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A case report of euglycemic ketoacidosis due to dapagliflozin treatment

Year 2021, , 85 - 86, 07.03.2021
https://doi.org/10.46310/tjim.877156

Abstract

Diabetic ketoacidosis (DKA) is a leading cause of mortality and morbidity in type 2 diabetic patients. Sodium-glucose co-transporter (SGLT-2) inhibitors are a new antidiabetic treatment class that increases the renal excretion of glucose. The Food and Drug Administration issued a warning in May 2015 notifying that patients using this class of anti-diabetic drugs may develop DKA. Risk factors for DKA development among patients who take SGLT-2 inhibitors include carbohydrate intake/starvation or acute illness. In the current report, we aimed to present a case of euglycemic DKA using dapagliflozin treatment.

References

  • 1. Chao EC, Henry RR. SGLT2 inhibition--a novel strategy for diabetes treatment. Nat Rev Drug Discov 2010;9(7):551–9.
  • 2. Dhatariya KK, Umpierrez GE. Guidelines for management of diabetic ketoacidosis: time to revise? Lancet Diabetes Endocrinol 2017;5(5):321–3.
  • 3. Yu X, Zhang S, Zhang L. Newer Perspectives of Mechanisms for Euglycemic Diabetic Ketoacidosis. Int J Endocrinol 2018;2018:7074868.
  • 4. Fralick M, Schneeweiss S, Patorno E. Risk of Diabetic Ketoacidosis after Initiation of an SGLT2 Inhibitor. N Engl J Med 2017;376(23):2300–2.
  • 5. Food and Drug Administration, FDA drug safety communication: FDA warns that SGLT2 inhibitors for diabetes may result in a serious condition of too much acid in the bloodNovember 2019 http://www.fda.gov/Drugs/Drug.Safety/ucm446845.htm.
  • 6. Taylor SI, Blau JE, Rother KI. SGLT2 Inhibitors May Predispose to Ketoacidosis. J Clin Endocrinol Metab 2015;100(8):2849–52.
  • 7. American Diabetes Association. 9. Pharmacologic Approaches to Glycemic Treatment: Standards of Medical Care in Diabetes-2021. Diabetes Care 2021;44(Suppl 1):S111–24.
  • 8. Burke KR, Schumacher CA, Harpe SE. SGLT2 Inhibitors: A Systematic Review of Diabetic Ketoacidosis and Related Risk Factors in the Primary Literature. Pharmacotherapy 2017;37(2):187–94.
Year 2021, , 85 - 86, 07.03.2021
https://doi.org/10.46310/tjim.877156

Abstract

References

  • 1. Chao EC, Henry RR. SGLT2 inhibition--a novel strategy for diabetes treatment. Nat Rev Drug Discov 2010;9(7):551–9.
  • 2. Dhatariya KK, Umpierrez GE. Guidelines for management of diabetic ketoacidosis: time to revise? Lancet Diabetes Endocrinol 2017;5(5):321–3.
  • 3. Yu X, Zhang S, Zhang L. Newer Perspectives of Mechanisms for Euglycemic Diabetic Ketoacidosis. Int J Endocrinol 2018;2018:7074868.
  • 4. Fralick M, Schneeweiss S, Patorno E. Risk of Diabetic Ketoacidosis after Initiation of an SGLT2 Inhibitor. N Engl J Med 2017;376(23):2300–2.
  • 5. Food and Drug Administration, FDA drug safety communication: FDA warns that SGLT2 inhibitors for diabetes may result in a serious condition of too much acid in the bloodNovember 2019 http://www.fda.gov/Drugs/Drug.Safety/ucm446845.htm.
  • 6. Taylor SI, Blau JE, Rother KI. SGLT2 Inhibitors May Predispose to Ketoacidosis. J Clin Endocrinol Metab 2015;100(8):2849–52.
  • 7. American Diabetes Association. 9. Pharmacologic Approaches to Glycemic Treatment: Standards of Medical Care in Diabetes-2021. Diabetes Care 2021;44(Suppl 1):S111–24.
  • 8. Burke KR, Schumacher CA, Harpe SE. SGLT2 Inhibitors: A Systematic Review of Diabetic Ketoacidosis and Related Risk Factors in the Primary Literature. Pharmacotherapy 2017;37(2):187–94.
There are 8 citations in total.

Details

Primary Language English
Subjects ​Internal Diseases
Journal Section Case Reports
Authors

Murat Çalapkulu 0000-0002-7445-2275

Muhammed Erkam Sencar 0000-0001-5581-4886

İlknur Öztürk Ünsal 0000-0003-3999-6426

Hayri Bostan 0000-0002-4957-9856

Erman Çakal 0000-0003-4455-7276

Publication Date March 7, 2021
Submission Date February 8, 2021
Acceptance Date March 6, 2021
Published in Issue Year 2021

Cite

EndNote Çalapkulu M, Sencar ME, Öztürk Ünsal İ, Bostan H, Çakal E (March 1, 2021) A case report of euglycemic ketoacidosis due to dapagliflozin treatment. Turkish Journal of Internal Medicine 3 Supplement 1 85–86.

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