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Clinical Citations: Can HDL cholesterol level predict outcomes in patients with sepsis?

Publication
Article
The Journal of Respiratory DiseasesThe Journal of Respiratory Diseases Vol 5 No 12
Volume 5
Issue 12

Although lipoprotein levels are known to be reduced in critically ill patients, the prognostic significance of this in patients with sepsis has not been established. However, a study recently conducted in Taiwan is worth noting; it found that low levels of high-density lipoprotein (HDL) cholesterol on day 1 of severe sepsis were associated with increased risk of death.

Although lipoprotein levels are known to be reduced in critically ill patients, the prognostic significance of this in patients with sepsis has not been established. However, a study recently conducted in Taiwan is worth noting; it found that low levels of high-density lipoprotein (HDL) cholesterol on day 1 of severe sepsis were associated with increased risk of death.

Chien and associates studied 63 patients who had severe sepsis. Blood samples were obtained within the first day and in the subsequent 14 days. Patients were followed up for at least 30 days after recruitment or until death.

Patients who died had significantly lower levels of HDL cholesterol and apolipoprotein A-I during the first 4 days of sepsis compared with the patients who survived. HDL cholesterol levels correlated inversely with concentrations of interleukin-6 and tumor necrosis factor on day 1. Overall mortality, sepsis-related mortality, risk of prolonged ICU stay, and rate of hospital-acquired infection were increased in patients who had HDL cholesterol levels of less than 20 mg/dL and apolipoprotein A-I levels of less than 100 mg/dL. Multivariate analysis indicated that a low HDL cholesterol level was an independent predictor of mortality.

It is not clear whether there is a causal relationship between low HDL levels and outcomes. It also is not known whether a low HDL level on day 1 of sepsis is the result of low baseline levels before sepsis, higher amounts of endotoxin production during severe infection, or suppression of production by proinflammatory cytokines.

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