diabetestalk.net

Euglycemic Dka Mechanism

A Can't Miss Ed Diagnosis: Euglycemic Dka

A Can't Miss Ed Diagnosis: Euglycemic Dka

The FDA has approved these three SGLT2 inhibitors for Type 2 diabetics, and at times, they are prescribed off-label for Type 1. The mechanism involves decreasingglucose reabsorption in the nephrons proximal tubule (via inhibition of the sodium-glucose linked cotransporter-2 protein). This results in increased urinary excretion of glucose that is independent of the bodys insulin secretion.1 Other potential benefits of this class of medications include:13 In 2015 the FDA issued a warning, however, that SGLT2 inhibitors may cause ketoacidosis, urinary tract infections, and urosepsis.4 Since then, multiple case reports have been published showing an association between SGLT2 inhibitors and the development of euglycemic DKA. Euglycemic DKA is an uncommon and likely under-diagnosed phenomenon, best defined as DKA with alower than expected blood glucose (less than 250 mg/dL according to the American Diabetes Association).46 Potential precipitants, in addition to SGLT2 inhibitors, include:7 EPs may delay diagnosis, given the modest glucose levels at the time of presentation. This, however, is false reassurance because DKA is not defined by an absolute blood glucose. Interestingly, patients with euglycemic DKA may have a normal mental status despite marked ketoacidosis, and vomiting seems to be a common complaint.5 Euglycemic DKA treatment is the same as traditional DKA, and includes hydration, insulin, and supportive care. Patients with euglycemic DKA may also need a dextrose infusion given the lower glucose levels. SGLT2 Inhibitors and Euglycemic DKA: Mechanism The mechanisms by which SGLT2 inhibitors cause or predispose to euglycemic DKA are unclear and likely complex. SGLT2 inhibitors may lead to a decrease in either endogenous or exogenous insulin, and an increase in gluca Continue reading >>

Euglycemic Diabetic Ketoacidosis: The Clinical Concern Of Sglt2 Inhibitors

Euglycemic Diabetic Ketoacidosis: The Clinical Concern Of Sglt2 Inhibitors

Euglycemic diabetic ketoacidosis is a post market warning in patients with type 1 diabetes and type 2 diabetes treated with SGLT-2 inhibitors. We report a case of a 39-year-old obese female with presumed type 2 diabetes for seven years who presented to the emergency department with three days of nausea, vomiting, and abdominal pain. Due to previous total non-adherence with a prescribed insulin regimen, she was recently started on canagliflozin and liraglutide. The diagnosis of euDKA was missed in the initial evaluation as the blood glucose level was only 167 mg/dL. Further work up showed severe metabolic acidosis with an anion gap of 25 and positive ketones in the urine. She was treated successfully with dextrose water 5%/half normal saline and an insulin drip. As part of the work up, she tested positive for glutamic acid decarboxylase autoantibodies. Given the increasing utilization of SGLT-2 inhibitors and the fact that patients can present with near-normal glycemia, the diagnosis can be missed. Vigilance with the use of SGLT-2 inhibitors is necessary to decrease morbidity and potentially mortality particularly in patients with long-standing type 2 diabetes associated with marked β-cell insufficiency, type 1 diabetes mellitus, or latent autoimmune diabetes of adult onset. Continue reading >>

Risk Of Diabetic Ketoacidosis After Initiation Of An Sglt2 Inhibitor

Risk Of Diabetic Ketoacidosis After Initiation Of An Sglt2 Inhibitor

To the Editor: Inhibitors of sodium–glucose cotransporter 2 (SGLT2) decrease plasma glucose by blocking the reabsorption of glucose at the proximal tubule.1,2 Case reports have suggested that SGLT2 inhibitors may be associated with an increased risk of diabetic ketoacidosis, which led to a warning from the Food and Drug Administration (FDA) in May 2015.3,4 The objective of our study was to assess the risk of diabetic ketoacidosis after the initiation of an SGLT2 inhibitor. Using a large claims database of commercially insured patients in the United States (Truven MarketScan), we identified a cohort of adult patients (≥18 years of age) who had newly started treatment with either an SGLT2 inhibitor or a dipeptidyl peptidase-4 (DPP4) inhibitor between April 1, 2013, and December 31, 2014 (before the FDA warning). DPP4 inhibitors were chosen as the comparator medication because they are similarly used as a second-line treatment for diabetes but have no known association with diabetic ketoacidosis. We excluded patients with human immunodeficiency virus infection, end-stage renal disease, cancer, type 1 diabetes, or past diabetic ketoacidosis. Our primary outcome was hospitalization for diabetic ketoacidosis (using the primary position code of the International Classification of Diseases, Ninth Revision) within 180 days after the initiation of an SGLT2 inhibitor or a DPP4 inhibitor. We censored data for patients at the time that they discontinued the initial medication, had the outcome, lost insurance coverage, or died. We used 1:1 propensity-score matching to balance 46 characteristics of the patients and Cox regression to estimate hazard ratios and 95% confidence intervals for diabetic ketoacidosis within 180 days after treatment initiation. Predefined sensitivity analy Continue reading >>

Euglycemic Diabetic Ketoacidosis: A Review.

Euglycemic Diabetic Ketoacidosis: A Review.

Abstract INTRODUCTION: Diabetic ketoacidosis (DKA) is one of the most serious complications of diabetes. It is characterised by the triad of hyperglycemia (blood sugar >250 mg/dl), metabolic acidosis (arterial pH <7.3 and serum bicarbonate <18 mEq/L) and ketosis. Rarely these patients can present with blood glucose (BG) levels of less than 200 mg/dl, which is defined as euglycemic DKA. The possible etiology of euglycemic DKA includes the recent use of insulin, decreased caloric intake, heavy alcohol consumption, chronic liver disease and glycogen storage disorders. DKA in pregnancy has also been reported to present with euglycemia. The recent use of sodium glucose cotransporter 2 (SGLT2) inhibitors has shed light on another possible mechanism of euglycemic DKA. Clinicians may also be misled by the presence of pseudonormoglycemia. CONCLUSION: Euglycemic DKA thus poses a challenge to physicians, as patients presenting with normal BG levels in ketoacidosis may be overlooked, leading to a delay in appropriate management strategies. In this article, we review all the possible etiologies and the associated pathophysiology of patients presenting with euglycemic DKA. We also discuss the approach to diagnosis and management of such patients. Despite euglycemia, ketoacidosis in diabetic patients remains a medical emergency and must be treated in a quick and appropriate manner. Copyright© Bentham Science Publishers; For any queries, please email at [email protected] Continue reading >>

Euglycemic Diabetic Ketoacidosis In Type 2 Diabetes Treated With A Sodium-glucose Cotransporter-2 Inhibitor

Euglycemic Diabetic Ketoacidosis In Type 2 Diabetes Treated With A Sodium-glucose Cotransporter-2 Inhibitor

Go to: Case A 51-year-old man with a known history of T2DM and hypertension presented to the emergency department with a 1-week history of malaise, cough, and intermittent shortness of breath. Over the preceding 2 days, he admitted to a history of decreased oral intake and fever, and he had abstained from taking his antihyperglycemic medications (canagliflozin and linagliptin-metformin). He reported 3 episodes of clear emesis the day of his presentation in the emergency department. He denied any other symptoms, sick contacts, or travel history. He reported no substance use, alcohol consumption, or other ingestions. He was not vaccinated against the flu. He was not taking insulin. Vital signs at triage were within normal limits except for a heart rate of 122 beats/min. The patient looked well and was in no acute distress. The only relevant physical examination findings were mild inspiratory crackles at the left lower lobe on auscultation of the lungs. A 12-lead electrocardiogram showed sinus tachycardia at 101 beats/min. Initial bloodwork revealed a hemoglobin level of 159 g/L (normal range 130 to 170 g/L); a white blood cell count of 12.1 × 109/L (normal range 4.8 × 109/L to 10.8 × 109/L); a neutrophil count of 11.0 × 109/L (normal range 2.0 × 109/L to 7.0 × 109/L); a platelet count of 405 × 109/L (normal range 130 × 109/L to 400 × 109/L); a random blood glucose level of 11.9 mmol/L (normal range 3.9 to 11.2 mmol/L); a sodium concentration of 139 mmol/L (normal range 136 to 144 mmol/L); a potassium level of 5.0 mmol/L (normal range 3.5 to 5.5 mmol/L); a chloride level of 93 mmol/L (normal range 98 to 109 mmol/L); a total CO2 level of 8 mmol/L (normal range 22 to 29 mmol/L); an anion gap of 38 mmol/L (normal range 4 to 12 mmol/L); a urea level of 9.3 mmol/L (nor Continue reading >>

Sglt2 Inhibitors May Predispose To Ketoacidosis

Sglt2 Inhibitors May Predispose To Ketoacidosis

SGLT2 Inhibitors May Predispose to Ketoacidosis Diabetes, Endocrinology, and Obesity Branch (S.I.T., J.E.B., K.I.R.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; Division of Diabetes, Endocrinology, and Nutrition (S.I.T.), Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland 21201 Address all correspondence and requests for reprints to: Simeon I. Taylor, MD, PhD, Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Mail Stop 1453, 9000 Rockville Pike, Bethesda, MD 20892. Search for other works by this author on: Diabetes, Endocrinology, and Obesity Branch (S.I.T., J.E.B., K.I.R.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; Search for other works by this author on: Diabetes, Endocrinology, and Obesity Branch (S.I.T., J.E.B., K.I.R.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; Search for other works by this author on: The Journal of Clinical Endocrinology & Metabolism, Volume 100, Issue 8, 1 August 2015, Pages 28492852, Simeon I. Taylor, Jenny E. Blau, Kristina I. Rother; SGLT2 Inhibitors May Predispose to Ketoacidosis, The Journal of Clinical Endocrinology & Metabolism, Volume 100, Issue 8, 1 August 2015, Pages 28492852, Sodium glucose cotransporter 2 (SGLT2) inhibitors are antidiabetic drugs that increase urinary excretion of glucose, thereby improving glycemic control and promoting weight loss. Since approval of the first-in-class drug in 2013, data have emerged suggesting that these drugs increase the risk of di Continue reading >>

Get Unlimited Access On Medscape.

Get Unlimited Access On Medscape.

You’ve become the New York Times and the Wall Street Journal of medicine. A must-read every morning. ” Continue reading >>

Euglycemic Dka: It’s Not A Myth

Euglycemic Dka: It’s Not A Myth

Background: Diabetic ketoacidosis (DKA) is traditionally defined as a triad of hyperglycemia (>250mg/dL), anion gap acidosis, and increased plasma ketones. There is another entity that providers must be aware of known as euglycemic DKA (euDKA), which is essentially DKA without the hyperglycemia (Serum glucose <200 mg/dL). Euglycemic DKA is a rare entity that mostly occurs in patients with type 1 diabetes, but can possibly occur in type 2 diabetes as well. The exact mechanism of euDKA is not entirely known, but has been associated with partial treatment of diabetes, carbohydrate food restriction, alcohol intake, and inhibition of gluconeogenesis. euDKA, can also be associated with sodium-glucose cotransporter 2 (SGLT-2) inhibitor medications. These medications first came onto the market in 2013 and are FDA approved for the treatment of type 2 diabetes, however many physicians use them off-label for type I diabetes due to their ability to improve average glucose levels, reduce glycemic variability without increasing hypoglycemia, and finally promote weight loss. Does euDKA Exist even in Patients not Using SGLT-2 Inhibitors? The short answer is YES. Munro JF et al [5] reviewed a case series of 37 episodes of euDKA in a publication from 1973. Although, dated and not robust evidence some take home messages can be derived: All but one episode was in insulin dependent diabetics Vomiting was the most frequent symptom of euDKA in 32% of patients Management in most cases consisted of: Intravenous fluids and electrolyte replacement. No deaths occurred in this case series What are the Names of the SGLT-2 Inhibitors? Ipragliflozin (Suglat) – Approved in Japan Dapagliflozin (Farxiga) – 1st SGLT2 Inhibitor Approved; Approved in US Luseogliflozin (Lusefi) – Approved in Japan Tofo Continue reading >>

Euglycemic Diabetic Ketoacidosis Sometimes Seen With Sglt2 Inhibitors

Euglycemic Diabetic Ketoacidosis Sometimes Seen With Sglt2 Inhibitors

Craig Cocchio, PharmD, BCPS, is an Emergency Medicine Clinical Pharmacist at Trinity Mother Frances Hospital in Tyler, Texas. Follow on Twitter @iEMPharmD and on his blog at empharmd.blogspot.com Diabetic ketoacidosis (DKA) in patients with presenting serum blood glucose <200 mg/dL isn’t common. More often, it’s seen in patients with type 1 diabetes in conjunction with starvation and acute illness.1 It’s difficult to determine an incidence of euglycemic DKA (euDKA) among all DKA cases in the literature, given the migration of the serum glucose cutoff from ≤300 mg/dL to ≤200 mg/dL. The best estimation based on an analysis of case reports suggests an incidence anywhere between 0.8% and 7.5%.1 However, the sodium-glucose cotransporter-2 (SGLT2) inhibitors canagliflozin, dapagliflozin, and empagliflozin can apparently induce this once-rare form of DKA.2,3 SGLT2 inhibitors are a class of oral hypoglycemic drugs indicated only for type 2 diabetes. Their novel mechanism of action prevents glucose reabsorption from the proximal renal tubules, resulting in increased glucosuria and decreasing plasma glucose. SGLT2 inhibitors lower serum glucose and HBA1C levels, and even produce weight loss. However, the increased glucose concentration in the bladder is a terrific incubation environment for fungi and bacteria, so much so that the FDA stuck a post-marketing warning on the drug class for the increased risk of serious urinary tract infections and urosepsis, in addition to euglycemic DKA. The proposed mechanism suggests that while SGLT2 inhibitors lower serum glucose, they also reduce insulin secretion from pancreatic beta cells in a negative feedback fashion. The lower serum insulin coupled with lower serum glucose consequently shifts energy metabolism to antilipolytic act Continue reading >>

Euglycemic Dka From Sglt2 Inhibitors: Don't Worry, I Can't Pronounce Them Either

Euglycemic Dka From Sglt2 Inhibitors: Don't Worry, I Can't Pronounce Them Either

Diabetic ketoacidosis in patients with presenting serum blood glucose less than 200 is not common. Particularly when practicing in the Bible/Diabetes belt of the United States. This euglycemic DKA (euDKA) is more often associated in patients with type 1 diabetes in conjunction with starvation and acute illness.[1] It's difficult to determine an incidence of euglycemic serum glucose among all DKA cases in the literature given the migration of the serum glucose cutoff from 300 or less to 200 or less. The best estimation based on an analysis of case reports suggests an incidence anywhere from 0.8% to 7.5%.[1] However, the newest class of unpronounceable medications, the sodium-glucose co-transporter 2 inhibitors (SGLT2inh) (canagliflozin, dapagliflozin, empagliflozin) are making their presence known by inducing this once rare form of DKA.[2-3] SGLT2inhs are a class of oral hypoglycemic drugs indicated only for type 2 diabetes. Their novel mechanism of action prevents glucose reabsorption from the proximal renal tubules resulting in increased glucosuria and decreasing plasma glucose. The resulting effects include lower serum glucose levels, lower HBA1C, and even weight loss. But that's not all. The increased glucose concentration in the bladder is a terrific incubation environment for fungi and bacteria. So much so that the FDA has slapped a post-marketing warning on the drug class for the increased risk of UTI and urosepsis. In other patients, euglycemic DKA may occur. This too has led to the FDA issuing a similar warning of this possible life threat. The proposed mechanism suggests that SGLT2inhs while lowering serum glucose, also reduces insulin secretion from pancreatic beta cells in a negative feedback fashion. The lower serum insulin coupled with lower serum glucose c Continue reading >>

Diabetic Ketoacidosis With Sglt2 Inhibitors Is Manageable

Diabetic Ketoacidosis With Sglt2 Inhibitors Is Manageable

Diabetic Ketoacidosis With SGLT2 Inhibitors Is Manageable The euglycemic diabetic ketoacidosis (DKA) that has recently been associated with the use of sodiumglucose cotransporter 2 (SGLT2) inhibitors will probably turn out to be very infrequent in patients with type 2 diabetes and "predictable, detectable, and preventable" in those with type 1 diabetes, two leading clinical trialists assert in a new editorial published in the September issue of Diabetes Care. The piece by Julio Rosenstock, MD, of the Dallas Diabetes and Endocrine Center at Medical City, Texas, and Ele Ferrannini, MD, of the Institute of Clinical Physiology, Consiglio Nazionale delle Ricerche, Pisa, Italy accompanies the published versions of two related articles that had previously appeared online: a Janssen article demonstrating a low (but not zero) risk for DKA in a clinical-trial program of canagliflozin (Invokana, Janssen Pharmaceuticals, Inc), and a case series report of 13 episodes of euglycemic DKA in nine patients, seven with type 1 diabetes and two with type 2 diabetes, who developed the condition postoperatively. The issue initially came to light in May 2015, when the US Food and Drug Administration issued a notice on the basis of 20 cases of DKA associated with SGLT2 inhibitors reported to the agency's adverse-event reporting system database. A month later, the European Medicines Agency initiated a review and identified 101 cases worldwide associated with type 2 diabetes. Dr Rosenstock and Dr Ferrannini provide unpublished data from the other manufacturers of SGLT2 inhibitors on the US market, suggesting rates of DKA symptoms of 0.1% or less in randomized trials in more than 18,000 patients receiving dapagliflozin (multiple brands) and 7000 patients receiving empagliflozin (Jardiance, Boehri Continue reading >>

Euglycemic Diabetic Ketoacidosis: A Diagnostic And Therapeutic Dilemma

Euglycemic Diabetic Ketoacidosis: A Diagnostic And Therapeutic Dilemma

Euglycemic diabetic ketoacidosis: a diagnostic and therapeutic dilemma 1Department of Internal Medicine, Memorial Hospital of Martinsville and Henry County, Martinsville, Virginia, USA, 2Texas Tech University Health Sciences Center, El Paso, Texas, USA, 3Senior Research Associate, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA, 4Department of Pharmacology, St Johns Medical College, Bangalore, India, Received 2017 Jul 18; Accepted 2017 Aug 4. This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License . Euglycemic diabetic ketoacidosis (EDKA) is a clinical triad comprising increased anion gap metabolic acidosis, ketonemia or ketonuria and normal blood glucose levels <200 mg/dL. This condition is a diagnostic challenge as euglycemia masquerades the underlying diabetic ketoacidosis. Thus, a high clinical suspicion is warranted, and other diagnosis ruled out. Here, we present two patients on regular insulin treatment who were admitted with a diagnosis of EDKA. The first patient had insulin pump failure and the second patient had urinary tract infection and nausea, thereby resulting in starvation. Both of them were aggressively treated with intravenous fluids and insulin drip as per the protocol for the blood glucose levels till the anion gap normalized, and the metabolic acidosis reversed. This case series summarizes, in brief, the etiology, pathophysiology and treatment of EDKA. Euglycemic diabetic ketoacidosis is rare. Consider ketosis in patients with DKA even if their serum glucose levels are normal. High clinical suspicion is required to diagnose EDKA as normal blood sugar levels masquerade the underlying DKA and cause a diagnostic and therapeutic dilemma. Blood pH and blood or urine Continue reading >>

Euglycemic Dka Secondary To Sglt2 Inhibitors

Euglycemic Dka Secondary To Sglt2 Inhibitors

Authors: Priyanka Kailash (MS-4, Campbell University School of Osteopathic Medicine), Kevin Weaver, DO (Program Director, Lehigh Valley Health Network), and Krystle Shafer, MD (Attending Physician, York Hospital) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit) A 35-year-old male with a past medical history of type 2 diabetes arrives at the Emergency Department (ED) with altered mental status, nausea, vomiting, and diffuse abdominal pain that started 10 hours ago. The patient was recently started on an SGLT2 inhibitor. On examination, the patient is tachycardic (HR 126) and tachypneic (RR 25), with normal blood pressure (110/90). He is further noted to have dry mucous membranes and poor skin turgor. Blood glucose is noted to be 140 mg/dl, serum ketones 6.2 mmol/L, and arterial pH of 6.9. The patient is diagnosed with euglycemic DKA and quickly admitted to ICU for treatment. Pathogenesis of Typical DKA Two major complications from type 1 diabetes mellitus and type 2 diabetes mellitus are diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). DKA is typically seen in younger individuals, while HHS is typically seen in older patients(1). In the pathogenesis of typical DKA, the body experiences a starved state. Insulin deficiency (either through decreased production or decrease sensitivity) leads to the inactivation of GLUT4 receptors on cells. GLUT4 receptors function to help transport glucose molecules into cells so that it can be converted into energy. Without GLUT4 receptor activation, the glucose entry into cells remains shut. Thus, the cells start to experience a starved state. To compensate, the body activates an alternative energy pathway Continue reading >>

Euglycemic Diabetic Ketoacidosis: A Predictable, Detectable, And Preventable Safety Concern With Sglt2 Inhibitors

Euglycemic Diabetic Ketoacidosis: A Predictable, Detectable, And Preventable Safety Concern With Sglt2 Inhibitors

The Case At Hand Recently, the U.S. Food and Drug Administration (FDA) issued a Drug Safety Communication that warns of an increased risk of diabetic ketoacidosis (DKA) with uncharacteristically mild to moderate glucose elevations (euglycemic DKA [euDKA]) associated with the use of all the approved sodium–glucose cotransporter 2 (SGLT2) inhibitors (1). This Communication was based on 20 clinical cases requiring hospitalization captured between March 2013 and June 2014 in the FDA Adverse Event Reporting System database. The scarce clinical data provided suggested that most of the DKA cases were reported in patients with type 2 diabetes (T2D), for whom this class of agents is indicated; most likely, however, they were insulin-treated patients, some with type 1 diabetes (T1D). The FDA also identified potential triggering factors such as intercurrent illness, reduced food and fluid intake, reduced insulin doses, and history of alcohol intake. The following month, at the request of the European Commission, the European Medicines Agency (EMA) announced on 12 June 2015 that the Pharmacovigilance Risk Assessment Committee has started a review of all of the three approved SGLT2 inhibitors (canagliflozin, dapagliflozin, and empagliflozin) to evaluate the risk of DKA in T2D (2). The EMA announcement claimed that as of May 2015 a total of 101 cases of DKA have been reported worldwide in EudraVigilance in T2D patients treated with SGLT2 inhibitors, with an estimated exposure over 0.5 million patient-years. No clinical details were provided except for the mention that “all cases were serious and some required hospitalisation. Although [DKA] is usually accompanied by high blood sugar levels, in a number of these reports blood sugar levels were only moderately increased” (2). Wit Continue reading >>

Euglycemic Diabetic Ketoacidosis Due To Canagliflozin In A Patient With An Uncertain Diagnosis Of Type 2 Diabetes: A Case Report

Euglycemic Diabetic Ketoacidosis Due To Canagliflozin In A Patient With An Uncertain Diagnosis Of Type 2 Diabetes: A Case Report

University of Pittsburgh Medical Center, Pittsburgh, PA, USA *Corresponding Author: Bonnie B. Lu University of Pittsburgh Medical Center Pittsburgh, PA, USA Tel: +1 412-647-2345 E-mail: [email protected] Citation: Lu BB, Rivera-Lebron B, Ng J (2017) Euglycemic Diabetic Ketoacidosis Due to Canagliflozin in A Patient with an Uncertain Diagnosis of Type 2 Diabetes: A Case Report. Diabetes Case Rep 2:127. doi: 10.4172/2572-5629.1000127 Copyright: © 2017 Lu BB, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Diabetes Case Reports Abstract Sodium-glucose cotransport 2 (SGLT2) inhibitors are approved for use only in patients with type 2 diabetes and work by blocking glucose reabsorption in the proximal renal tubule. There is also evidence that SGLT2 inhibitors directly act on pancreatic α-cells to stimulate glucagon secretion, leading to additional ketone body production, and that SGLT2 inhibitors decrease renal clearance of ketone bodies. While the risk of euglycemic diabetic ketoacidosis (eDKA) associated with offlabel use in patients with type 1 diabetes is well known, there are currently no guidelines for SGLT2 inhibitor use in patients with diabetes of uncertain or transitioning pathology. We report a case of eDKA associated with canagliflozin in a patient with rapid progression of noninsulin dependent to insulin-dependent diabetes within the span of 2 years to illustrate the risk of eDKA when SGLT2 inhibitors are used in patients with an uncertain insulin treatment requirement in T2D. Keywords SGLT2 inhibitor; Euglycemic diabetic ketoacidosis Continue reading >>

More in ketosis