Antiphospholipid syndrome: an update
Identifieur interne : 000530 ( Istex/Corpus ); précédent : 000529; suivant : 000531Antiphospholipid syndrome: an update
Auteurs : Mira Merashli ; Mohammad Hassan A. Noureldine ; Imad Uthman ; Munther KhamashtaSource :
- European Journal of Clinical Investigation [ 0014-2972 ] ; 2015-06.
Abstract
Background: Antiphospholipid syndrome (APS) or ‘Hughes syndrome’ is a prothrombotic disease characterized by thrombosis and pregnancy morbidity in the presence of antiphospholipid antibodies (aPL). More than three decades have passed, and experts are still uncovering new pieces of this disease complex pathogenesis and management. Materials and methods: We searched in literature using MEDLINE and PubMed databases focusing on the latest development on disease pathogenesis, risk assessment of thrombosis and treatment of APS. Results: The phosphatidylinositol 3‐kinase (PI3K)–AKT‐mTORC pathway was most recently identified to have a crucial role in activating inflammation among endothelial vessel wall causing vascular lesions in APS. Additionally, new variables are being implemented to assess the risk of thrombosis in patients with APS. Global APS Score (GAPSS) utilizes cardiovascular risk factors and new autoimmune antibodies as part of the score assessment and is the most valid so far. It can be a promising tool in the future for prediction of thrombosis. Anticoagulation remains the cornerstone in APS; however, many new potential therapeutic agents are developing and are currently under investigation. Conclusions: The most recent advances in pathogenesis, risk stratification and treatment provide a platform for high yield studies with the ultimate goal of providing the optimal management to patients with APS.
Url:
DOI: 10.1111/eci.12449
Links to Exploration step
ISTEX:AFD9D4431996A6136C0F155C2F97074B408B20D8Le document en format XML
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Noureldine</name><affiliation><mods:affiliation>Faculty of Medicine, Lebanese American University Medical Center‐Rizk Hospital, Beirut, Lebanon</mods:affiliation></affiliation></author><author><name sortKey="Uthman, Imad" sort="Uthman, Imad" uniqKey="Uthman I" first="Imad" last="Uthman">Imad Uthman</name><affiliation><mods:affiliation>Division of Rheumatology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon</mods:affiliation></affiliation></author><author><name sortKey="Khamashta, Munther" sort="Khamashta, Munther" uniqKey="Khamashta M" first="Munther" last="Khamashta">Munther Khamashta</name><affiliation><mods:affiliation>Graham Hughes Lupus Research Laboratory, Division of Women's Health King's College London, The Rayne Institute, St Thomas' Hospital, London, UK</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: munther.khamashta@kcl.ac.uk</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:AFD9D4431996A6136C0F155C2F97074B408B20D8</idno><date when="2015" year="2015">2015</date><idno type="doi">10.1111/eci.12449</idno><idno type="url">https://api.istex.fr/ark:/67375/WNG-JMPPPK7T-M/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000530</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000530</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">Antiphospholipid syndrome: an update</title><author><name sortKey="Merashli, Mira" sort="Merashli, Mira" uniqKey="Merashli M" first="Mira" last="Merashli">Mira Merashli</name><affiliation><mods:affiliation>Division of Rheumatology, Faculty of Medicine, The Royal London Hospital, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Noureldine, Mohammad Hassan A" sort="Noureldine, Mohammad Hassan A" uniqKey="Noureldine M" first="Mohammad Hassan A." last="Noureldine">Mohammad Hassan A. Noureldine</name><affiliation><mods:affiliation>Faculty of Medicine, Lebanese American University Medical Center‐Rizk Hospital, Beirut, Lebanon</mods:affiliation></affiliation></author><author><name sortKey="Uthman, Imad" sort="Uthman, Imad" uniqKey="Uthman I" first="Imad" last="Uthman">Imad Uthman</name><affiliation><mods:affiliation>Division of Rheumatology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon</mods:affiliation></affiliation></author><author><name sortKey="Khamashta, Munther" sort="Khamashta, Munther" uniqKey="Khamashta M" first="Munther" last="Khamashta">Munther Khamashta</name><affiliation><mods:affiliation>Graham Hughes Lupus Research Laboratory, Division of Women's Health King's College London, The Rayne Institute, St Thomas' Hospital, London, UK</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: munther.khamashta@kcl.ac.uk</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">European Journal of Clinical Investigation</title><title level="j" type="alt">EUROPEAN JOURNAL OF CLINICAL INVESTIGATION</title><idno type="ISSN">0014-2972</idno><idno type="eISSN">1365-2362</idno><imprint><biblScope unit="vol">45</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="653">653</biblScope><biblScope unit="page" to="662">662</biblScope><biblScope unit="page-count">10</biblScope><date type="published" when="2015-06">2015-06</date></imprint><idno type="ISSN">0014-2972</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0014-2972</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">Background: Antiphospholipid syndrome (APS) or ‘Hughes syndrome’ is a prothrombotic disease characterized by thrombosis and pregnancy morbidity in the presence of antiphospholipid antibodies (aPL). More than three decades have passed, and experts are still uncovering new pieces of this disease complex pathogenesis and management. Materials and methods: We searched in literature using MEDLINE and PubMed databases focusing on the latest development on disease pathogenesis, risk assessment of thrombosis and treatment of APS. Results: The phosphatidylinositol 3‐kinase (PI3K)–AKT‐mTORC pathway was most recently identified to have a crucial role in activating inflammation among endothelial vessel wall causing vascular lesions in APS. Additionally, new variables are being implemented to assess the risk of thrombosis in patients with APS. Global APS Score (GAPSS) utilizes cardiovascular risk factors and new autoimmune antibodies as part of the score assessment and is the most valid so far. It can be a promising tool in the future for prediction of thrombosis. Anticoagulation remains the cornerstone in APS; however, many new potential therapeutic agents are developing and are currently under investigation. Conclusions: The most recent advances in pathogenesis, risk stratification and treatment provide a platform for high yield studies with the ultimate goal of providing the optimal management to patients with APS.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>antiphospholipid</json:string><json:string>antiphospholipid syndrome</json:string><json:string>lupus</json:string><json:string>thrombosis</json:string><json:string>syndrome</json:string><json:string>thrombotic</json:string><json:string>antiphospholipid antibody</json:string><json:string>anticoagulant</json:string><json:string>khamashta</json:string><json:string>warfarin</json:string><json:string>heparin</json:string><json:string>rituximab</json:string><json:string>hydroxychloroquine</json:string><json:string>venous</json:string><json:string>rheumatology</json:string><json:string>autoimmun</json:string><json:string>pathway</json:string><json:string>thromboprophylaxis</json:string><json:string>obstetric</json:string><json:string>cervera</json:string><json:string>autoimmune</json:string><json:string>thromboembolism</json:string><json:string>lmwh</json:string><json:string>ivig</json:string><json:string>erkan</json:string><json:string>anticoagulation</json:string><json:string>merashli</json:string><json:string>randomized</json:string><json:string>rheumatol</json:string><json:string>cuadrado</json:string><json:string>clin</json:string><json:string>engl</json:string><json:string>eculizumab</json:string><json:string>cohort</json:string><json:string>renal</json:string><json:string>transplantation</json:string><json:string>intravenous</json:string><json:string>haemost</json:string><json:string>catastrophic antiphospholipid syndrome</json:string><json:string>sciascia</json:string><json:string>morbidity</json:string><json:string>thromb</json:string><json:string>immunoglobulin</json:string><json:string>refractory</json:string><json:string>rheum</json:string><json:string>primary antiphospholipid syndrome</json:string><json:string>systemic lupus erythematosus</json:string><json:string>international congress</json:string><json:string>intravenous immunoglobulin</json:string><json:string>recurrent thrombosis</json:string><json:string>clinical investigation</json:string><json:string>refractory case</json:string><json:string>stichting european society</json:string><json:string>systematic review</json:string><json:string>thromb haemost</json:string><json:string>aspirin</json:string><json:string>datum</json:string><json:string>tissue factor</json:string><json:string>european journal</json:string><json:string>haemolytic anaemia</json:string><json:string>thrombotic microangiopathy</json:string><json:string>pregnancy loss</json:string><json:string>risk stratification</json:string><json:string>antiphospholipid antibody syndrome</json:string><json:string>endothelial cell</json:string><json:string>arthritis rheum</json:string><json:string>renal transplantation</json:string><json:string>pathogenesis</json:string><json:string>endothelial</json:string><json:string>venous thromboembolism</json:string><json:string>refractory obstetric</json:string><json:string>obstetric morbidity</json:string><json:string>lupus patient</json:string><json:string>antiprothrombin antibody</json:string><json:string>systemic lupus erythromatosus</json:string><json:string>oral anticoagulant</json:string><json:string>conventional therapy</json:string><json:string>health college london</json:string><json:string>venous thrombosis</json:string><json:string>recent advance</json:string><json:string>cardiovascular risk factor</json:string><json:string>clinical investigation journal foundation antiphospholipid syndrome</json:string><json:string>risk assessment</json:string><json:string>clinical significance</json:string><json:string>molecular weight heparin</json:string><json:string>combination therapy</json:string><json:string>rayne institute</json:string><json:string>arthritis care</json:string><json:string>pregnancy morbidity</json:string><json:string>hughes syndrome</json:string><json:string>pregnant patient</json:string><json:string>heparin combination</json:string><json:string>pregnancy</json:string><json:string>inhibitor</json:string><json:string>antibody</json:string><json:string>recurrent</json:string></teeft></keywords><author><json:item><name>Mira Merashli</name><affiliations><json:string>Division of Rheumatology, Faculty of Medicine, The Royal London Hospital, London, UK</json:string></affiliations></json:item><json:item><name>Mohammad Hassan A. Noureldine</name><affiliations><json:string>Faculty of Medicine, Lebanese American University Medical Center‐Rizk Hospital, Beirut, Lebanon</json:string></affiliations></json:item><json:item><name>Imad Uthman</name><affiliations><json:string>Division of Rheumatology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon</json:string></affiliations></json:item><json:item><name>Munther Khamashta</name><affiliations><json:string>Graham Hughes Lupus Research Laboratory, Division of Women's Health King's College London, The Rayne Institute, St Thomas' Hospital, London, UK</json:string><json:string>E-mail: munther.khamashta@kcl.ac.uk</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Antiphospholipid antibodies</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>antiphospholipid syndrome</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>management</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>pathogenesis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>risk stratification</value></json:item></subject><articleId><json:string>ECI12449</json:string></articleId><arkIstex>ark:/67375/WNG-JMPPPK7T-M</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>reviewArticle</json:string></originalGenre><abstract>Background: Antiphospholipid syndrome (APS) or ‘Hughes syndrome’ is a prothrombotic disease characterized by thrombosis and pregnancy morbidity in the presence of antiphospholipid antibodies (aPL). More than three decades have passed, and experts are still uncovering new pieces of this disease complex pathogenesis and management. Materials and methods: We searched in literature using MEDLINE and PubMed databases focusing on the latest development on disease pathogenesis, risk assessment of thrombosis and treatment of APS. Results: The phosphatidylinositol 3‐kinase (PI3K)–AKT‐mTORC pathway was most recently identified to have a crucial role in activating inflammation among endothelial vessel wall causing vascular lesions in APS. Additionally, new variables are being implemented to assess the risk of thrombosis in patients with APS. Global APS Score (GAPSS) utilizes cardiovascular risk factors and new autoimmune antibodies as part of the score assessment and is the most valid so far. It can be a promising tool in the future for prediction of thrombosis. Anticoagulation remains the cornerstone in APS; however, many new potential therapeutic agents are developing and are currently under investigation. 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<orgName type="institution">Lebanese American University Medical Center‐Rizk Hospital</orgName>
<address><settlement>Beirut</settlement>
<country key="LB" xml:lang="en">LEBANON</country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Imad</forename><surname>Uthman</surname></persName><affiliation><orgName type="division">Division of Rheumatology</orgName>
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<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract style="main" xml:id="eci12449-abs-0001"><head>Abstract</head><head>Background</head><p>Antiphospholipid syndrome (<hi rend="fc">APS</hi>) or ‘Hughes syndrome’ is a prothrombotic disease characterized by thrombosis and pregnancy morbidity in the presence of antiphospholipid antibodies (<hi rend="fc">aPL</hi>). More than three decades have passed, and experts are still uncovering new pieces of this disease complex pathogenesis and management.</p><head>Materials and methods</head><p>We searched in literature using <hi rend="fc">MEDLINE</hi> and PubMed databases focusing on the latest development on disease pathogenesis, risk assessment of thrombosis and treatment of <hi rend="fc">APS</hi>.</p><head>Results</head><p>The phosphatidylinositol 3‐kinase (<hi rend="fc">PI</hi>3K)–<hi rend="fc">AKT</hi>‐<hi rend="fc">mTORC</hi> pathway was most recently identified to have a crucial role in activating inflammation among endothelial vessel wall causing vascular lesions in <hi rend="fc">APS</hi>. Additionally, new variables are being implemented to assess the risk of thrombosis in patients with <hi rend="fc">APS</hi>. Global <hi rend="fc">APS</hi> Score (<hi rend="fc">GAPSS</hi>) utilizes cardiovascular risk factors and new autoimmune antibodies as part of the score assessment and is the most valid so far. It can be a promising tool in the future for prediction of thrombosis. Anticoagulation remains the cornerstone in <hi rend="fc">APS</hi>; however, many new potential therapeutic agents are developing and are currently under investigation.</p><head>Conclusions</head><p>The most recent advances in pathogenesis, risk stratification and treatment provide a platform for high yield studies with the ultimate goal of providing the optimal management to patients with <hi rend="fc">APS</hi>.</p></abstract><textClass><keywords><term xml:id="eci12449-kwd-0001">Antiphospholipid antibodies</term><term xml:id="eci12449-kwd-0002">antiphospholipid syndrome</term><term xml:id="eci12449-kwd-0003">management</term><term xml:id="eci12449-kwd-0004">pathogenesis</term><term xml:id="eci12449-kwd-0005">risk stratification</term></keywords><keywords rend="articleCategory"><term>Review</term></keywords><keywords rend="tocHeading1"><term>REVIEWS</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-JMPPPK7T-M/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component type="serialArticle" version="2.0" xml:id="eci12449" xml:lang="en"><header><publicationMeta level="product"><doi origin="wiley" registered="yes">10.1111/(ISSN)1365-2362</doi><issn type="print">0014-2972</issn><issn type="electronic">1365-2362</issn><idGroup><id type="product" value="ECI"></id></idGroup><titleGroup><title sort="EUROPEAN JOURNAL OF CLINICAL INVESTIGATION" type="main">European Journal of Clinical Investigation</title><title type="short">Eur J Clin Invest</title></titleGroup></publicationMeta><publicationMeta level="part" position="60"><doi origin="wiley">10.1111/eci.2015.45.issue-6</doi><copyright ownership="publisher">Copyright © 2015 Stichting European Society for Clinical Investigation Journal Foundation. Published by John Wiley & Sons Ltd</copyright><numberingGroup><numbering type="journalVolume" number="45">45</numbering><numbering type="journalIssue">6</numbering></numberingGroup><coverDate startDate="2015-06">June 2015</coverDate></publicationMeta><publicationMeta level="unit" position="160" status="forIssue" type="reviewArticle"><doi>10.1111/eci.12449</doi><idGroup><id type="unit" value="ECI12449"></id></idGroup><countGroup><count number="10" type="pageTotal"></count></countGroup><titleGroup><title type="articleCategory">Review</title><title type="tocHeading1">REVIEWS</title></titleGroup><copyright ownership="thirdParty">© 2015 Stichting European Society for Clinical Investigation Journal Foundation</copyright><eventGroup><event date="2015-03-16" type="manuscriptReceived"></event><event date="2015-04-04" type="manuscriptAccepted"></event><event agent="SPS" date="2015-04-11" type="xmlCreated"></event><event type="publishedOnlineAccepted" date="2015-04-08"></event><event type="publishedOnlineEarlyUnpaginated" date="2015-04-24"></event><event type="firstOnline" date="2015-04-24"></event><event type="publishedOnlineFinalForm" date="2015-05-18"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.7.2 mode:FullText" date="2016-01-05"></event></eventGroup><numberingGroup><numbering type="pageFirst">653</numbering><numbering type="pageLast">662</numbering></numberingGroup><correspondenceTo><b>Correspondence to:</b> Munther Khamashta, Graham Hughes Lupus Research Laboratory, Division of Women's Health King's College London, The Rayne Institute, Lambeth Wing, 4th Floor, St Thomas' Hospital, London SE1 7EH, UK. Tel.: 0207 188 3571; fax: 0207 620 2658; e‐mail: <email>munther.khamashta@kcl.ac.uk</email></correspondenceTo><selfCitationGroup><citation type="self" xml:id="eci12449-cit-1001"><journalTitle>Eur J Clin Invest</journalTitle> <pubYear year="2015">2015</pubYear>; <vol>45</vol> (<issue>6</issue>):<pageFirst>653</pageFirst>–<pageLast>662</pageLast></citation></selfCitationGroup><linkGroup><link type="toTypesetVersion" href="file:ECI.ECI12449.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">Antiphospholipid syndrome: an update</title><title type="shortAuthors">M. Merashli <i>et al</i>.</title></titleGroup><creators><creator affiliationRef="#eci12449-aff-0001" creatorRole="author" xml:id="eci12449-cr-0001"><personName><givenNames>Mira</givenNames> <familyName>Merashli</familyName></personName></creator><creator affiliationRef="#eci12449-aff-0002" creatorRole="author" xml:id="eci12449-cr-0002"><personName><givenNames>Mohammad Hassan A.</givenNames> <familyName>Noureldine</familyName></personName></creator><creator affiliationRef="#eci12449-aff-0003" creatorRole="author" xml:id="eci12449-cr-0003"><personName><givenNames>Imad</givenNames> <familyName>Uthman</familyName></personName></creator><creator affiliationRef="#eci12449-aff-0004" corresponding="yes" creatorRole="author" xml:id="eci12449-cr-0004"><personName><givenNames>Munther</givenNames> <familyName>Khamashta</familyName></personName></creator></creators><affiliationGroup><affiliation countryCode="GB" type="organization" xml:id="eci12449-aff-0001"><orgDiv>Division of Rheumatology</orgDiv> <orgDiv>Faculty of Medicine</orgDiv> <orgName>The Royal London Hospital</orgName> <address><city>London</city> <country>UK</country></address></affiliation><affiliation countryCode="LB" type="organization" xml:id="eci12449-aff-0002"><orgDiv>Faculty of Medicine</orgDiv> <orgName>Lebanese American University Medical Center‐Rizk Hospital</orgName> <address><city>Beirut</city> <country>Lebanon</country></address></affiliation><affiliation countryCode="LB" type="organization" xml:id="eci12449-aff-0003"><orgDiv>Division of Rheumatology</orgDiv> <orgDiv>Faculty of Medicine</orgDiv> <orgName>American University of Beirut</orgName> <address><city>Beirut</city> <country>Lebanon</country></address></affiliation><affiliation countryCode="GB" type="organization" xml:id="eci12449-aff-0004"><orgDiv>Graham Hughes Lupus Research Laboratory</orgDiv><orgDiv>Division of Women's Health King's College London</orgDiv> <orgDiv>The Rayne Institute</orgDiv> <orgName>St Thomas' Hospital</orgName> <address><city>London</city> <country>UK</country></address></affiliation></affiliationGroup><keywordGroup type="author"><keyword xml:id="eci12449-kwd-0001">Antiphospholipid antibodies</keyword><keyword xml:id="eci12449-kwd-0002">antiphospholipid syndrome</keyword><keyword xml:id="eci12449-kwd-0003">management</keyword><keyword xml:id="eci12449-kwd-0004">pathogenesis</keyword><keyword xml:id="eci12449-kwd-0005">risk stratification</keyword></keywordGroup><abstractGroup><abstract type="main" xml:id="eci12449-abs-0001"><title type="main">Abstract</title><section xml:id="eci12449-sec-0001"><title type="main">Background</title><p>Antiphospholipid syndrome (<fc>APS</fc>) or ‘Hughes syndrome’ is a prothrombotic disease characterized by thrombosis and pregnancy morbidity in the presence of antiphospholipid antibodies (<fc>aPL</fc>). More than three decades have passed, and experts are still uncovering new pieces of this disease complex pathogenesis and management.</p></section><section xml:id="eci12449-sec-0002"><title type="main">Materials and methods</title><p>We searched in literature using <fc>MEDLINE</fc> and PubMed databases focusing on the latest development on disease pathogenesis, risk assessment of thrombosis and treatment of <fc>APS</fc>.</p></section><section xml:id="eci12449-sec-0003"><title type="main">Results</title><p>The phosphatidylinositol 3‐kinase (<fc>PI</fc>3K)–<fc>AKT</fc>‐<fc>mTORC</fc> pathway was most recently identified to have a crucial role in activating inflammation among endothelial vessel wall causing vascular lesions in <fc>APS</fc>. Additionally, new variables are being implemented to assess the risk of thrombosis in patients with <fc>APS</fc>. Global <fc>APS</fc> Score (<fc>GAPSS</fc>) utilizes cardiovascular risk factors and new autoimmune antibodies as part of the score assessment and is the most valid so far. It can be a promising tool in the future for prediction of thrombosis. Anticoagulation remains the cornerstone in <fc>APS</fc>; however, many new potential therapeutic agents are developing and are currently under investigation.</p></section><section xml:id="eci12449-sec-0004"><title type="main">Conclusions</title><p>The most recent advances in pathogenesis, risk stratification and treatment provide a platform for high yield studies with the ultimate goal of providing the optimal management to patients with <fc>APS</fc>.</p></section></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Antiphospholipid syndrome: an update</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Antiphospholipid syndrome: an update</title></titleInfo><name type="personal"><namePart type="given">Mira</namePart><namePart type="family">Merashli</namePart><affiliation>Division of Rheumatology, Faculty of Medicine, The Royal London Hospital, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mohammad Hassan A.</namePart><namePart type="family">Noureldine</namePart><affiliation>Faculty of Medicine, Lebanese American University Medical Center‐Rizk Hospital, Beirut, Lebanon</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Imad</namePart><namePart type="family">Uthman</namePart><affiliation>Division of Rheumatology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Munther</namePart><namePart type="family">Khamashta</namePart><affiliation>Graham Hughes Lupus Research Laboratory, Division of Women's Health King's College London, The Rayne Institute, St Thomas' Hospital, London, UK</affiliation><affiliation>E-mail: munther.khamashta@kcl.ac.uk</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-L5L7X3NF-P">review-article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><dateIssued encoding="w3cdtf">2015-06</dateIssued><dateCreated encoding="w3cdtf">2015-04-11</dateCreated><dateCaptured encoding="w3cdtf">2015-03-16</dateCaptured><dateValid encoding="w3cdtf">2015-04-04</dateValid><edition>Eur J Clin Invest 2015; 45 (6):653–662</edition><copyrightDate encoding="w3cdtf">2015</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract>Background: Antiphospholipid syndrome (APS) or ‘Hughes syndrome’ is a prothrombotic disease characterized by thrombosis and pregnancy morbidity in the presence of antiphospholipid antibodies (aPL). More than three decades have passed, and experts are still uncovering new pieces of this disease complex pathogenesis and management. Materials and methods: We searched in literature using MEDLINE and PubMed databases focusing on the latest development on disease pathogenesis, risk assessment of thrombosis and treatment of APS. Results: The phosphatidylinositol 3‐kinase (PI3K)–AKT‐mTORC pathway was most recently identified to have a crucial role in activating inflammation among endothelial vessel wall causing vascular lesions in APS. Additionally, new variables are being implemented to assess the risk of thrombosis in patients with APS. Global APS Score (GAPSS) utilizes cardiovascular risk factors and new autoimmune antibodies as part of the score assessment and is the most valid so far. It can be a promising tool in the future for prediction of thrombosis. Anticoagulation remains the cornerstone in APS; however, many new potential therapeutic agents are developing and are currently under investigation. Conclusions: The most recent advances in pathogenesis, risk stratification and treatment provide a platform for high yield studies with the ultimate goal of providing the optimal management to patients with APS.</abstract><subject><genre>keywords</genre><topic>Antiphospholipid antibodies</topic><topic>antiphospholipid syndrome</topic><topic>management</topic><topic>pathogenesis</topic><topic>risk stratification</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Clinical Investigation</title></titleInfo><titleInfo type="abbreviated"><title>Eur J Clin Invest</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><subject><genre>article-category</genre><topic>Review</topic><topic>REVIEWS</topic></subject><identifier type="ISSN">0014-2972</identifier><identifier type="eISSN">1365-2362</identifier><identifier type="DOI">10.1111/(ISSN)1365-2362</identifier><identifier type="PublisherID">ECI</identifier><part><date>2015</date><detail type="volume"><caption>vol.</caption><number>45</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>653</start><end>662</end><total>10</total></extent></part></relatedItem><relatedItem type="references" displayLabel="eci12449-cit-0001"><titleInfo><title>Diagnosis and classification of the antiphospholipid syndrome</title></titleInfo><name type="personal"><namePart type="given">JA</namePart><namePart type="family">Gomez‐Puerta</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Cervera</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Gomez‐Puerta JA, Cervera R. 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