SLE, atherosclerosis and cardiovascular disease
. Atherosclerosis is an inflammatory disease and the major cause of cardiovascular disease (CVD) in general. Atherosclerotic plaques are characterized by the presence of activated immune competent cells, but antigens and underlying mechanisms causing this immune activation are not well defined. Duri...
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Veröffentlicht in: | Journal of internal medicine 2005-06, Vol.257 (6), p.485-495 |
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Atherosclerosis is an inflammatory disease and the major cause of cardiovascular disease (CVD) in general. Atherosclerotic plaques are characterized by the presence of activated immune competent cells, but antigens and underlying mechanisms causing this immune activation are not well defined. During recent years and with improved treatment of acute disease manifestations, it has become clear that the risk of CVD is very high in a prototypic autoimmune disease, systemic lupus erythematosus (SLE). SLE‐related CVD and atherosclerosis are important clinical problems but may in addition also shed light on how immune reactions are related to premature atherosclerosis and atherothrombosis. A combination of traditional and nontraditional risk factors, including dyslipidaemia (and to a varying degree hypertension, diabetes and smoking), inflammation, antiphospholipid antibodies (aPL) and lipid oxidation are related to CVD in SLE. Premature atherosclerosis in some form leading to atherothrombosis is likely to be a major underlying mechanism, though distinctive features if any, of SLE‐related atherosclerosis when compared with ‘normal’ atherosclerosis are not clear. One interesting possibility is that factors such as inflammation or aPL make atherosclerotic lesions in autoimmune disease more prone to rupture than in ‘normal’ atherosclerosis. Whether premature atherosclerosis is a general feature of SLE or only affects a subgroup of patients remains to be demonstrated. Treatment of SLE patients should also include a close monitoring of traditional risk factors for CVD. In addition, attention should also be paid to nontraditional risk factors such as inflammation and SLE‐related factors such as aPL. Hopefully novel therapeutic principles will be developed that target the causes of the inflammation and immune reactions present in atherosclerotic lesions. |
doi_str_mv | 10.1111/j.1365-2796.2005.01502.x |
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Atherosclerosis is an inflammatory disease and the major cause of cardiovascular disease (CVD) in general. Atherosclerotic plaques are characterized by the presence of activated immune competent cells, but antigens and underlying mechanisms causing this immune activation are not well defined. During recent years and with improved treatment of acute disease manifestations, it has become clear that the risk of CVD is very high in a prototypic autoimmune disease, systemic lupus erythematosus (SLE). SLE‐related CVD and atherosclerosis are important clinical problems but may in addition also shed light on how immune reactions are related to premature atherosclerosis and atherothrombosis. A combination of traditional and nontraditional risk factors, including dyslipidaemia (and to a varying degree hypertension, diabetes and smoking), inflammation, antiphospholipid antibodies (aPL) and lipid oxidation are related to CVD in SLE. Premature atherosclerosis in some form leading to atherothrombosis is likely to be a major underlying mechanism, though distinctive features if any, of SLE‐related atherosclerosis when compared with ‘normal’ atherosclerosis are not clear. One interesting possibility is that factors such as inflammation or aPL make atherosclerotic lesions in autoimmune disease more prone to rupture than in ‘normal’ atherosclerosis. Whether premature atherosclerosis is a general feature of SLE or only affects a subgroup of patients remains to be demonstrated. Treatment of SLE patients should also include a close monitoring of traditional risk factors for CVD. In addition, attention should also be paid to nontraditional risk factors such as inflammation and SLE‐related factors such as aPL. Hopefully novel therapeutic principles will be developed that target the causes of the inflammation and immune reactions present in atherosclerotic lesions.</description><identifier>ISSN: 0954-6820</identifier><identifier>EISSN: 1365-2796</identifier><identifier>DOI: 10.1111/j.1365-2796.2005.01502.x</identifier><identifier>PMID: 15910552</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Adrenal Cortex Hormones - therapeutic use ; Antibodies, Antiphospholipid - immunology ; antiphospholipid antibodies ; Arteriosclerosis - drug therapy ; Arteriosclerosis - immunology ; atherosclerosis ; Biological and medical sciences ; Cardiovascular Diseases - drug therapy ; Cardiovascular Diseases - immunology ; Cytokines - immunology ; General aspects ; Humans ; Hyperlipidemias - immunology ; inflammation ; Inflammation - immunology ; Lipoproteins, LDL - metabolism ; Lupus Erythematosus, Systemic - complications ; Lupus Erythematosus, Systemic - drug therapy ; Lupus Erythematosus, Systemic - immunology ; Medical sciences ; Medicin och hälsovetenskap ; Oxidation-Reduction ; plaque rupture ; Risk Factors ; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis ; SLE</subject><ispartof>Journal of internal medicine, 2005-06, Vol.257 (6), p.485-495</ispartof><rights>2005 INIST-CNRS</rights><rights>Copyright Blackwell Publishing Jun 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5772-9e86d8dc5cea28f99271be9c462cf21ec7ae25d5871f4da410aedc363c7ad18e3</citedby><cites>FETCH-LOGICAL-c5772-9e86d8dc5cea28f99271be9c462cf21ec7ae25d5871f4da410aedc363c7ad18e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1365-2796.2005.01502.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1365-2796.2005.01502.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,780,784,885,1417,1433,27924,27925,45574,45575,46409,46833</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16792429$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15910552$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:1940978$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>FROSTEGARD, J</creatorcontrib><title>SLE, atherosclerosis and cardiovascular disease</title><title>Journal of internal medicine</title><addtitle>J Intern Med</addtitle><description>.
Atherosclerosis is an inflammatory disease and the major cause of cardiovascular disease (CVD) in general. Atherosclerotic plaques are characterized by the presence of activated immune competent cells, but antigens and underlying mechanisms causing this immune activation are not well defined. During recent years and with improved treatment of acute disease manifestations, it has become clear that the risk of CVD is very high in a prototypic autoimmune disease, systemic lupus erythematosus (SLE). SLE‐related CVD and atherosclerosis are important clinical problems but may in addition also shed light on how immune reactions are related to premature atherosclerosis and atherothrombosis. A combination of traditional and nontraditional risk factors, including dyslipidaemia (and to a varying degree hypertension, diabetes and smoking), inflammation, antiphospholipid antibodies (aPL) and lipid oxidation are related to CVD in SLE. Premature atherosclerosis in some form leading to atherothrombosis is likely to be a major underlying mechanism, though distinctive features if any, of SLE‐related atherosclerosis when compared with ‘normal’ atherosclerosis are not clear. One interesting possibility is that factors such as inflammation or aPL make atherosclerotic lesions in autoimmune disease more prone to rupture than in ‘normal’ atherosclerosis. Whether premature atherosclerosis is a general feature of SLE or only affects a subgroup of patients remains to be demonstrated. Treatment of SLE patients should also include a close monitoring of traditional risk factors for CVD. In addition, attention should also be paid to nontraditional risk factors such as inflammation and SLE‐related factors such as aPL. Hopefully novel therapeutic principles will be developed that target the causes of the inflammation and immune reactions present in atherosclerotic lesions.</description><subject>Adrenal Cortex Hormones - therapeutic use</subject><subject>Antibodies, Antiphospholipid - immunology</subject><subject>antiphospholipid antibodies</subject><subject>Arteriosclerosis - drug therapy</subject><subject>Arteriosclerosis - immunology</subject><subject>atherosclerosis</subject><subject>Biological and medical sciences</subject><subject>Cardiovascular Diseases - drug therapy</subject><subject>Cardiovascular Diseases - immunology</subject><subject>Cytokines - immunology</subject><subject>General aspects</subject><subject>Humans</subject><subject>Hyperlipidemias - immunology</subject><subject>inflammation</subject><subject>Inflammation - immunology</subject><subject>Lipoproteins, LDL - metabolism</subject><subject>Lupus Erythematosus, Systemic - complications</subject><subject>Lupus Erythematosus, Systemic - drug therapy</subject><subject>Lupus Erythematosus, Systemic - immunology</subject><subject>Medical sciences</subject><subject>Medicin och hälsovetenskap</subject><subject>Oxidation-Reduction</subject><subject>plaque rupture</subject><subject>Risk Factors</subject><subject>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</subject><subject>SLE</subject><issn>0954-6820</issn><issn>1365-2796</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkV9LHDEUxUNRdLv1K5ShoE-d8SYz-fdSENFWWfGh-hyyyR0629mdbeK4-u2b6Y4uFATzkFxyf-dwuYeQjEJB0zldFLQUPGdSi4IB8AIoB1Y8fSCT18YemYDmVS4Ug0PyMcYFAC1BwAE5pFxT4JxNyOnP2cXXzD78wtBF1w53EzO78pmzwTfdo42ub23IfBPRRvxE9mvbRjwa3ym5v7y4O_-Rz26_X52fzXLHpWS5RiW88o47tEzVWjNJ56hdJZirGUUnLTLuuZK0rrytKFj0rhRlaniqsJySfOsbN7ju52YdmqUNz6azjRm_fqcKDVcgWZl4-Sa_Dp3fiV6EVFegpUrKk60yYX96jA9m2USHbWtX2PXRCKkEcDGAX_4DF10fVmkLyUtqziUVCVJbyKVNxoD16yQUzJCdWZghIjNEZIbszL_szFOSfh79-_kS_U44hpWA4xFIodi2DnblmrjjhNSsYjpx37bcpmnx-d0DmOvbq5uhLP8Cvyu1eA</recordid><startdate>200506</startdate><enddate>200506</enddate><creator>FROSTEGARD, J</creator><general>Blackwell Science Ltd</general><general>Blackwell Science</general><general>Blackwell Publishing Ltd</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>C1K</scope><scope>K9.</scope><scope>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope></search><sort><creationdate>200506</creationdate><title>SLE, atherosclerosis and cardiovascular disease</title><author>FROSTEGARD, J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5772-9e86d8dc5cea28f99271be9c462cf21ec7ae25d5871f4da410aedc363c7ad18e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adrenal Cortex Hormones - therapeutic use</topic><topic>Antibodies, Antiphospholipid - immunology</topic><topic>antiphospholipid antibodies</topic><topic>Arteriosclerosis - drug therapy</topic><topic>Arteriosclerosis - immunology</topic><topic>atherosclerosis</topic><topic>Biological and medical sciences</topic><topic>Cardiovascular Diseases - drug therapy</topic><topic>Cardiovascular Diseases - immunology</topic><topic>Cytokines - immunology</topic><topic>General aspects</topic><topic>Humans</topic><topic>Hyperlipidemias - immunology</topic><topic>inflammation</topic><topic>Inflammation - immunology</topic><topic>Lipoproteins, LDL - metabolism</topic><topic>Lupus Erythematosus, Systemic - complications</topic><topic>Lupus Erythematosus, Systemic - drug therapy</topic><topic>Lupus Erythematosus, Systemic - immunology</topic><topic>Medical sciences</topic><topic>Medicin och hälsovetenskap</topic><topic>Oxidation-Reduction</topic><topic>plaque rupture</topic><topic>Risk Factors</topic><topic>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</topic><topic>SLE</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>FROSTEGARD, J</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>SwePub</collection><collection>SwePub Articles</collection><jtitle>Journal of internal medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>FROSTEGARD, J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SLE, atherosclerosis and cardiovascular disease</atitle><jtitle>Journal of internal medicine</jtitle><addtitle>J Intern Med</addtitle><date>2005-06</date><risdate>2005</risdate><volume>257</volume><issue>6</issue><spage>485</spage><epage>495</epage><pages>485-495</pages><issn>0954-6820</issn><eissn>1365-2796</eissn><abstract>.
Atherosclerosis is an inflammatory disease and the major cause of cardiovascular disease (CVD) in general. Atherosclerotic plaques are characterized by the presence of activated immune competent cells, but antigens and underlying mechanisms causing this immune activation are not well defined. During recent years and with improved treatment of acute disease manifestations, it has become clear that the risk of CVD is very high in a prototypic autoimmune disease, systemic lupus erythematosus (SLE). SLE‐related CVD and atherosclerosis are important clinical problems but may in addition also shed light on how immune reactions are related to premature atherosclerosis and atherothrombosis. A combination of traditional and nontraditional risk factors, including dyslipidaemia (and to a varying degree hypertension, diabetes and smoking), inflammation, antiphospholipid antibodies (aPL) and lipid oxidation are related to CVD in SLE. Premature atherosclerosis in some form leading to atherothrombosis is likely to be a major underlying mechanism, though distinctive features if any, of SLE‐related atherosclerosis when compared with ‘normal’ atherosclerosis are not clear. One interesting possibility is that factors such as inflammation or aPL make atherosclerotic lesions in autoimmune disease more prone to rupture than in ‘normal’ atherosclerosis. Whether premature atherosclerosis is a general feature of SLE or only affects a subgroup of patients remains to be demonstrated. Treatment of SLE patients should also include a close monitoring of traditional risk factors for CVD. In addition, attention should also be paid to nontraditional risk factors such as inflammation and SLE‐related factors such as aPL. Hopefully novel therapeutic principles will be developed that target the causes of the inflammation and immune reactions present in atherosclerotic lesions.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>15910552</pmid><doi>10.1111/j.1365-2796.2005.01502.x</doi><tpages>11</tpages></addata></record> |
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subjects | Adrenal Cortex Hormones - therapeutic use Antibodies, Antiphospholipid - immunology antiphospholipid antibodies Arteriosclerosis - drug therapy Arteriosclerosis - immunology atherosclerosis Biological and medical sciences Cardiovascular Diseases - drug therapy Cardiovascular Diseases - immunology Cytokines - immunology General aspects Humans Hyperlipidemias - immunology inflammation Inflammation - immunology Lipoproteins, LDL - metabolism Lupus Erythematosus, Systemic - complications Lupus Erythematosus, Systemic - drug therapy Lupus Erythematosus, Systemic - immunology Medical sciences Medicin och hälsovetenskap Oxidation-Reduction plaque rupture Risk Factors Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis SLE |
title | SLE, atherosclerosis and cardiovascular disease |
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