04-30 /pmc/articles/PMC6552746/ http://dx.doi.org/10.1210/js.2019-SUN-LB030 Text en Copyright © 2019 Endocrine Society https://creativecommons.org/licenses/by-nc-nd/4.0/ This article has been published under the terms of the Creative Commons Attribution Non-Commercial, No-Derivatives License (CC BY-NC-ND; https://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Diabetes Mellitus and Glucose Metabolism
Thomas, Mathew
Tran, Ly
White, Christopher
Deppe, John
Davidson, James
SUN-LB030 Empagliflozin Causing Euglycemic Diabetic Ketoacidosis
title SUN-LB030 Empagliflozin Causing Euglycemic Diabetic Ketoacidosis
title_full SUN-LB030 Empagliflozin Causing Euglycemic Diabetic Ketoacidosis
title_fullStr SUN-LB030 Empagliflozin Causing Euglycemic Diabetic Ketoacidosis
title_full_unstemmed SUN-LB030 Empagliflozin Causing Euglycemic Diabetic Ketoacidosis
title_short SUN-LB030 Empagliflozin Causing Euglycemic Diabetic Ketoacidosis
title_sort sun-lb030 empagliflozin causing euglycemic diabetic ketoacidosis
topic Diabetes Mellitus and Glucose Metabolism
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6552746/
http://dx.doi.org/10.1210/js.2019-SUN-LB030
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