Document Detail

Anti-(apolipoprotein A-1) IgGs are associated with high levels of oxidized low-density lipoprotein in acute coronary syndrome.
MedLine Citation:
PMID:  18088236     Owner:  NLM     Status:  MEDLINE    
ApoA-1 (apolipoprotein A-1) is the main component of HDL (high-density lipoprotein) and stabilizes PON-1 (paraoxonase-1), which prevents lipid peroxidation and oxLDL (oxidized low-density lipoprotein) formation. Autoantibodies against apoA-1 [anti-(apoA-1) IgG] have been found in antiphospholipid syndrome and systemic lupus erythematosous, two diseases with an increased risk of thrombotic events, as well as in ACS (acute coronary syndrome). OxLDL levels are also elevated in these diseases. Whether anti-(apoA-1) IgGs exist in other prothrombotic conditions, such as APE (acute pulmonary embolism) and stroke, has not been studied and their potential association with oxLDL and PON-1 activity is not known. In the present study, we determined prospectively the prevalence of anti-(apoA-1) IgG in patients with ACS (n=127), APE (n=58) and stroke (n=34), and, when present, we tested their association with oxLDL levels. The prevalance of anti-(apoA-1) IgG was 11% in the ACS group, 2% in the control group and 0% in the APE and stroke groups. The ACS group had significantly higher median anti-(apoA-1) IgG titres than the other groups of patients. Patients with ACS positive for anti-(apoA-1) IgG had significantly higher median oxLDL values than those who tested negative (226.5 compared with 47.7 units/l; P<0.00001) and controls. The Spearman ranked test revealed a significant correlation between anti-(apoA-1) IgG titres and serum oxLDL levels (r=0.28, P<0.05). No association was found between PON-1 activity and oxLDL or anti-(apoA-1) IgG levels. In conclusion, anti-(apoA-1) IgG levels are positive in ACS, but not in stroke or APE. In ACS, their presence is associated with higher levels of oxLDL and is directly proportional to the serum concentration of oxLDL. These results emphasize the role of humoral autoimmunity as a mediator of inflammation and coronary atherogenesis.
Nicolas Vuilleumier; Emmanuel Charbonney; Lionel Fontao; Montserrat Alvarez; Natacha Turck; Jean-Charles Sanchez; Pierre R Burkhard; Noury Mensi; Marc Righini; Guido Reber; Richard James; François Mach; Jean-Claude Chevrolet; Jean-Michel Dayer; Johan Frostegard; Pascale Roux-Lombard
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Clinical science (London, England : 1979)     Volume:  115     ISSN:  1470-8736     ISO Abbreviation:  Clin. Sci.     Publication Date:  2008 Jul 
Date Detail:
Created Date:  2008-11-21     Completed Date:  2009-01-07     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7905731     Medline TA:  Clin Sci (Lond)     Country:  England    
Other Details:
Languages:  eng     Pagination:  25-33     Citation Subset:  IM    
Division of Immunology and Allergy, Department of Internal Medicine, University Hospital, Geneva, Switzerland.
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MeSH Terms
Acute Coronary Syndrome / blood*,  immunology
Acute Disease
Aged, 80 and over
Apolipoprotein A-I / immunology*
Autoantibodies / blood*
Biological Markers / blood
Enzyme-Linked Immunosorbent Assay / methods
Immunoglobulin G / blood*
Lipoproteins, LDL / blood*
Middle Aged
Prospective Studies
Pulmonary Embolism / immunology
Stroke / immunology
Young Adult
Reg. No./Substance:
0/Apolipoprotein A-I; 0/Autoantibodies; 0/Biological Markers; 0/Immunoglobulin G; 0/Lipoproteins, LDL; 0/oxidized low density lipoprotein

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