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Insulin infusion to treat severe hypertriglyceridemia associated with pegaspargase therapy: a case report
Eileen B Lawson1, Michael Gottschalk, Deborah E Schiff
1UCSD Skaggs School of Pharmacy and Pharmaceutical Sciences, La Jolla, San Diego, CA, USA. ebrigid@ucsd.edu
Insights
Pegaspargase therapy for acute leukemia can cause severe hypertriglyceridemia (hyperTG). Continuous insulin infusion effectively managed this metabolic complication in a pediatric patient, highlighting the role of apolipoprotein E genetics.
Area of Science:
- Biochemistry
- Pediatric Oncology
- Pharmacology
Background:
- Pegaspargase is a crucial chemotherapeutic agent for acute lymphoblastic leukemia (ALL).
- Asparaginase therapy can lead to metabolic complications, including hypertriglyceridemia (hyperTG).
- Understanding these adverse events is vital for patient management.
Observation:
- A pediatric patient with acute leukemia developed severe hyperTG during pegaspargase treatment.
- The patient's triglyceride levels were critically high upon admission.
- Genetic testing identified the patient as an apolipoprotein E (ApoE) 3/4 heterozygote.
Findings:
- Continuous insulin infusion therapy was administered to manage the severe hyperTG.
- This treatment significantly reduced triglyceride levels from 4640 mg/dL to 522 mg/dL within 9 days.
- ApoE polymorphism may be a risk factor for developing asparaginase-induced hyperTG.
Implications:
- Continuous insulin infusion is a viable treatment for pegaspargase-induced hyperTG.
- ApoE genotyping may help identify patients at high risk for this metabolic complication.
- This case highlights the importance of monitoring metabolic parameters during asparaginase therapy in pediatric ALL patients.
Abstract:
We describe a pediatric patient with acute leukemia who developed an uncommon but significant metabolic consequence of pegaspargase therapy-severe hypertriglyceridemia (hyperTG). We also relate our experience with continuous insulin infusion treatment for pegaspargase-induced hyperTG. This treatment approach led to a decrease in triglycerides from 4640 mg/dL on admission to 522 mg/dL at discharge 9 days later. Genetic testing revealed that our patient was an apolipoprotein E 3/4 heterozygote. Our review of the literature suggests that apolipoprotein E polymorphism may influence the development of hyperlipidemia in acute lymphoblastic leukemia patients receiving asparaginase therapy and may identify patients at high risk for developing asparaginase-induced hyperTG.
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