4.3 Article

From rheumatic fever to Libman-Sacks endocarditis: is there any possible pathogenetic link?

Journal

LUPUS
Volume 14, Issue 9, Pages 697-701

Publisher

SAGE PUBLICATIONS LTD
DOI: 10.1191/0961203305lu2203oa

Keywords

anti-beta 2GPI; antiphosphplipid syndrome; autoimmunity; Libman-Sacks endocarditis; M-protein; rheumatic fever

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The heart lesions of rheumatic fever and the heart involvement in antiphospholipid syndrome (APS), have different clinical pictures. Yet, there are several common characteristics linking both diseases: 1) central nervous system (CNS) and heart involvement; 2) molecular mimicry between the a pathogen and the origin of the disease; 3) cross reacting antibodies between the pathogen and self molecules; 4) endothelial cell activation in the 'crime-area' i.e., the valves; 5) some of the patients with RF have circulating antiphospholipid antibodies, while APS may be associated with streptococcal infection; and 6) recently, a cross-reactivity between antibodies directed to the streptococcal M-protein and its synthetic derivative in rheumatic fever (RF) and antibodies derived from APS patients targeting the beta-2-glycoprotein-I (beta 2GPI) and a beta 2GPI related synthetic peptide. In the current paper, we summarize the possible links between the heart involvement in RF and APS.

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