© 2000 American Heart Association, Inc.
Atherosclerosis and Lipoproteins |
Major Reduction in Plasma Lp(a) Levels During Sepsis and Burns
From the Department of Medicine (V.M., P.N.), Surgical Intensive Care Unit (M.M.B., C.C., R.C.), Institute of Physiology (L.T.), and Medical Policlinic (R.D.), CHUV University Hospital, Lausanne, Switzerland, and the Northwest Lipid Research Laboratories (S.M.M.), Seattle, Wash.
Correspondence to Vincent Mooser, MD, Department of Medicine, CHUV University Hospital, BH 19-135, CH-1011 CHUV Lausanne, Switzerland. E-mail vincent.mooser{at}hola.hospv.ch
Abstract—Plasma levels of lipoprotein(a) [Lp(a)], an atherogenic particle, vary widely between individuals and are highly genetically determined. Whether Lp(a) is a positive acute-phase reactant is debated. The present study was designed 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 urinary apo(a), were measured serially in 9 patients admitted to the intensive care unit for sepsis and 4 patients with extensive burns. Sepsis and burns elicited a major increase in plasma CRP levels. In both conditions, plasma concentrations of Lp(a) declined abruptly and transiently in parallel with plasma low density lipoprotein cholesterol levels and closely mirrored plasma 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 change 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, these data demonstrate that Lp(a) behaves as a negative acute-phase reactant during major inflammatory response. Nongenetic factors have a major, acute, and unexpected impact on Lp(a) metabolism in burns and sepsis. Identification of these factors may provide new tools to lower elevated plasma Lp(a) levels.
Key Words: lipoprotein(a) • apolipoprotein(a) • sepsis • burns • inflammation
This article has been cited by other articles:
 |
|
 |
|
  E. Anuurad, J. Rubin, A. Chiem, R. P. Tracy, T. A. Pearson, and L. Berglund High Levels of Inflammatory Biomarkers Are Associated with Increased Allele-Specific Apolipoprotein(a) Levels in African-Americans J. Clin. Endocrinol. Metab., April 1, 2008; 93(4): 1482 - 1488. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. Khovidhunkit, M.-S. Kim, R. A. Memon, J. K. Shigenaga, A. H. Moser, K. R. Feingold, and C. Grunfeld Thematic review series: The Pathogenesis of Atherosclerosis. Effects of infection and inflammation on lipid and lipoprotein metabolism mechanisms and consequences to the host J. Lipid Res., July 1, 2004; 45(7): 1169 - 1196. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. L. Kitchens, P. A. Thompson, R. S. Munford, and G. E. O'Keefe Acute inflammation and infection maintain circulating phospholipid levels and enhance lipopolysaccharide binding to plasma lipoproteins J. Lipid Res., December 1, 2003; 44(12): 2339 - 2348. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Liberopoulos, G. Alexandridis, E. Bairaktari, and M. Elisaf Severe Hypocholesterolemia with Reduced Serum Lipoprotein(a) in a Patient with Visceral Leishmaniasis Ann. Clin. Lab. Sci., July 1, 2002; 32(3): 305 - 308. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Busso, J. Dudler, R. Salvi, V. Peclat, V. Lenain, S. Marcovina, R. Darioli, P. Nicod, A. K. So, and V. Mooser Plasma Apolipoprotein(a) Co-Deposits with Fibrin in Inflammatory Arthritic Joints Am. J. Pathol., October 1, 2001; 159(4): 1445 - 1453. [Abstract] [Full Text]
|
|
|
|
 |
|
 W. Korte, J. Greiner, A. Feldges, and W. F. Riesen Increased Lipoprotein(a) levels are not a steady prothrombotic defect Blood, September 15, 2001; 98(6): 1993 - 1994. [Full Text] [PDF]
|
|