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Presence of Circulating Anti-Myosin Antibodies in Endomyocardial Fibrosis

BACKGROUND: Endomyocardial Fibrosis (EMF) is a tropical restrictive cardiomyopathy of unknown etiology with high prevalence in Sub-Saharan Africa, for which it is unclear whether the primary target of injury is the endocardial endothelium, the subendocardial fibroblast, the coronary microcirculation...

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Autores principales: Mocumbi, Ana Olga, Latif, Najma, Yacoub, Magdi H.
Formato: Texto
Lenguaje:English
Publicado: Public Library of Science 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2857887/
https://www.ncbi.nlm.nih.gov/pubmed/20422043
http://dx.doi.org/10.1371/journal.pntd.0000661
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author Mocumbi, Ana Olga
Latif, Najma
Yacoub, Magdi H.
author_facet Mocumbi, Ana Olga
Latif, Najma
Yacoub, Magdi H.
author_sort Mocumbi, Ana Olga
collection PubMed
description BACKGROUND: Endomyocardial Fibrosis (EMF) is a tropical restrictive cardiomyopathy of unknown etiology with high prevalence in Sub-Saharan Africa, for which it is unclear whether the primary target of injury is the endocardial endothelium, the subendocardial fibroblast, the coronary microcirculation or the myocyte. In an attempt to explore the possibility of endocardial lesions being a result of an immune response against the myocyte we assessed the presence and frequency of circulating anti-myocardial antibodies in EMF patients. METHODOLOGY/PRINCIPAL FINDINGS: EMF classification, assessment of severity and staging was based on echocardiography. We used sodium dodecylsulfate polyacrylamide gel electrophoresis (SDS-PAGE) of myocardial proteins followed by western blotting to screen serum samples for antiheart antibodies G and M classes. The degree of serum reactivity was correlated with the severity and activity of EMF. We studied 56 EMF patients and 10 healthy controls. IgG reactivity against myocardial proteins was stronger and more frequent in patients with EMF when compared to controls (30/56; 53.6% vs. 1/10; 10%, respectively). IgM reactivity was weak in both groups, although higher in EMF patients (11/56; 19.6%) when compared to controls (n = 0). EMF patients showed greater frequency and reactivity of IgG antibodies against myocardial proteins of molecular weights 35 kD, 42 kD and 70 kD (p values <0.01, <0.01 and <0.05 respectively). CONCLUSIONS: The presence of antibodies against myocardial proteins was demonstrated in a subset of EMF patients. These immune markers seem to be related with activity and might provide an adjunct tool for diagnosis and classification of EMF, therefore improving its management by identifying patients who may benefit from immunosuppressive therapy. Further research is needed to clarify the role of autoimmunity in the pathogenesis of EMF.
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spelling pubmed-28578872010-04-26 Presence of Circulating Anti-Myosin Antibodies in Endomyocardial Fibrosis Mocumbi, Ana Olga Latif, Najma Yacoub, Magdi H. PLoS Negl Trop Dis Research Article BACKGROUND: Endomyocardial Fibrosis (EMF) is a tropical restrictive cardiomyopathy of unknown etiology with high prevalence in Sub-Saharan Africa, for which it is unclear whether the primary target of injury is the endocardial endothelium, the subendocardial fibroblast, the coronary microcirculation or the myocyte. In an attempt to explore the possibility of endocardial lesions being a result of an immune response against the myocyte we assessed the presence and frequency of circulating anti-myocardial antibodies in EMF patients. METHODOLOGY/PRINCIPAL FINDINGS: EMF classification, assessment of severity and staging was based on echocardiography. We used sodium dodecylsulfate polyacrylamide gel electrophoresis (SDS-PAGE) of myocardial proteins followed by western blotting to screen serum samples for antiheart antibodies G and M classes. The degree of serum reactivity was correlated with the severity and activity of EMF. We studied 56 EMF patients and 10 healthy controls. IgG reactivity against myocardial proteins was stronger and more frequent in patients with EMF when compared to controls (30/56; 53.6% vs. 1/10; 10%, respectively). IgM reactivity was weak in both groups, although higher in EMF patients (11/56; 19.6%) when compared to controls (n = 0). EMF patients showed greater frequency and reactivity of IgG antibodies against myocardial proteins of molecular weights 35 kD, 42 kD and 70 kD (p values <0.01, <0.01 and <0.05 respectively). CONCLUSIONS: The presence of antibodies against myocardial proteins was demonstrated in a subset of EMF patients. These immune markers seem to be related with activity and might provide an adjunct tool for diagnosis and classification of EMF, therefore improving its management by identifying patients who may benefit from immunosuppressive therapy. Further research is needed to clarify the role of autoimmunity in the pathogenesis of EMF. Public Library of Science 2010-04-20 /pmc/articles/PMC2857887/ /pubmed/20422043 http://dx.doi.org/10.1371/journal.pntd.0000661 Text en Mocumbi et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Mocumbi, Ana Olga
Latif, Najma
Yacoub, Magdi H.
Presence of Circulating Anti-Myosin Antibodies in Endomyocardial Fibrosis
title Presence of Circulating Anti-Myosin Antibodies in Endomyocardial Fibrosis
title_full Presence of Circulating Anti-Myosin Antibodies in Endomyocardial Fibrosis
title_fullStr Presence of Circulating Anti-Myosin Antibodies in Endomyocardial Fibrosis
title_full_unstemmed Presence of Circulating Anti-Myosin Antibodies in Endomyocardial Fibrosis
title_short Presence of Circulating Anti-Myosin Antibodies in Endomyocardial Fibrosis
title_sort presence of circulating anti-myosin antibodies in endomyocardial fibrosis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2857887/
https://www.ncbi.nlm.nih.gov/pubmed/20422043
http://dx.doi.org/10.1371/journal.pntd.0000661
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