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Autoimmune rheumatic diseases

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dc.creatorAnaya, Juan-Manuel
dc.creatorShoenfeld, Yehuda
dc.creatorButtgereit, Frank
dc.creatorGonzalez-Gay, Miguel
dc.creator.googleAnaya, Juan-Manuelspa
dc.creator.googleShoenfeld, Yehudaspa
dc.creator.googleButtgereit, Frankspa
dc.creator.googleGonzalez-Gay, Miguel A.spa
dc.date.accessioned2020-04-27T20:19:25Z
dc.date.available2020-04-27T20:19:25Z
dc.date.created2014
dc.date.issued2014
dc.description.abstractThe term autoimmune rheumatic diseases (ARDs) encompasses a heterogeneous group of conditions characterized by joint involvement along with a wide spectrum of systemic manifestations. The most common ARDs are rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Nevertheless, all these conditions share similar pathophysiological mechanisms [1, 2] and a common risk of developing a process of accelerated atherosclerosis [3]. In this regard, in this special issue J. Amaya-Amaya and colleagues discussed the mechanisms associated with the increased risk of cardiovascular disease (CVD) in patients with autoimmune diseases. These authors emphasize the relevance of the CVD in rheumatic conditions and its connection with inflammation and autoimmunity. They also highlight the need of a more aggressive management of these conditions, both of disease activity and classic cardiovascular risk factors. A good example of accelerated atherosclerosis in the setting of an ARD is SLE, in which endothelial dysfunction, an early step in the atherogenesis process, is observed before cardiovascular events can occur. With respect to this, A. Mak and N. Y. Kow performed a comprehensive review of the mechanisms that are involved in endothelial damage.These authors focused on the factors involved in endothelial damage and repair and, therefore, in the development of CVD in patients with SLE. They discussed the relevant role of factors such as type 1 interferon, proinflammatory cytokines, inflammatory cells, immune complexes, costimulatory molecules, neutrophils extracellular traps, lupus-related autoantibodies, oxidative stress, and dyslipidemia that along with the aberrant function of the endothelial progenitor cells lead to endothelial dysfunction and increased susceptibility to develop CVD in patients with SLE. Based on these lines of evidence, the authors’ claim is in favor of early intervention at the preclinical stage of atherogenesis in these patients.eng
dc.format.mimetypeapplication/pdf
dc.identifier.doihttps://doi.org/10.1155/2014/952159
dc.identifier.issn2314-6133
dc.identifier.urihttps://repository.urosario.edu.co/handle/10336/21783
dc.language.isoengspa
dc.relation.citationTitleBioMed Research International
dc.relation.citationVolumeVol. 2014
dc.relation.ispartofBioMed Research International, ISSN: 2314-6133 Vol. 2014, (2014)spa
dc.relation.urihttp://www.sherpa.ac.uk/romeo/issn/2314-6133/spa
dc.rights.accesRightsinfo:eu-repo/semantics/openAccess
dc.rights.accesoAbierto (Texto Completo)spa
dc.source.instnameinstname:Universidad del Rosario
dc.source.reponamereponame:Repositorio Institucional EdocUR
dc.subject.ddcEnfermedadesspa
dc.subject.keywordEtanerceptspa
dc.subject.keywordSystemiceng
dc.subject.keywordRituximabspa
dc.subject.keywordAutoimmune diseasespa
dc.subject.keywordCardiovascular diseasespa
dc.subject.keywordEditorialspa
dc.subject.keywordHumanspa
dc.subject.keywordImmunogenicityspa
dc.subject.keywordKidney transplantationspa
dc.subject.keywordMorbidityspa
dc.subject.keywordMortalityspa
dc.subject.keywordRheumatic diseasespa
dc.subject.keywordRrheumatoid arthritisspa
dc.subject.keywordSystemic lupus erythematosusspa
dc.subject.keywordAutoimmune diseasespa
dc.subject.keywordImmunologyspa
dc.subject.keywordJointspa
dc.subject.keywordPathologyspa
dc.subject.keywordRheumatoid arthritisspa
dc.subject.keywordArthritiseng
dc.subject.keywordAutoimmune Diseasesspa
dc.subject.keywordHumansspa
dc.subject.keywordJointsspa
dc.subject.keywordLupus Erythematosuseng
dc.titleAutoimmune rheumatic diseasesspa
dc.typearticleeng
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersion
dc.type.spaEditorialspa
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