Tyler Brouse, PharmD
PGY2 Critical Care Pharmacy Resident
Baylor Scott & White Health
Dallas, Texas
Disclosure information not submitted.
Klayton Ryman, PharmD, BCCCP
Baylor University Medical Center - Dallas
Dallas, Texas
Disclosure information not submitted.
Vivek Kataria, PharmD, BCCCP
Clinical Pharmacist - MICU
Baylor University Medical Center, United States
Disclosure information not submitted.
Title: L-Carnitine for Propofol-Induced Hypertriglyceridemia: A Case Series
INTRODUCTION/HYPOTHESIS: Propofol is a short-acting sedative utilized in mechanically ventilated patients in the intensive care unit (ICU) and is known to cause hypertriglyceridemia due to its lipid emulsion formulation. This often leads to discontinuation of the medication to prevent pancreatitis. L-carnitine is an essential component of lipid metabolism, and deficiency of this amino acid derivative may contribute to hypertriglyceridemia. This case series aims to describe the use of L-carnitine for the reduction of triglycerides in patients with propofol-induced hypertriglyceridemia.
Methods: We performed a retrospective review of patients who received L-carnitine for hypertriglyceridemia while on a propofol infusion at a 1,008-bed tertiary care hospital from January 1st, 2020 to July 29th, 2021. Patients were excluded if propofol was discontinued prior to a repeat triglyceride level being checked, or if they received an insulin infusion after the diagnosis of hypertriglyceridemia.
Results: There were seven patients identified for review, and of these five patients met criteria for inclusion. The average propofol infusion rate was 36 mcg/kg/min, and the average infusion duration was 5.2 days prior to L-carnitine initiation. L-carnitine at a dose of 990 mg three times daily was used in three (60%) patients, where 990 mg twice daily was used in two (40%) patients. The mean triglyceride level at initiation of L-carnitine was 396 mg/dL. Three (60%) of our patients experienced a decrease in triglyceride levels within one to three days with the addition of L-carnitine without a decrease in the propofol infusion rate. The average decrease in triglycerides was 205 mg/dL. Out of the two patients who did not have a decrease in triglyceride levels, one patient (who was receiving 990 mg twice daily) experienced an increase in triglycerides of 85 mg/dL on day 3 of therapy and an increase of 349 mg/dL on day 4 of therapy with a concomitant increase in the propofol infusion rate. The other patient had a slight 8 mg/dL increase in triglycerides on day 2 of L-carnitine therapy.
Conclusion: L-carnitine may decrease triglycerides in patients with propofol-induced hypertriglyceridemia, allowing for continuation of treatment. Larger trials are needed to confirm these hypothesis-generating results.