Document Detail

Basic science for the clinician 44: atherosclerosis: an immunologically mediated (autoimmune?) disease.
MedLine Citation:
PMID:  17551386     Owner:  NLM     Status:  MEDLINE    
There has been a sea change in our understanding of atherosclerosis. We have come a long way from the days where eating too much fat and not getting enough exercise and having the wrong genetic background was thought to be the entire story. A few years ago, the cardiologists began to embrace inflammation as a possible pathogenetic mechanism and from that came high-sensitivity C-reactive protein testing for just about everyone. Chronic systemic inflammation became an area of interest. We have learned that it is more than just corticosteroid use that causes accelerated atherosclerosis in our rheumatoid and lupus patients. Even C-reactive protein may be a pathogenetic player, not only a diagnostic clue. Oxidized phospholipids and the cells that recognize them may be crucial in the evolution of the atherosclerotic plaque. Statins may be useful in suppressing inflammation, not only in suppressing cholesterol levels. And now even cardiologists are thinking about immune mechanisms! A strange world, but the beneficiaries of going through this looking glass will be our patients. A true understanding of this seems to have required a most circuitous route-sometimes you have to leave for a long journey before you can return and really see home for the first time.
Leonard H Sigal
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Journal of clinical rheumatology : practical reports on rheumatic & musculoskeletal diseases     Volume:  13     ISSN:  1076-1608     ISO Abbreviation:  J Clin Rheumatol     Publication Date:  2007 Jun 
Date Detail:
Created Date:  2007-06-06     Completed Date:  2007-07-31     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  9518034     Medline TA:  J Clin Rheumatol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  160-8     Citation Subset:  IM    
Research and Development, Bristol-Myers Squibb, Princeton, NJ, USA.
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MeSH Terms
Atherosclerosis / immunology*,  physiopathology
Autoantibodies / blood
Immunity, Innate
Inflammation / physiopathology
Lipoproteins, HDL / metabolism
Lipoproteins, LDL / metabolism
Reg. No./Substance:
0/Autoantibodies; 0/Lipoproteins, HDL; 0/Lipoproteins, LDL

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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