Sodium Glucose Transporter 2 Inhibitors and Diabetic Ketoacidosis in Three Patients with Diabetes: Underlying Causation

Abstract

Sodium glucose transporter 2 inhibitors (SGLT2i) inhibit the reabsorption of glucose in the renal tubules reducing glycemia and increasing glucosuria. The increased glucosuria causes a shift in normal flora and colonization of pathogenic microorganisms leading to an increase in mycotic genital infections. Recent Food and Drug Administration reported cases of diabetic ketoacidosis (DKA) after initiation of SGLT2i probes the question of safety with such agents. The mechanisms of ketoacidosis and the breakdown of lipids are often misunderstood, and blame is placed on lack of insulin or on medications used to treat diabetes. However, many patients living with diabetes do not experience DKA if the proper treatment and management of concomitant comorbidities are addressed. After a retrospective chart review of 250 patients, three patients were identified with DKA while on SGLT2i, but for three distinct contrasting reasons. Assessment of the pharmacodynamics of SGLT2i and the pathophysiology of DKA infers that emphasis for prevention of SGLT2i-associated DKA should be placed on appropriate diagnosis, infection, and electrolyte abnormalities.

Keywords: Case series; diabetes; diabetic ketoacidosis; electrolyte abnormalities; latent autoimmune diabetes in adults; sodium glucose transporter 2 inhibitors.

Figure 1

Mechanisms of diabetic ketoacidosis resulting from glucose transporter 2 inhibitors