%0 Journal Article %1 floris2018protective %A Floris, Alberto %A Piga, Matteo %A Mangoni, Arduino Aleksander %A Bortoluzzi, Alessandra %A Erre, Gian Luca %A Cauli, Alberto %D 2018 %J Mediators of Inflammation %K (h)cq lupus %P 11 %T Protective Effects of Hydroxychloroquine against Accelerated Atherosclerosis in Systemic Lupus Erythematosus %U https://doi.org/10.1155/2018/3424136 %V 2018 %X Cardiovascular (CV) morbidity and mortality are a challenge in management of patients with systemic lupus erythematosus (SLE). Higher risk of CV disease in SLE patients is mostly related to accelerated atherosclerosis. Nevertheless, high prevalence of traditional cardiovascular risk factors in SLE patients does not fully explain the increased CV risk. Despite the pathological bases of accelerated atherosclerosis are not fully understood, it is thought that this process is driven by the complex interplay between SLE and atherosclerosis pathogenesis. Hydroxychloroquine (HCQ) is a cornerstone in treatment of SLE patients and has been thought to exert a broad spectrum of beneficial effects on disease activity, prevention of damage accrual, and mortality. Furthermore, HCQ is thought to protect against accelerated atherosclerosis targeting toll-like receptor signaling, cytokine production, T-cell and monocyte activation, oxidative stress, and endothelial dysfunction. HCQ was also described to have beneficial effects on traditional CV risk factors, such as dyslipidemia and diabetes. In conclusion, despite lacking randomized controlled trials unambiguously proving the protection of HCQ against accelerated atherosclerosis and incidence of CV events in SLE patients, evidence analyzed in this review is in favor of its beneficial effect."/><meta name="citation_pdf_url" content="http://downloads.hindawi.com/journals/mi/2018/3424136.pdf"/><meta name="citation_xml_url" content="http://downloads.hindawi.com/journals/mi/2018/3424136.xml"/><meta name="citation_fulltext_html_url" content="https://www.hindawi.com/journals/mi/2018/3424136/"/><meta name="citation_doi" content="https://doi.org/10.1155/2018/3424136"/><meta name="citation_online_date" content="2018/02/18"/><meta name="dcterms.issued" content="2018/02/18"/><meta name="dc.creator" content="Floris, Alberto"/><meta name="dc.creator" content="Piga, Matteo"/><meta name="dc.creator" content="Mangoni, Arduino Aleksander"/><meta name="dc.creator" content="Bortoluzzi, Alessandra"/><meta name="dc.creator" content="Erre, Gian Luca"/><meta name="dc.creator" content="Cauli, Alberto"/><meta name="dc.title" content="Protective Effects of Hydroxychloroquine against Accelerated Atherosclerosis in Systemic Lupus Erythematosus"/><meta name="dc.description" content="Cardiovascular (CV) morbidity and mortality are a challenge in management of patients with systemic lupus erythematosus (SLE). Higher risk of CV disease in SLE patients is mostly related to accelerated atherosclerosis. Nevertheless, high prevalence of traditional cardiovascular risk factors in SLE patients does not fully explain the increased CV risk. Despite the pathological bases of accelerated atherosclerosis are not fully understood, it is thought that this process is driven by the complex interplay between SLE and atherosclerosis pathogenesis. Hydroxychloroquine (HCQ) is a cornerstone in treatment of SLE patients and has been thought to exert a broad spectrum of beneficial effects on disease activity, prevention of damage accrual, and mortality. Furthermore, HCQ is thought to protect against accelerated atherosclerosis targeting toll-like receptor signaling, cytokine production, T-cell and monocyte activation, oxidative stress, and endothelial dysfunction. HCQ was also described to have beneficial effects on traditional CV risk factors, such as dyslipidemia and diabetes. In conclusion, despite lacking randomized controlled trials unambiguously proving the protection of HCQ against accelerated atherosclerosis and incidence of CV events in SLE patients, evidence analyzed in this review is in favor of its beneficial effect."/><meta name="dc.publisher" content="Hindawi"/><meta name="dc.format" content="text/html"/><meta name="dc.language" content="en"/><meta name="dc.identifier" content="https://doi.org/10.1155/2018/3424136"/><meta name="dc.type" content="Review Article"/><meta name="dc.date" content="2018/02/18"/><meta name="dcterms.issued" content="2018/02/18"/><meta name="prism.publicationDate" content="2018/02/18"/><meta name="prism.volume" content="2018"/><meta name="prism.number" content=""/><meta name="prism.startingPage" content=""/><meta name="prism.section" content="Review Article"/><meta name="prism.doi" content="https://doi.org/10.1155/2018/3424136"/><meta name="citation_issn" content="0962-9351"/><meta name="prism.issn" content="0962-9351"/><meta name="dc.source" content="Mediators of Inflammation"/><meta name="citation_journal_title" content="Mediators of Inflammation"/><meta name="prism.publicationName" content="Mediators of Inflammation"/><meta name=äuthors" content=Älberto Floris | Matteo Piga | ... | Alberto Cauli"/><link rel="stylesheet" href="//fonts.googleapis.com/css?family=IBM+Plex+Sans:400,400i,500,500i,700,700i"/><link rel="shortcut icon" type="image/x-icon" href="data:image/vnd.microsoft.icon;base64,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"/><meta name=Äuthor" content="Hindawi"/><meta name="robots" content="index"/><meta name="google-site-verification" content=ÄxEuDsL7vXGOxRe53-uFhOk2ODN0bbXMeuBy6Pfq4ww"/><script src="https://cdn.cookielaw.org/scripttemplates/otSDKStub.js" type="text/javascript" charset=ÜTF-8" data-domain-script="790048b6-f010-4ac2-b5f6-108356336b09"></script><link href="https://static-01.hindawi.com/next_assets/e4dXiy6wXnQD3-DFzWQ0d/static/lib/basictable.css" rel="stylesheet" media="none" class="next-head"/><link rel="stylesheet" href="https://static-01.hindawi.com/next_assets/e4dXiy6wXnQD3-DFzWQ0d/static/lib/owl.carousel.min.css" media="none" class="next-head"/><link rel="stylesheet" href="https://static-01.hindawi.com/next_assets/e4dXiy6wXnQD3-DFzWQ0d/static/lib/owl.theme.default.min.css" media="none" class="next-head

@article{floris2018protective, abstract = {Cardiovascular (CV) morbidity and mortality are a challenge in management of patients with systemic lupus erythematosus (SLE). Higher risk of CV disease in SLE patients is mostly related to accelerated atherosclerosis. Nevertheless, high prevalence of traditional cardiovascular risk factors in SLE patients does not fully explain the increased CV risk. Despite the pathological bases of accelerated atherosclerosis are not fully understood, it is thought that this process is driven by the complex interplay between SLE and atherosclerosis pathogenesis. Hydroxychloroquine (HCQ) is a cornerstone in treatment of SLE patients and has been thought to exert a broad spectrum of beneficial effects on disease activity, prevention of damage accrual, and mortality. Furthermore, HCQ is thought to protect against accelerated atherosclerosis targeting toll-like receptor signaling, cytokine production, T-cell and monocyte activation, oxidative stress, and endothelial dysfunction. HCQ was also described to have beneficial effects on traditional CV risk factors, such as dyslipidemia and diabetes. In conclusion, despite lacking randomized controlled trials unambiguously proving the protection of HCQ against accelerated atherosclerosis and incidence of CV events in SLE patients, evidence analyzed in this review is in favor of its beneficial effect."/><meta name="citation_pdf_url" content="http://downloads.hindawi.com/journals/mi/2018/3424136.pdf"/><meta name="citation_xml_url" content="http://downloads.hindawi.com/journals/mi/2018/3424136.xml"/><meta name="citation_fulltext_html_url" content="https://www.hindawi.com/journals/mi/2018/3424136/"/><meta name="citation_doi" content="https://doi.org/10.1155/2018/3424136"/><meta name="citation_online_date" content="2018/02/18"/><meta name="dcterms.issued" content="2018/02/18"/><meta name="dc.creator" content="Floris, Alberto"/><meta name="dc.creator" content="Piga, Matteo"/><meta name="dc.creator" content="Mangoni, Arduino Aleksander"/><meta name="dc.creator" content="Bortoluzzi, Alessandra"/><meta name="dc.creator" content="Erre, Gian Luca"/><meta name="dc.creator" content="Cauli, Alberto"/><meta name="dc.title" content="Protective Effects of Hydroxychloroquine against Accelerated Atherosclerosis in Systemic Lupus Erythematosus"/><meta name="dc.description" content="Cardiovascular (CV) morbidity and mortality are a challenge in management of patients with systemic lupus erythematosus (SLE). Higher risk of CV disease in SLE patients is mostly related to accelerated atherosclerosis. Nevertheless, high prevalence of traditional cardiovascular risk factors in SLE patients does not fully explain the increased CV risk. Despite the pathological bases of accelerated atherosclerosis are not fully understood, it is thought that this process is driven by the complex interplay between SLE and atherosclerosis pathogenesis. Hydroxychloroquine (HCQ) is a cornerstone in treatment of SLE patients and has been thought to exert a broad spectrum of beneficial effects on disease activity, prevention of damage accrual, and mortality. Furthermore, HCQ is thought to protect against accelerated atherosclerosis targeting toll-like receptor signaling, cytokine production, T-cell and monocyte activation, oxidative stress, and endothelial dysfunction. HCQ was also described to have beneficial effects on traditional CV risk factors, such as dyslipidemia and diabetes. In conclusion, despite lacking randomized controlled trials unambiguously proving the protection of HCQ against accelerated atherosclerosis and incidence of CV events in SLE patients, evidence analyzed in this review is in favor of its beneficial effect."/><meta name="dc.publisher" content="Hindawi"/><meta name="dc.format" content="text/html"/><meta name="dc.language" content="en"/><meta name="dc.identifier" content="https://doi.org/10.1155/2018/3424136"/><meta name="dc.type" content="Review Article"/><meta name="dc.date" content="2018/02/18"/><meta name="dcterms.issued" content="2018/02/18"/><meta name="prism.publicationDate" content="2018/02/18"/><meta name="prism.volume" content="2018"/><meta name="prism.number" content=""/><meta name="prism.startingPage" content=""/><meta name="prism.section" content="Review Article"/><meta name="prism.doi" content="https://doi.org/10.1155/2018/3424136"/><meta name="citation_issn" content="0962-9351"/><meta name="prism.issn" content="0962-9351"/><meta name="dc.source" content="Mediators of Inflammation"/><meta name="citation_journal_title" content="Mediators of Inflammation"/><meta name="prism.publicationName" content="Mediators of Inflammation"/><meta name="authors" content="Alberto Floris | Matteo Piga | ... | Alberto Cauli"/><link rel="stylesheet" href="//fonts.googleapis.com/css?family=IBM+Plex+Sans:400,400i,500,500i,700,700i"/><link rel="shortcut icon" type="image/x-icon" href="data:image/vnd.microsoft.icon;base64,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"/><meta name="Author" content="Hindawi"/><meta name="robots" content="index"/><meta name="google-site-verification" content="AxEuDsL7vXGOxRe53-uFhOk2ODN0bbXMeuBy6Pfq4ww"/><script src="https://cdn.cookielaw.org/scripttemplates/otSDKStub.js" type="text/javascript" charset="UTF-8" data-domain-script="790048b6-f010-4ac2-b5f6-108356336b09"></script><link href="https://static-01.hindawi.com/next_assets/e4dXiy6wXnQD3-DFzWQ0d/static/lib/basictable.css" rel="stylesheet" media="none" class="next-head"/><link rel="stylesheet" href="https://static-01.hindawi.com/next_assets/e4dXiy6wXnQD3-DFzWQ0d/static/lib/owl.carousel.min.css" media="none" class="next-head"/><link rel="stylesheet" href="https://static-01.hindawi.com/next_assets/e4dXiy6wXnQD3-DFzWQ0d/static/lib/owl.theme.default.min.css" media="none" class="next-head}, added-at = {2020-04-30T17:18:25.000+0200}, author = {Floris, Alberto and Piga, Matteo and Mangoni, Arduino Aleksander and Bortoluzzi, Alessandra and Erre, Gian Luca and Cauli, Alberto}, biburl = {https://www.bibsonomy.org/bibtex/28e76933b33e99324093c82778dd0fe03/fordham1}, description = {Protective Effects of Hydroxychloroquine against Accelerated Atherosclerosis in Systemic Lupus Erythematosus}, interhash = {eb252d15f2528e234617b6e6ce556e42}, intrahash = {8e76933b33e99324093c82778dd0fe03}, journal = {Mediators of Inflammation}, keywords = {(h)cq lupus}, pages = 11, timestamp = {2020-04-30T17:18:25.000+0200}, title = {Protective Effects of Hydroxychloroquine against Accelerated Atherosclerosis in Systemic Lupus Erythematosus}, url = {https://doi.org/10.1155/2018/3424136}, volume = 2018, year = 2018 }