Cargando…

Euglycemic diabetic ketoacidosis caused by canagliflozin: a case report

BACKGROUND: Diabetic ketoacidosis (DKA) is seen relatively frequently in the emergency department (ED). DKA is characterized by hyperglycemia, acidosis, and ketonemia, and sodium glucose transporter 2 inhibitors (SGLT2i) represent a new diabetes medication that has been associated with euglycemic DK...

Descripción completa

Detalles Bibliográficos
Autores principales: Fukuda, Masafumi, Nabeta, Masakazu, Muta, Takanori, Fukami, Kei, Takasu, Osamu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6977311/
https://www.ncbi.nlm.nih.gov/pubmed/31969112
http://dx.doi.org/10.1186/s12245-020-0261-8
_version_ 1783490481434394624
author Fukuda, Masafumi
Nabeta, Masakazu
Muta, Takanori
Fukami, Kei
Takasu, Osamu
author_facet Fukuda, Masafumi
Nabeta, Masakazu
Muta, Takanori
Fukami, Kei
Takasu, Osamu
author_sort Fukuda, Masafumi
collection PubMed
description BACKGROUND: Diabetic ketoacidosis (DKA) is seen relatively frequently in the emergency department (ED). DKA is characterized by hyperglycemia, acidosis, and ketonemia, and sodium glucose transporter 2 inhibitors (SGLT2i) represent a new diabetes medication that has been associated with euglycemic DKA (eu-DKA). CASE PRESENTATION: A 71-year-old female who was being treated for type 2 diabetes with canagliflozin, metformin, and saxagliptin orally presented to the ED for evaluation of reduced oral intake, malaise, nausea, and abdominal pain. Although her blood glucose was not severely elevated (259 mg/dL), there was notable ketoacidosis (pH 6.89; CO(2), 11.4 mmHg; HCO(3), 1.9 mEq/L; base excess, − 31.3 mmol/L; 3-hydroxybutyric acid > 10,000 μmol/L) was observed. The uncontrolled acidosis improved following 3 days of continuous renal replacement therapy, but elevated urinary glucose continued for more than 10 days. Ringer’s lactated fluid supplementation was continued for management of polyurea and glucosuria. Urinary glucose turned negative on day 16, and there was improvement in the patient’s overall state; hence, she was discharged on day 18. CONCLUSION: Although it is difficult to diagnose eu-DKA because of the absence of substantial blood glucose abnormalities in the ED, there is a need to consider eu-DKA when evaluating acidosis in a patient treated with SGLT2i. Moreover, even after discontinuing the SGLT2i, attention should be given to the possibility of continuing glucosuria. Regular measurements of urinary glucose should be obtained, and the patient should be monitored for dehydration.
format Online
Article
Text
id pubmed-6977311
institution National Center for Biotechnology Information
language English
publishDate 2020
publisher Springer Berlin Heidelberg
record_format MEDLINE/PubMed
spelling pubmed-69773112020-01-28 Euglycemic diabetic ketoacidosis caused by canagliflozin: a case report Fukuda, Masafumi Nabeta, Masakazu Muta, Takanori Fukami, Kei Takasu, Osamu Int J Emerg Med Case Report BACKGROUND: Diabetic ketoacidosis (DKA) is seen relatively frequently in the emergency department (ED). DKA is characterized by hyperglycemia, acidosis, and ketonemia, and sodium glucose transporter 2 inhibitors (SGLT2i) represent a new diabetes medication that has been associated with euglycemic DKA (eu-DKA). CASE PRESENTATION: A 71-year-old female who was being treated for type 2 diabetes with canagliflozin, metformin, and saxagliptin orally presented to the ED for evaluation of reduced oral intake, malaise, nausea, and abdominal pain. Although her blood glucose was not severely elevated (259 mg/dL), there was notable ketoacidosis (pH 6.89; CO(2), 11.4 mmHg; HCO(3), 1.9 mEq/L; base excess, − 31.3 mmol/L; 3-hydroxybutyric acid > 10,000 μmol/L) was observed. The uncontrolled acidosis improved following 3 days of continuous renal replacement therapy, but elevated urinary glucose continued for more than 10 days. Ringer’s lactated fluid supplementation was continued for management of polyurea and glucosuria. Urinary glucose turned negative on day 16, and there was improvement in the patient’s overall state; hence, she was discharged on day 18. CONCLUSION: Although it is difficult to diagnose eu-DKA because of the absence of substantial blood glucose abnormalities in the ED, there is a need to consider eu-DKA when evaluating acidosis in a patient treated with SGLT2i. Moreover, even after discontinuing the SGLT2i, attention should be given to the possibility of continuing glucosuria. Regular measurements of urinary glucose should be obtained, and the patient should be monitored for dehydration. Springer Berlin Heidelberg 2020-01-22 /pmc/articles/PMC6977311/ /pubmed/31969112 http://dx.doi.org/10.1186/s12245-020-0261-8 Text en © The Author(s). 2020 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Case Report
Fukuda, Masafumi
Nabeta, Masakazu
Muta, Takanori
Fukami, Kei
Takasu, Osamu
Euglycemic diabetic ketoacidosis caused by canagliflozin: a case report
title Euglycemic diabetic ketoacidosis caused by canagliflozin: a case report
title_full Euglycemic diabetic ketoacidosis caused by canagliflozin: a case report
title_fullStr Euglycemic diabetic ketoacidosis caused by canagliflozin: a case report
title_full_unstemmed Euglycemic diabetic ketoacidosis caused by canagliflozin: a case report
title_short Euglycemic diabetic ketoacidosis caused by canagliflozin: a case report
title_sort euglycemic diabetic ketoacidosis caused by canagliflozin: a case report
topic Case Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6977311/
https://www.ncbi.nlm.nih.gov/pubmed/31969112
http://dx.doi.org/10.1186/s12245-020-0261-8
work_keys_str_mv AT fukudamasafumi euglycemicdiabeticketoacidosiscausedbycanagliflozinacasereport
AT nabetamasakazu euglycemicdiabeticketoacidosiscausedbycanagliflozinacasereport
AT mutatakanori euglycemicdiabeticketoacidosiscausedbycanagliflozinacasereport
AT fukamikei euglycemicdiabeticketoacidosiscausedbycanagliflozinacasereport
AT takasuosamu euglycemicdiabeticketoacidosiscausedbycanagliflozinacasereport