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SUN-188 Contributing Factors Precipitation Diabetic Ketoacidosis in Patients Using Sodium-Glucose Cotransporter-2 Inhibitor

Background: Euglycemic diabetic ketosis acidosis (DKA) is a possible adverse event with sodium-glucose cotransporter-2 inhibitor (SGLT2i). A number of contributing factor(s) have been identified precipitating DKA with the use of SGLT2i. Here we present three cases developing DKA on SGLT2i. Clinical...

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Autores principales: Attia, Jonven, Elsheikh, Arwa, Shafiq, Ismat, Valle, Valle
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Endocrine Society 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6553402/
http://dx.doi.org/10.1210/js.2019-SUN-188
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author Attia, Jonven
Elsheikh, Arwa
Shafiq, Ismat
Valle, Valle
author_facet Attia, Jonven
Elsheikh, Arwa
Shafiq, Ismat
Valle, Valle
author_sort Attia, Jonven
collection PubMed
description Background: Euglycemic diabetic ketosis acidosis (DKA) is a possible adverse event with sodium-glucose cotransporter-2 inhibitor (SGLT2i). A number of contributing factor(s) have been identified precipitating DKA with the use of SGLT2i. Here we present three cases developing DKA on SGLT2i. Clinical Case 1: A 64-year-old Caucasian female with history of type 2 diabetes (T2DM) presented to the emergency department (ED) with nausea, vomiting and abdominal pain 24 hours after evisceration of her eyes with implantation. She was on Jardiance for the last 3 months. Laboratory evaluation revealed a serum glucose of 95 mg/dl (n:70-100mg/dL), pH: 7.3 (n: 7.32 - 7.42), anion gap of 22 (n:7 - 16), carbon dioxide of 10 mmol/L (n: 20 - 28 mmol/L ), beta- hydroxybutyrate of 4.88 mmol/L (n: 0.02 - 0.27 mmol/L), plasma lactate of 0.9 mmol/L (n: 0.5 - 2.2 mmol/L) and urinalysis of glucose greater than 500 mg/dl and plus ketone. She was treated for euglycemic DKA with an insulin drip and intravenous fluids. She was discharge on insulin. Glutamic acid decarboxylase and islet cell antibodies were negative, c-peptide and insulin levels were normal. Perioperative continuation of Jardiance was attributed to be the cause of euglycemic DKA. Clinical Case 2: A 62-year-old male with T2DM presented to the ED for persistent nausea and vomiting. He has been on Jardiance for almost 8 months. A month ago, he started following intermittent fasting diet. Laboratory evaluation was consistent with euglycemic DKA. He had elevated Glutamic acid decarboxylase antibody thus was diagnosed with LADA. Intermittent fasting and LADA was attributed to be the cause euglycemic DKA. Clinical Case 3: 77-years-old male with T2DM well controlled on Jardiance, presented to the ED with nausea and abdominal pain. CT scan of the abdomen revealed gallbladder wall thickness and sludge with pericholecystic fluid. He underwent a percutaneous drainage and antibiotics treatment. A week into his hospitalization, he clinically deteriorated with laboratory findings consistent euglycemic DKA. Systemic illness was considered to be the underlying factor precipitating DKA. Conclusion: SGLT2i are reported to cause euglycemic DKA with underlying contributing factor(s). Physician and patients should be aware of the contributing factors precipitating DKA. Taking a thorough history, defining the type of diabetes, dietary education and discontinuation of medication in the setting of procedure/illness can prevent DKA and potential serious outcomes.
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spelling pubmed-65534022019-06-13 SUN-188 Contributing Factors Precipitation Diabetic Ketoacidosis in Patients Using Sodium-Glucose Cotransporter-2 Inhibitor Attia, Jonven Elsheikh, Arwa Shafiq, Ismat Valle, Valle J Endocr Soc Diabetes Mellitus and Glucose Metabolism Background: Euglycemic diabetic ketosis acidosis (DKA) is a possible adverse event with sodium-glucose cotransporter-2 inhibitor (SGLT2i). A number of contributing factor(s) have been identified precipitating DKA with the use of SGLT2i. Here we present three cases developing DKA on SGLT2i. Clinical Case 1: A 64-year-old Caucasian female with history of type 2 diabetes (T2DM) presented to the emergency department (ED) with nausea, vomiting and abdominal pain 24 hours after evisceration of her eyes with implantation. She was on Jardiance for the last 3 months. Laboratory evaluation revealed a serum glucose of 95 mg/dl (n:70-100mg/dL), pH: 7.3 (n: 7.32 - 7.42), anion gap of 22 (n:7 - 16), carbon dioxide of 10 mmol/L (n: 20 - 28 mmol/L ), beta- hydroxybutyrate of 4.88 mmol/L (n: 0.02 - 0.27 mmol/L), plasma lactate of 0.9 mmol/L (n: 0.5 - 2.2 mmol/L) and urinalysis of glucose greater than 500 mg/dl and plus ketone. She was treated for euglycemic DKA with an insulin drip and intravenous fluids. She was discharge on insulin. Glutamic acid decarboxylase and islet cell antibodies were negative, c-peptide and insulin levels were normal. Perioperative continuation of Jardiance was attributed to be the cause of euglycemic DKA. Clinical Case 2: A 62-year-old male with T2DM presented to the ED for persistent nausea and vomiting. He has been on Jardiance for almost 8 months. A month ago, he started following intermittent fasting diet. Laboratory evaluation was consistent with euglycemic DKA. He had elevated Glutamic acid decarboxylase antibody thus was diagnosed with LADA. Intermittent fasting and LADA was attributed to be the cause euglycemic DKA. Clinical Case 3: 77-years-old male with T2DM well controlled on Jardiance, presented to the ED with nausea and abdominal pain. CT scan of the abdomen revealed gallbladder wall thickness and sludge with pericholecystic fluid. He underwent a percutaneous drainage and antibiotics treatment. A week into his hospitalization, he clinically deteriorated with laboratory findings consistent euglycemic DKA. Systemic illness was considered to be the underlying factor precipitating DKA. Conclusion: SGLT2i are reported to cause euglycemic DKA with underlying contributing factor(s). Physician and patients should be aware of the contributing factors precipitating DKA. Taking a thorough history, defining the type of diabetes, dietary education and discontinuation of medication in the setting of procedure/illness can prevent DKA and potential serious outcomes. Endocrine Society 2019-04-30 /pmc/articles/PMC6553402/ http://dx.doi.org/10.1210/js.2019-SUN-188 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
Attia, Jonven
Elsheikh, Arwa
Shafiq, Ismat
Valle, Valle
SUN-188 Contributing Factors Precipitation Diabetic Ketoacidosis in Patients Using Sodium-Glucose Cotransporter-2 Inhibitor
title SUN-188 Contributing Factors Precipitation Diabetic Ketoacidosis in Patients Using Sodium-Glucose Cotransporter-2 Inhibitor
title_full SUN-188 Contributing Factors Precipitation Diabetic Ketoacidosis in Patients Using Sodium-Glucose Cotransporter-2 Inhibitor
title_fullStr SUN-188 Contributing Factors Precipitation Diabetic Ketoacidosis in Patients Using Sodium-Glucose Cotransporter-2 Inhibitor
title_full_unstemmed SUN-188 Contributing Factors Precipitation Diabetic Ketoacidosis in Patients Using Sodium-Glucose Cotransporter-2 Inhibitor
title_short SUN-188 Contributing Factors Precipitation Diabetic Ketoacidosis in Patients Using Sodium-Glucose Cotransporter-2 Inhibitor
title_sort sun-188 contributing factors precipitation diabetic ketoacidosis in patients using sodium-glucose cotransporter-2 inhibitor
topic Diabetes Mellitus and Glucose Metabolism
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6553402/
http://dx.doi.org/10.1210/js.2019-SUN-188
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