SUN-621 - A Decade of Morbidity after ERCP-Induced Pancreatitis in A Young Patient: Teaching Points in the Long-Term Management of Type 3C Diabetes

Type 3c diabetes mellitus arises from pancreatic disease leading to combined exocrine and endocrine dysfunction. It is characterized by marked glycemic instability, exocrine pancreatic insufficiency, and progressive malnutrition. Optimal long-term outcomes require early, continuous, and multidisciplinary management addressing glycemic control, pancreatic enzyme replacement, and nutritional support. When longitudinal care is fragmented, patients are at risk for preventable metabolic complications and progressive morbidity. We present a 34-year-old woman with no prior metabolic disease who developed severe post–endoscopic retrograde cholangiopancreatography (ERCP) necrotizing pancreatitis at age 24 for Mirizzi syndrome. Imaging demonstrated pancreatic necrosis exceeding 75% of the gland (Balthazar grade E), requiring prolonged intensive care and multiple readmissions for recurrent necrotizing pancreatitis, sepsis, and abdominal pain. Her course necessitated open cystgastrostomy, partial pancreatectomy, and temporary gastrostomy tube placement, resulting in exocrine pancreatic insufficiency. During initial hospitalizations, she developed hyperglycemia after initiation of total parenteral nutrition and was diagnosed with pancreatogenic (type 3c) diabetes mellitus, with autoimmune and secondary causes excluded. Over the following decade, she experienced recurrent hospitalizations for abdominal pain, malabsorption, and progressive weight loss, with worsening glycemic control despite insulin therapy, culminating in recurrent diabetic ketoacidosis and hemoglobin A1c levels reaching 18.9%. At recent presentation, she had severe cachexia (BMI 15 kg/m²), steatorrhea, and poor oral intake. Despite years of recurrent abdominal pain contributing to repeated hospitalizations, advanced pain-directed interventions were not pursued until her most recent admission, when a celiac plexus block was performed. This case illustrates the profound long-term morbidity that can develop in pancreatogenic diabetes when management is not consistently comprehensive. Although the diagnosis was recognized early, longitudinal care focused primarily on glycemic control without sustained integration of nutritional optimization, pancreatic enzyme adequacy, weight monitoring, and prevention of metabolic decompensation. Severe malnutrition, exocrine insufficiency, and recurrent inflammatory stress likely contributed to progressive glycemic instability and recurrent diabetic ketoacidosis. Pancreatogenic diabetes is a multisystem disease requiring continuous, coordinated endocrine, gastrointestinal, and nutritional care. This patient’s trajectory underscores the need for structured, proactive strategies to interrupt disease progression and improve quality of life in patients with pancreatogenic diabetes.

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