Abstract 4347475: Dostarlimab-Induced Diabetic Ketoacidosis in a Non-Diabetic Patient with Acute Myocardial Infarction: A Case Report

Background: Diabetic ketoacidosis (DKA) is a life-threatening complication commonly associated with type 1 diabetes. However, it can also develop in patients without a known history of diabetes, particularly in the context of acute stress or medication-induced side effects. Dostarlimab, an anti-PD-1 monoclonal antibody, has been linked to immune-mediated type 1 diabetes. Case Presentation: We present the case of a 76-year-old female with a history of uterine cancer (ER+, PR+, HER2+) who presented to the emergency department with altered mental status, and ketoacidosis. The patient had no prior history of diabetes and been receiving dostarlimab therapy for several months for uterine cancer. On admission, blood glucose level was 800 mg/dL, with a hemoglobin A1c was 6.1%. Arterial blood gas revealed severe acidosis with a pH of 6.88, pCO 2 of 28 mmHg, and HCO 3 of 5 mEq/L. Beta-hydroxybutyrate levels unremarkable. EKG demonstrated nonspecific ST-T changes consistent with an anterolateral infarct, and initial troponin levels were elevated in 5000s. The patient was started on heparin, insulin, and bicarbonate drips. A transthoracic echocardiogram (TTE) was ordered. Due to the patient’s hemodynamic instability and pressor requirements, cardiac catheterization was deferred until stabilization. Subsequent TTE revealed a decreased ejection fraction of 45-50% and apical inferior hypokinesis, representing new findings compared to prior imaging. Further evaluation confirmed hyperglycemic ketoacidosis consistent with DKA, with no existing diabetes diagnosis. The etiology of DKA in this patient was likely multifactorial from MI vs medication side effects. Acute myocardial infarction (MI) may have triggered activation of sympathetic nervous system; release of glucagon and cortisol, impairing insulin function leading to hyperglycemia. Additionally, dostarlimab therapy may have played a role in the new onset of DKA through immune-mediated beta-cell destruction. Conclusion: This case underscores the importance of recognizing DKA in patients without a prior history of diabetes, especially those receiving immune checkpoint inhibitors like dostarlimab. Acute stressors, such as MI, should be carefully evaluated, as they may synergize with medication-induced effects to precipitate DKA. Early recognition and comprehensive management are essential in mitigating the risks associated with this critical condition. Keywords: Ketoacidosis, insulin, DKA, myocardial infarction, dostarlimab