MON-274 - "Extreme Hypertriglyceridemia >10,000 mg/dL With Mild Clinical Presentation: A Case Report"

Background: Severe hypertriglyceridemia is an uncommon cause of acute pancreatitis. The degree of triglyceride elevation may not correlate with clinical severity, and patients may present with a clinically mild course despite extreme hypertriglyceridemia.

Case Presentation: A female in her 40s with type 2 diabetes, chronic hypertriglyceridemia with no prior genetic evaluation, fibromyalgia, and a history of pancreatitis six years ago , presented with acute epigastric pain associated with one episode of vomiting and poor oral intake. She was hemodynamically stable and afebrile. Her abdominal pain and gastrointestinal symptoms resolved within hours, and examination demonstrated a soft, non-tender abdomen without guarding. Initial laboratory evaluation revealed glucose 25.2 mmol/L (453 mg/dL), sodium 129 mmol/L, potassium 4.5 mmol/L, bicarbonate 17 mmol/L, and anion gap 17. Beta-hydroxybutyrate was 1.91 mmol/L, venous pH was 7.34, creatinine was 0.56 mg/dL, and urea was 9 mg/dL. White blood cell count was 8.2 ×10⁹/L. AST was 54 U/L and ALT was 75 U/L. Triglycerides were >113 mmol/L (>10,000 mg/dL), total cholesterol 42.2 mmol/L (1,632 mg/dL), and HDL 0.88 mmol/L (34 mg/dL). Lipase was within normal limits (72 U/L). Computed tomography demonstrated mild peripancreatic fat stranding, along with hepatomegaly and diffuse hepatic steatosis. Seven months prior to presentation, she had an emergency department visit for right upper quadrant abdominal pain, at which time triglycerides were 8.2 mmol/L (724 mg/dL) with normal lipase and unremarkable abdominal imaging; symptoms resolved, and she was discharged the same day. History revealed multiple contributing factors, including discontinuation of insulin glargine one month prior and metformin one week prior, along with cessation of atorvastatin 20 mg daily six months earlier due to persistent myalgias attributed to fibromyalgia. She was also receiving tirzepatide, with recent exposure to antipsychotic therapy and norethindrone. She was managed with intravenous fluids, a clear liquid diet low in carbohydrates and fat, and continuous insulin infusion at 15 units/hour with dextrose supplementation. Triglyceride levels declined rapidly from >113 mmol/L (>10,000 mg/dL) to 47.3 mmol/L (4,184 mg/dL) and further to 21.4 mmol/L (1,892 mg/dL) over 3 days, with sustained clinical improvement and no requirement for plasmapheresis. She was initiated on rosuvastatin 40 mg daily, fenofibrate 145 mg daily, and prescription-strength omega-3 fatty acids, with plans for outpatient initiation of olezarsen.

Conclusion: Extreme hypertriglyceridemia can present with a clinically mild and rapidly resolving course. This case emphasizes the disconnect between triglyceride levels and clinical severity and supports the effectiveness of conservative management with dietary modification and insulin therapy.

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