SGLT2 Inhibitors May Precipitate DKA in Type 1 Diabetes Mellitus Patients

Abstract

Sodium-glucose co-transporter 2 (SGLT2) inhibitors have emerged as a valuable class of drugs in managing diabetes, primarily due to their hypoglycemic effects and additional benefits such as weight loss and cardiovascular protection. Although they are mainly used in type 2 diabetes, their potential as an add-on treatment in type 1 diabetes (T1D) has attracted attention. SGLT2 inhibitors improve glycemic control in T1D by promoting renal glucose excretion, which reduces insulin requirements and stabilizes blood sugar levels. They also aid in weight loss and improve metabolic parameters, making them an attractive option for people with T1D struggling to achieve optimal blood sugar goals. However, the use of SGLT2 inhibitors in type 1 diabetes is associated with a significant risk of diabetic ketoacidosis (DKA). This serious complication can be life-threatening if not treated and supported promptly. This risk is increased by the risk of euglycemic diabetic ketoacidosis, where blood glucose levels remain near normal despite the presence of significant ketoacidosis. The mechanism involves decreased insulin levels, increased lipolysis, and increased ketone production, coupled with the glucagon-enhancing effects of SGLT2 inhibitors. These factors promote ketogenesis, especially during illness, dehydration, or insulin failure. The risk of diabetic ketoacidosis emphasizes the need. Caution should be exercised when prescribing SGLT2 inhibitors to people with type 1 diabetes. Their use should be limited to carefully selected patients who are well-informed about their condition, able to monitor their blood sugar and ketone levels regularly, and aware of the early signs of diabetic ketoacidosis. Education on maintaining adequate insulin therapy and adherence to sick leave protocols are essential to minimize the risk of complications. Further research is needed to improve the safety profile of SGLT2 inhibitors in type 1 diabetes, identify strategies to mitigate the risk of diabetic ketoacidosis and determine the most appropriate candidates for treatment. Until these measures are established, SGLT2 inhibitors in type 1 diabetes should be reserved for selected cases under close medical supervision, ensuring that the potential benefits do not outweigh the risks.

Materials and Methods: 50 patients with type 1 diabetes, the results show a statistically significant occurrence of DKA in patients with type 1 diabetes on SGL2 inhibitors with p value less than 0.0001. The results show a statistically insignificant difference in DKA occurrence between patients on empagliflozin and dapagliflozin with a p-value less than 0.7532.

Conclusion: Although SGLT2 inhibitors show promise as add-on therapy in type 1 diabetes, their potential to induce DKA requires a careful and individualized approach to prescribing. With careful patient selection, thorough education, and careful monitoring, the benefits of these drugs can be realized while minimizing their risks. However, until more evidence becomes available, SGLT2 inhibitors in type 1 diabetes should be reserved for carefully selected cases under close medical supervision.