Propofol 2% in critically ill patients: effect on lipids.

Abstract

To investigate the concentrations of triglyceride, cholesterol, and high-density lipoprotein during a 50-hr infusion of 2% propofol, starting within 24 hrs of admission to the intensive care unit (ICU). Prospective, clinical study. ICU, university hospital. Thirty adult patients, who were ventilated and expected to be sedated for >2 days, were studied for 50 hrs, beginning at 1800 hrs on the first day of ICU admission. Triglyceride, cholesterol, and high-density lipoprotein were measured at 2000, 0400, and 0800 hrs. Tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and C-reactive protein were measured at 2000 hrs. Median cholesterol and high-density lipoprotein concentrations were at the low end of the normal range. In seven patients, peak triglyceride concentrations were >3 mmol/L up to a maximum of 4.83 mmol/L. Although there was no statistical difference in lipid concentrations between days 1 and 2, there was an apparent pattern of increasing triglyceride concentrations. There was a correlation between peak triglyceride concentration and total propofol consumption, but there was no correlation between lipids and age, gender, or Acute Physiology and Chronic Health Evaluation II scores. There was a direct correlation between triglyceride and C-reactive protein concentrations, and an inverse correlation between cholesterol and C-reactive protein. Twenty-two patients had evidence of TNF and 11 patients had an IL-6 of >1000 pg/mL, but there was no relationship between concentrations of cytokines and triglycerides in plasma. Infusion of 2% propofol to critically ill patients over a 50-hr period does not result in a significant increase in triglyceride concentrations. Mean cholesterol and high-density lipoprotein concentrations were low throughout the study period. There was a significant direct correlation between triglyceride and C-reactive protein and an inverse correlation between cholesterol and C-reactive protein, suggesting that the changes in lipids in critically ill patients may be partly attributable to the acute-phase response.