Major reduction in plasma Lp(a) levels during sepsis and burns

Plasma levels of lipoprotein(a) [Lp(a)], an atherogenic particle, vary wide ly between individuals and are highly genetically determined. Whether Lp(a) is a positive acute-phase reactant is debated. The present study was desig ned to evaluate the impact of major inflammatory responses on plasma Lp(a) levels. Plasma levels of C-reactive protein (CRP), low density lipoprotein cholesterol, Lp(a), and apolipoprotein(a) [apo(a)] fragments, as well as ur inary apo(a), were measured serially in 9 patients admitted to the intensiv e care unit for sepsis and 4 patients with extensive burns. Sepsis and burn s elicited a major increase in plasma CRP levels. In both conditions, plasm a concentrations of Lp(a) declined abruptly and transiently in parallel wit h plasma low density lipoprotein cholesterol levels and closely mirrored pl asma CRP levels. In 5 survivors, the nadir of plasma Lp(a) levels was 5- to 15-fold lower than levels 16 to 18 months after the study period. No chang e in plasma levels of apo(a) fragments or urinary apo(a) was noticed during the study period. Turnover studies in mice indicated that clearance of Lp( a) was retarded in lipopolysaccharide-treated animals. Taken together, thes e data demonstrate that Lp(a) behaves as al negative acute-phase reactant d uring major inflammatory response. Nongenetic factors have a major, acute, and unexpected impact on Lp(a) metabolism in burns and sepsis, Identificati on of these factors may provide new tools to lower elevated plasma Lp(a) le vels.