Case of ketoacidosis by a sodium‐glucose cotransporter 2 inhibitor in a diabetic patient with a low‐carbohydrate diet

Abstract

We present a case of a 32-year-old diabetic woman with Prader–Willi syndrome who developed severe ketoacidosis caused by a sodium-glucose cotransporter 2 (SGLT2) inhibitor, a novel class of antihyperglycemic agents, during a strict low-carbohydrate diet. At admission, a serum glucose level of 191 mg/dL was relatively low, though laboratory evaluations showed severe ketoacidosis. This is the first report of ketoacidosis caused by a SGLT2 inhibitor. It is necessary to not only pay attention when using a SGLT2 inhibitor in patients following a low-carbohydrate diet, but also to start a low-carbohydrate diet in patients treated with a SGLT2 inhibitor because of a high risk for developing ketoacidosis.

Possible risk factors for the development of sodium-glucose co-transporter 2 inhibitor- associated diabetic ketoacidosis in type 2 diabetes

“…One of the limitations of studies of SGLT-2 inhibitors is that no analysis has been done on the effectiveness of these drugs after different durations of diabetes, nor whether this is a factor in determining the risk of developing DKA. 9 Hayami et al also hypothesised that this class of oral hypoglycaemic agent may be particularly useful in patients who have had diabetes for a longer duration in whom sulphonylureas have become less effective due to reduced beta cell activity. 9 However, we would postulate the opposite: if an SGLT-2 inhibitor is to be used, it should be early where beta cell reserve function is retained.…”

“…9 Hayami et al also hypothesised that this class of oral hypoglycaemic agent may be particularly useful in patients who have had diabetes for a longer duration in whom sulphonylureas have become less effective due to reduced beta cell activity. 9 However, we would postulate the opposite: if an SGLT-2 inhibitor is to be used, it should be early where beta cell reserve function is retained. The lack of data reporting the duration of diabetes in those who have developed DKA means that this postulated mechanism remains speculative.…”

“…These include a faster than predicted weight loss because this may indicate reduced beta cell function. 1,9 We also suggest immediate cessation of the medication if the patient becomes acutely unwell or has reduced oral intake. Finally, in the acute management of possible SGLT-2 inhibitor-induced DKA, the increased glycosuria has been shown for up to 11 days following cessation of the SGLT-2 inhibitor, 6 meaning that metabolic correction may be slower than expected.…”

“…8 The last case described a patient who followed a strictly reduced carbohydrate diet in the time period leading up to presentation with DKA. 9 Case report In May 2015 a 48-year-old woman with a 16-year history of T2DM and hypertension presented to the emergency department with a 4-week history of back pain and malaise. She had no other medical history and denied alcohol use.…”

Cetosis normoglicémica en adolescente con diabetes tipo 1 recibiendo insulina y dapaglifozina: Reporte de un caso

“…Since then, a few other DKA cases have been published 13,14 . However, large series of patients report a very low incidence of this association [15][16][17] .…”