While sodium-glucose cotransporter-2 (SGLT2) inhibitors draw praise for their weight-loss and blood pressure reduction benefits, medical experts continue to puzzle over their more immediate metabolic and immune system effects. Specifically, researchers are worried about their possible link to diabetic ketoacidosis, a potentially fatal condition caused by excess blood acids, or ketones. In an article published by the Journal of Diabetes Investigation, two Japanese researchers provide a possible explanation for how SGLT2 inhibitors may be inducing ketoacidosis in diabetic patients.
SGLT2 inhibitors are a new line of oral medication for the treatment of type 2 diabetes. Popular brands include Janssen Pharmaceutica’s Invokana (canagliflozin), Bristol-Myers Squibb and AstraZeneca’s Farxiga (dapagliflozin), and Boehringer Ingelheim and Eli Lilly & Co.’s Jardiance (empagliflozin). These drugs work by preventing the reabsorption of blood sugar in the kidneys, instead rerouting it for disposal through urine. As a result, SGLT2 inhibitors are claimed to help with weight-loss and blood pressure reduction, side effects that may or may not be beneficial.
Only two years after SGLT2 inhibitors hit the market, the U.S. Food and Drug Administration (FDA) came out with a safety communication warning of a potential link between the new drugs and diabetic ketoacidosis. Evidence also suggests SGLT2 inhibitors can make diabetic ketoacidosis more difficult for medical staff to detect, leading to misdiagnosis and delayed treatment of the condition. The problem may be especially prevalent in SGLT2 inhibitor users with Type I diabetes, in whom these medications are not approved for use.
The authors of the new article present a possible mechanism by which SGLT2 inhibitors may trigger euglycemic diabetic ketoacidosis, or diabetic ketoacidosis in patients who present with normal levels of blood sugar. They begin by stating that SGLT2 inhibitors lower blood glucose levels by increasing the amount of glucose eliminated through urine. This in turn reduces the amount of insulin secreted by certain pancreatic cells (which are triggered by high blood glucose concentrations). This decline in circulating insulin leads to a lowering of antilipolytic activity, meaning there is more breakdown of fat. This results in more fatty acids in the blood, which are converted to ketones, the blood acids responsible for diabetic ketoacidosis, in the liver. The authors of the study provide additional evidence supporting this mechanism.
Whether or not this newly proposed explanation is correct, the link between SGLT2 inhibitors and diabetic ketoacidosis still needs more research. To this end, the FDA and Health Canada have launched investigations into the potential risks of SGLT2 inhibitor use. For now, patients are advised to seek immediate medical attention if they experience any symptoms of ketoacidosis including difficulty breathing, nausea, vomiting, abdominal pain, confusion, and unusual fatigue or sleepiness.
If you or someone you know was diagnosed with ketoacidosis after using an SGLT2 inhibitor, contact Lopez McHugh now to schedule a free legal consultation with one of our pharmaceutical attorneys. We can help determine whether an SGLT2 inhibitor lawsuit is right for you.
