ODP155 Successful Treatment of PEG-Asparaginase Related Hypertriglyceridemia with Omega-3 Acid Ethyl Esters

INTRODUCTION: Young adults diagnosed with acute lymphoblastic leukemia (ALL) have been increasingly treated with a pediatric-inspired regimen including asparaginase, to improve both quality and quantity of survival. Peg-asparaginase (PEG-ASP) is a long-acting formulation of L-asparaginase (L-ASP), an enzyme that selectively kills leukemic cells by depleting plasma asparagine. Treatment with PEG-ASP provides multiple benefits including increased complete remission rates and overall survival, however, numerous toxicities can occur including fatigue, nausea, vomiting, hypersensitivity, thrombosis, pancreatitis, hepatotoxicity, and, less commonly, hypertriglyceridemia (HTG). Several treatment approaches have been reported for patients with PEG-ASP induced HTG but strong evidence supporting any specific option is lacking. Clinical case: A 24-year-old woman presented with sacral joint septic arthritis that led to the discovery of underlying B-cell acute lymphoblastic leukemia (B-ALL). Soon after diagnosis the CALGB 10403 protocol, which contains PEG-ASP, was initiated. Sixteen days after the initial PEG-ASP dose of 3,750 units it was noted her plasma serum was lipemic with TG of 669 mg/dL, which peaked the next day to 1,314 mg/dL while the patient remained asymptomatic and without signs or symptoms of pancreatitis. She was started on a brief course of insulin drip (lasting 6 hours) and a low-fat diet. Four days later fish oil (omega-3 acid ethyl esters) 2 gm twice daily was added, and two days later micronized fenofibrate 67 mg as well. She was tolerating this regimen for three days when fenofibrate had to be discontinued due to elevated liver enzymes while fish oil was continued. Triglycerides continued to successfully trend down over the course of two weeks, and after reaching a level of 111 mg/dL she was re-challenged with another dose of PEG-ASP 3,750 units. After the second dose of PEG-ASP, her TGs became elevated again but peaked at 542 mg/dL. She received a third dose of PEG-ASP 3,750 units two months later when TG remained below 200 mg/dL. A month later she received a fourth/final dose of PEG-ASP 3,750 units which led to transient elevation of TGs peaking at 437 mg/dL but returning to levels below 200 mg/dl within two months. Throughout the course of her treatment with PEG-ASP, she continued to take fish oil. CONCLUSION: Multiple studies showed that the benefit to toxicity ratio of asparaginase in young adults with ALL is favorable. Our conclusion is that in patients who develop HTG, fish oil can be utilized as a treatment and continued as long as they are receiving PEG-ASP, especially in patients unable to tolerate fenofibrate. We would like to bring attention to this case with the current positive outcome given the fact there is currently limited evidence on the safety of re-challenging patients with PEG-ASP after experiencing HTG. Presentation: No date and time listed