S3214 Acute Pancreatitis and Shock Liver in a Diabetic Patient on Dulaglutide: A Case Report

Introduction: Dulaglutide a glucagon-like peptide-1 (GLP-1) receptor agonist approved for weight loss and type 2 diabetes, has been associated with gastrointestinal side effects and rare cases of acute pancreatitis. While beneficial for glycemic control and weight reduction, its use in patients with complex metabolic profiles requires careful monitoring. We report a severe case of acute pancreatitis and subsequent multi-organ failure in a patient on dulaglutide, emphasizing the need for vigilance in showing potential drug-related complications. Case Description/Methods: A 56-year-old man with type 2 diabetes mellitus on metformin, glipizide, insulin and dulaglutide presented with 3 days of nausea and vomiting, few months after being started on the medication. On arrival, was confused with undifferentiated shock requiring vasopressors and stress-dose steroids. Initial labs showed AST >3750 U/L, ALT >3750 U/L, lipase 1279 U/L, serum CO₂ <6 mmol/L, glucose 289 mg/dL, and β-hydroxybutyrate >6 mmol/L. Computed tomography abdomen/pelvis revealed marked hepatic steatosis with hepatomegaly, gastric and esophageal fluid distention, and ascending colonic thickening concerning for colitis. Patient was diagnosed with diabetic ketoacidosis, ischemic colitis, shock liver, and presumed septic shock. He required mechanical ventilation and continuous renal replacement therapy due to worsening renal failure. Worsening leukocytosis prompted repeat imaging, which showed features consistent with acute interstitial edematous pancreatitis. The patient gradually stabilized in the intensive care unit and, after nearly a month, was transferred for liver transplant evaluation. Dulaglutide was discontinued post-discharge, with suspected drug-induced pancreatitis. Discussion: GLP-1 receptor agonists like dulaglutide are increasingly used but carry a risk of pancreatitis, particularly in patients with comorbid diabetes and hepatic steatosis. In this case, the clinical trajectory—including elevated lipase, shock liver, and pancreatic imaging findings—suggests acute pancreatitis likely triggered by dulaglutide. The resulting systemic inflammatory response contributed to multi-organ dysfunction, including DKA, acute kidney injury, and ischemic colitis. Discontinuation of dulaglutide and intensive critical care led to gradual improvement. This case underscores the importance of close monitoring for pancreatitis in patients on GLP-1 therapy, especially those with existing hepatic or metabolic vulnerabilities.