SUN-667 Giant Pancreatic Pseudocyst as a complication of Hypertriglyceridemia-Induced Pancreatitis

Abstract Disclosure: S. Azmat: None. A.M. Hernández: None. O.W. Lodhi: None. S. Rabbani: None. S. Ramroop: None. A. Havrylyan: None. Background: Hypertriglyceridemia-induced acute pancreatitis (HTG AP) is far more complex and severe than other forms of pancreatitis with a higher mortality rate. Besides this, there is lack of of randomized studies comparing specific therapies which makes it essential to classify hypertriglyceridemia as a significant cause of pancreatitis. We report a 36-year-old Hispanic male with a history of multiple episodes of HTG- HTG-associated pancreatitis who developed necrotizing pancreatitis and was subsequently found to have a giant pancreatic pseudocyst. Clinical Case: A 36 y.o. Hispanic male with a history of multiple episodes of hypertriglyceridemia-induced acute pancreatitis, presented with abdominal pain, nausea, and vomiting. Home medications included fenofibrate, atorvastatin, and metformin. On arrival, the patient was hypertensive and tachycardic. Labs were significant for lipase of 1643 U/L (<160 U/L), A1c 8.1, glucose 130 g/dL, bicarb 18.5 mEq/L (22-29), AG 15.5(4-12), Calcium 8.2 mg/dL, WBCs 21.9 10(3)/mcL, triglycerides 3000 mg/dL (150 mg/dL), LDL 170 mg/dL (<100 mg/dL), liver function test were within normal limits. The patient denied any excessive alcohol intake. CT abdomen showed fat stranding consistent with acute interstitial edematous pancreatitis with no focal fluid collections. The patient received IV fluids, insulin infusion, fenofibrate, atorvastatin, PRN analgesics, antiemetics, and bowel rest. Repeat CT abdomen and pelvis was performed five days later, due to worsening pain, revealing severe necrotizing pancreatitis with a 5 x 3 x 3.8 cm hypodense collection at the pancreatic head. Antibiotics were initiated, surgical team recommended the continuation of conservative management. On day tenth, given clinical and biochemical improvement and a multidisciplinary team discussion, patient was discharged on metformin, fenofibrate, atorvastatin, pioglitazone, and vascepa, with plan for GI follow-up for possible necrosectomy. A repeat CT abdomen two months later showed dramatic increase in size of pseudocyst measuring 16 cm, hence patient was referred for endoscopic drainage of the pseudocyst. Conclusion: This case reports rare occurrence of HTG-induced necrotizing pancreatitis with the formation of giant pancreatic pseudocyst. It also illustrates the importance of timely intervention and proper management of severe hypertriglyceridemia, to reduce the risk of complications including necrotizing pancreatitis and pseudocyst. Long-term management should be focused on alleviating the effects of metabolic syndrome by addressing related factors like diabetes and obesity. Understanding the pathophysiology and management approach can ultimately improve long-term patient outcomes. Presentation: Sunday, July 13, 2025