Abstract Introduction Pancreatitis is a potentially life-threatening inflammatory disorder most often triggered by gallstones or chronic alcohol consumption. Hypertriglyceridemia accounts for 5-10 % of cases and ranks as the third most common cause after gallstones and alcohol. When both alcohol and hypertriglyceridemia coexist, they exert a synergistic lipotoxic and oxidative injury to pancreatic tissue, often leading to more severe disease. Early identification of this dual-etiology variant is critical for prompt metabolic control and prevention of complications. Case Description A 47-year-old male with alcohol use disorder, prediabetes, bipolar I disorder, and schizophrenia presented with acute epigastric and left-lower-quadrant pain following ingestion of approximately 1 L of vodka. The pain was sharp, persistent, and associated with nausea and non-bilious vomiting. On arrival: HR 97 bpm, BP 149/104 mm Hg, Na 131 mmol/L, creatinine 1.74 mg/dL, AST 98 U/L, anion gap 18, lactic acid 3.4 mmol/L, ethanol 206 mg/dL. Lipase measured 1039 U/L and triglycerides 2533 mg/dL.CT abdomen revealed diffuse pancreatic inflammation with a 5.6 cm cystic lesion at the tail consistent with a pseudocyst. The patient was admitted to the ICU and treated with lactated Ringer’s, thiamine, folic acid, multivitamins, pain control, and a CIWA protocol for alcohol withdrawal. Continuous insulin infusion with dextrose was initiated for hypertriglyceridemia, resulting in triglyceride decline from 2533 to 199 mg/dL within 36 hours. Surgical consultation advised conservative management of the pseudocyst with interval MRI/MRCP follow-up. Renal function, lactic acidosis, and transaminase elevation improved with metabolic stabilization. Discussion This case underscores the uncommon but clinically important overlap between alcohol-induced and hypertriglyceridemic pancreatitis. Alcohol increases hepatic triglyceride synthesis and impairs lipoprotein lipase activity, amplifying lipid-mediated pancreatic injury. Severe hypertriglyceridemia (2000 mg/dL) causes free-fatty-acid toxicity and microvascular ischemia within the pancreas. Prompt insulin therapy enhances lipoprotein-lipase-mediated clearance of triglycerides, rapidly lowering levels and mitigating inflammation. Our patient’s insulin and supportive therapy improvement, without the need for plasmapheresis or drainage, highlights the efficacy of early biochemical correction and multidisciplinary management. Clinicians should routinely assess lipid panels in all alcohol-related pancreatitis cases to identify this dual pathology and prevent recurrence through counseling, lipid control, and abstinence. This abstract is funded by: “None”
Acherjee et al. (Fri,) studied this question.