Antiphospholipid syndrome: an update
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 comple...
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| Veröffentlicht in: | European journal of clinical investigation 2015-06, Vol.45 (6), p.653-662 |
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| container_title | European journal of clinical investigation |
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| creator | Merashli, Mira Noureldine, Mohammad Hassan A. Uthman, Imad Khamashta, Munther |
| description | 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. |
| doi_str_mv | 10.1111/eci.12449 |
| format | Article |
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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.</description><identifier>ISSN: 0014-2972</identifier><identifier>EISSN: 1365-2362</identifier><identifier>DOI: 10.1111/eci.12449</identifier><identifier>PMID: 25851448</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Adrenal Cortex Hormones - therapeutic use ; Animals ; Annexin A2 - antagonists & inhibitors ; Anticoagulants - therapeutic use ; Antiphospholipid antibodies ; antiphospholipid syndrome ; Antiphospholipid Syndrome - etiology ; Antiphospholipid Syndrome - therapy ; Drugs, Investigational ; Female ; Humans ; Hydroxychloroquine - therapeutic use ; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use ; Immunoglobulins, Intravenous - therapeutic use ; Immunosuppressive Agents - therapeutic use ; management ; MAP Kinase Signaling System - physiology ; Mice ; pathogenesis ; Phosphatidylinositol 3-Kinases - metabolism ; Plasmapheresis ; Pregnancy ; Pregnancy Complications, Cardiovascular - etiology ; Pregnancy Complications, Cardiovascular - prevention & control ; Risk Assessment ; risk stratification ; Rituximab ; Secondary Prevention ; Thromboplastin - antagonists & inhibitors ; Thrombosis - etiology ; Thrombosis - prevention & control ; TOR Serine-Threonine Kinases - metabolism</subject><ispartof>European journal of clinical investigation, 2015-06, Vol.45 (6), p.653-662</ispartof><rights>2015 Stichting European Society for Clinical Investigation Journal Foundation</rights><rights>2015 Stichting European Society for Clinical Investigation Journal Foundation.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4689-13dbbfb9d77763872051f0fb686bc176ac76cea640aad4d4c3c7e39c9c31d8943</citedby><cites>FETCH-LOGICAL-c4689-13dbbfb9d77763872051f0fb686bc176ac76cea640aad4d4c3c7e39c9c31d8943</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%2Feci.12449$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Feci.12449$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27929,27930,45579,45580</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25851448$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Merashli, Mira</creatorcontrib><creatorcontrib>Noureldine, Mohammad Hassan A.</creatorcontrib><creatorcontrib>Uthman, Imad</creatorcontrib><creatorcontrib>Khamashta, Munther</creatorcontrib><title>Antiphospholipid syndrome: an update</title><title>European journal of clinical investigation</title><addtitle>Eur J Clin Invest</addtitle><description>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.</description><subject>Adrenal Cortex Hormones - therapeutic use</subject><subject>Animals</subject><subject>Annexin A2 - antagonists & inhibitors</subject><subject>Anticoagulants - therapeutic use</subject><subject>Antiphospholipid antibodies</subject><subject>antiphospholipid syndrome</subject><subject>Antiphospholipid Syndrome - etiology</subject><subject>Antiphospholipid Syndrome - therapy</subject><subject>Drugs, Investigational</subject><subject>Female</subject><subject>Humans</subject><subject>Hydroxychloroquine - therapeutic use</subject><subject>Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use</subject><subject>Immunoglobulins, Intravenous - therapeutic use</subject><subject>Immunosuppressive Agents - therapeutic use</subject><subject>management</subject><subject>MAP Kinase Signaling System - physiology</subject><subject>Mice</subject><subject>pathogenesis</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Plasmapheresis</subject><subject>Pregnancy</subject><subject>Pregnancy Complications, Cardiovascular - etiology</subject><subject>Pregnancy Complications, Cardiovascular - prevention & control</subject><subject>Risk Assessment</subject><subject>risk stratification</subject><subject>Rituximab</subject><subject>Secondary Prevention</subject><subject>Thromboplastin - antagonists & inhibitors</subject><subject>Thrombosis - etiology</subject><subject>Thrombosis - prevention & control</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><issn>0014-2972</issn><issn>1365-2362</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kLtOwzAUQC0EoqUw8AOoAwMMaf2K7bBVVSmFFjoUMVqO7QhDXsSJoH9PIC0bV7q6y7lnOACcIzhC7YytdiOEKY0OQB8RFgaYMHwI-hAiGuCI4x448f4NQigQwcegh0MRIkpFH1xO8tqVr4VvN3WlM0O_zU1VZPZmqPJhUxpV21NwlKjU27PdHYDn29lmehcsn-aL6WQZaMpEFCBi4jiJI8M5Z0RwDEOUwCRmgsUacaY0Z9oqRqFShhqqieaWRDrSBBkRUTIAV523rIqPxvpaZs5rm6Yqt0XjJWICU0xCDlv0ukN1VXhf2USWlctUtZUIyp8oso0if6O07MVO28SZNX_kvkILjDvg06V2-79JzqaLvTLoPpyv7dffh6reJeOEh_LlcS7vV-v1-oFv5Ip8A6_5eTQ</recordid><startdate>201506</startdate><enddate>201506</enddate><creator>Merashli, Mira</creator><creator>Noureldine, Mohammad Hassan A.</creator><creator>Uthman, Imad</creator><creator>Khamashta, Munther</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</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>7X8</scope></search><sort><creationdate>201506</creationdate><title>Antiphospholipid syndrome: an update</title><author>Merashli, Mira ; Noureldine, Mohammad Hassan A. ; Uthman, Imad ; Khamashta, Munther</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4689-13dbbfb9d77763872051f0fb686bc176ac76cea640aad4d4c3c7e39c9c31d8943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adrenal Cortex Hormones - therapeutic use</topic><topic>Animals</topic><topic>Annexin A2 - antagonists & inhibitors</topic><topic>Anticoagulants - therapeutic use</topic><topic>Antiphospholipid antibodies</topic><topic>antiphospholipid syndrome</topic><topic>Antiphospholipid Syndrome - etiology</topic><topic>Antiphospholipid Syndrome - therapy</topic><topic>Drugs, Investigational</topic><topic>Female</topic><topic>Humans</topic><topic>Hydroxychloroquine - therapeutic use</topic><topic>Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use</topic><topic>Immunoglobulins, Intravenous - therapeutic use</topic><topic>Immunosuppressive Agents - therapeutic use</topic><topic>management</topic><topic>MAP Kinase Signaling System - physiology</topic><topic>Mice</topic><topic>pathogenesis</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Plasmapheresis</topic><topic>Pregnancy</topic><topic>Pregnancy Complications, Cardiovascular - etiology</topic><topic>Pregnancy Complications, Cardiovascular - prevention & control</topic><topic>Risk Assessment</topic><topic>risk stratification</topic><topic>Rituximab</topic><topic>Secondary Prevention</topic><topic>Thromboplastin - antagonists & inhibitors</topic><topic>Thrombosis - etiology</topic><topic>Thrombosis - prevention & control</topic><topic>TOR Serine-Threonine Kinases - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Merashli, Mira</creatorcontrib><creatorcontrib>Noureldine, Mohammad Hassan A.</creatorcontrib><creatorcontrib>Uthman, Imad</creatorcontrib><creatorcontrib>Khamashta, Munther</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of clinical investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Merashli, Mira</au><au>Noureldine, Mohammad Hassan A.</au><au>Uthman, Imad</au><au>Khamashta, Munther</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antiphospholipid syndrome: an update</atitle><jtitle>European journal of clinical investigation</jtitle><addtitle>Eur J Clin Invest</addtitle><date>2015-06</date><risdate>2015</risdate><volume>45</volume><issue>6</issue><spage>653</spage><epage>662</epage><pages>653-662</pages><issn>0014-2972</issn><eissn>1365-2362</eissn><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><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>25851448</pmid><doi>10.1111/eci.12449</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | Wiley Online Library - AutoHoldings Journals; MEDLINE |
| subjects | Adrenal Cortex Hormones - therapeutic use Animals Annexin A2 - antagonists & inhibitors Anticoagulants - therapeutic use Antiphospholipid antibodies antiphospholipid syndrome Antiphospholipid Syndrome - etiology Antiphospholipid Syndrome - therapy Drugs, Investigational Female Humans Hydroxychloroquine - therapeutic use Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use Immunoglobulins, Intravenous - therapeutic use Immunosuppressive Agents - therapeutic use management MAP Kinase Signaling System - physiology Mice pathogenesis Phosphatidylinositol 3-Kinases - metabolism Plasmapheresis Pregnancy Pregnancy Complications, Cardiovascular - etiology Pregnancy Complications, Cardiovascular - prevention & control Risk Assessment risk stratification Rituximab Secondary Prevention Thromboplastin - antagonists & inhibitors Thrombosis - etiology Thrombosis - prevention & control TOR Serine-Threonine Kinases - metabolism |
| title | Antiphospholipid syndrome: an update |
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