Double heterozygosity polymorphisms for platelet glycoproteins Ia/IIa and IIb/IIIa increases arterial thrombosis and arteriosclerosis in patients with the antiphospholipid syndrome or with systemic lupus erythematosus
Objective:We analysed the genetic polymorphisms in platelet glycoproteins (GP) Ib-α, Ia/IIa and IIb/IIIa and their correlation with the development of arterial thrombosis and preclinical arteriosclerosis in patients with antiphospholipid syndrome (APS) or with systemic lupus erythematosus (SLE).Meth...
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| Veröffentlicht in: | Annals of the rheumatic diseases 2008-06, Vol.67 (6), p.835-840 |
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| container_title | Annals of the rheumatic diseases |
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| creator | Jiménez, S Tàssies, D Espinosa, G García-Criado, Á Plaza, J Monteagudo, J Cervera, R Reverter, J C |
| description | Objective:We analysed the genetic polymorphisms in platelet glycoproteins (GP) Ib-α, Ia/IIa and IIb/IIIa and their correlation with the development of arterial thrombosis and preclinical arteriosclerosis in patients with antiphospholipid syndrome (APS) or with systemic lupus erythematosus (SLE).Methods:We included 131 patients with APS (86 with primary APS and 45 with APS associated with SLE), 102 patients with SLE and 160 healthy controls. GP Ib-α VNTR polymorphism, GP Ia/IIa 807 C/T polymorphism and GP IIb/IIIa PlA1/2 polymorphism were determined by polymerase chain reaction. Thrombotic events were assessed clinically and confirmed by objective methods. The presence of preclinical arteriosclerosis was evaluated by a carotid ultrasound study in a subgroup of 70 patients with SLE measuring the intima-media wall thickness and the presence of arteriosclerotic plaque.Results:A total of 50 episodes of arterial thrombosis in 36 patients with APS have been registered. We found a significant correlation between the 807 T/T genotype of GP Ia/IIa and arterial thrombosis (22% vs 7%, p = 0.04; OR 3.59, 95% CI 1.20 to 10.79). The VNTR Ib-α and P1A1/2 IIb/IIIa polymorphisms were not associated with arterial thrombosis in patients with APS when individually analysed. The coexistence of both 807 T and PlA2 alleles increased the arterial thrombosis risk (28% vs 7%, p = 0.005; OR 4.84, 95% CI 1.67 to 13.96). In patients with SLE, no relationship was found between the presence of carotid arteriosclerotic plaque and separate polymorphisms of platelet GP. The coexistence of alleles 807 T of GP Ia/IIa and PlA2 of GP IIb/IIIa was associated with the presence of carotid plaque (35% vs 4%, p = 0.002; OR 12.92, 95% CI 2.39 to 69.81).Conclusions:The T/T genotype of 807 C/T polymorphism of GP Ia/IIa may be an additional risk for the development of arterial thrombosis in APS. The coexistence of both 807 T and PlA2 alleles increased the arterial thrombosis risk in patients with APS and preclinical arteriosclerosis in patients with SLE. |
| doi_str_mv | 10.1136/ard.2007.077321 |
| format | Article |
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GP Ib-α VNTR polymorphism, GP Ia/IIa 807 C/T polymorphism and GP IIb/IIIa PlA1/2 polymorphism were determined by polymerase chain reaction. Thrombotic events were assessed clinically and confirmed by objective methods. The presence of preclinical arteriosclerosis was evaluated by a carotid ultrasound study in a subgroup of 70 patients with SLE measuring the intima-media wall thickness and the presence of arteriosclerotic plaque.Results:A total of 50 episodes of arterial thrombosis in 36 patients with APS have been registered. We found a significant correlation between the 807 T/T genotype of GP Ia/IIa and arterial thrombosis (22% vs 7%, p = 0.04; OR 3.59, 95% CI 1.20 to 10.79). The VNTR Ib-α and P1A1/2 IIb/IIIa polymorphisms were not associated with arterial thrombosis in patients with APS when individually analysed. The coexistence of both 807 T and PlA2 alleles increased the arterial thrombosis risk (28% vs 7%, p = 0.005; OR 4.84, 95% CI 1.67 to 13.96). In patients with SLE, no relationship was found between the presence of carotid arteriosclerotic plaque and separate polymorphisms of platelet GP. The coexistence of alleles 807 T of GP Ia/IIa and PlA2 of GP IIb/IIIa was associated with the presence of carotid plaque (35% vs 4%, p = 0.002; OR 12.92, 95% CI 2.39 to 69.81).Conclusions:The T/T genotype of 807 C/T polymorphism of GP Ia/IIa may be an additional risk for the development of arterial thrombosis in APS. The coexistence of both 807 T and PlA2 alleles increased the arterial thrombosis risk in patients with APS and preclinical arteriosclerosis in patients with SLE.</description><identifier>ISSN: 0003-4967</identifier><identifier>EISSN: 1468-2060</identifier><identifier>DOI: 10.1136/ard.2007.077321</identifier><identifier>PMID: 17728329</identifier><identifier>CODEN: ARDIAO</identifier><language>eng</language><publisher>England: BMJ Publishing Group Ltd and European League Against Rheumatism</publisher><subject>Adult ; Analysis of Variance ; Antiphospholipid Syndrome - blood ; Antiphospholipid Syndrome - complications ; Antiphospholipid Syndrome - genetics ; Arteriosclerosis - blood ; Arteriosclerosis - complications ; Arteriosclerosis - genetics ; Atherosclerosis ; Autoimmune diseases ; Blood platelets ; Carotid Arteries - diagnostic imaging ; Case-Control Studies ; Chi-Square Distribution ; Disease ; Female ; Genetic Predisposition to Disease ; Hemophilia ; Heterozygote ; Humans ; Integrin alpha2 - genetics ; Lupus ; Lupus Erythematosus, Systemic - blood ; Lupus Erythematosus, Systemic - complications ; Lupus Erythematosus, Systemic - genetics ; Male ; Middle Aged ; Patients ; Platelet Glycoprotein GPIIb-IIIa Complex - genetics ; Platelet Membrane Glycoproteins - genetics ; Polymorphism, Genetic ; Risk Factors ; Studies ; Thrombosis ; Thrombosis - blood ; Thrombosis - complications ; Thrombosis - genetics ; Ultrasonography ; Womens health</subject><ispartof>Annals of the rheumatic diseases, 2008-06, Vol.67 (6), p.835-840</ispartof><rights>2008 BMJ Publishing Group and European League Against Rheumatism</rights><rights>Copyright: 2008 2008 BMJ Publishing Group and European League Against Rheumatism</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b396t-f9a8b9c21559388f8b9b225bdab99c363f6fdc4f251735e006c11644ab9e48163</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttp://ard.bmj.com/content/67/6/835.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttp://ard.bmj.com/content/67/6/835.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,314,780,784,3195,23570,27923,27924,77471,77502</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17728329$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiménez, S</creatorcontrib><creatorcontrib>Tàssies, D</creatorcontrib><creatorcontrib>Espinosa, G</creatorcontrib><creatorcontrib>García-Criado, Á</creatorcontrib><creatorcontrib>Plaza, J</creatorcontrib><creatorcontrib>Monteagudo, J</creatorcontrib><creatorcontrib>Cervera, R</creatorcontrib><creatorcontrib>Reverter, J C</creatorcontrib><title>Double heterozygosity polymorphisms for platelet glycoproteins Ia/IIa and IIb/IIIa increases arterial thrombosis and arteriosclerosis in patients with the antiphospholipid syndrome or with systemic lupus erythematosus</title><title>Annals of the rheumatic diseases</title><addtitle>Ann Rheum Dis</addtitle><description>Objective:We analysed the genetic polymorphisms in platelet glycoproteins (GP) Ib-α, Ia/IIa and IIb/IIIa and their correlation with the development of arterial thrombosis and preclinical arteriosclerosis in patients with antiphospholipid syndrome (APS) or with systemic lupus erythematosus (SLE).Methods:We included 131 patients with APS (86 with primary APS and 45 with APS associated with SLE), 102 patients with SLE and 160 healthy controls. GP Ib-α VNTR polymorphism, GP Ia/IIa 807 C/T polymorphism and GP IIb/IIIa PlA1/2 polymorphism were determined by polymerase chain reaction. Thrombotic events were assessed clinically and confirmed by objective methods. The presence of preclinical arteriosclerosis was evaluated by a carotid ultrasound study in a subgroup of 70 patients with SLE measuring the intima-media wall thickness and the presence of arteriosclerotic plaque.Results:A total of 50 episodes of arterial thrombosis in 36 patients with APS have been registered. We found a significant correlation between the 807 T/T genotype of GP Ia/IIa and arterial thrombosis (22% vs 7%, p = 0.04; OR 3.59, 95% CI 1.20 to 10.79). The VNTR Ib-α and P1A1/2 IIb/IIIa polymorphisms were not associated with arterial thrombosis in patients with APS when individually analysed. The coexistence of both 807 T and PlA2 alleles increased the arterial thrombosis risk (28% vs 7%, p = 0.005; OR 4.84, 95% CI 1.67 to 13.96). In patients with SLE, no relationship was found between the presence of carotid arteriosclerotic plaque and separate polymorphisms of platelet GP. The coexistence of alleles 807 T of GP Ia/IIa and PlA2 of GP IIb/IIIa was associated with the presence of carotid plaque (35% vs 4%, p = 0.002; OR 12.92, 95% CI 2.39 to 69.81).Conclusions:The T/T genotype of 807 C/T polymorphism of GP Ia/IIa may be an additional risk for the development of arterial thrombosis in APS. The coexistence of both 807 T and PlA2 alleles increased the arterial thrombosis risk in patients with APS and preclinical arteriosclerosis in patients with SLE.</description><subject>Adult</subject><subject>Analysis of Variance</subject><subject>Antiphospholipid Syndrome - blood</subject><subject>Antiphospholipid Syndrome - complications</subject><subject>Antiphospholipid Syndrome - genetics</subject><subject>Arteriosclerosis - blood</subject><subject>Arteriosclerosis - complications</subject><subject>Arteriosclerosis - genetics</subject><subject>Atherosclerosis</subject><subject>Autoimmune diseases</subject><subject>Blood platelets</subject><subject>Carotid Arteries - diagnostic imaging</subject><subject>Case-Control Studies</subject><subject>Chi-Square Distribution</subject><subject>Disease</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Hemophilia</subject><subject>Heterozygote</subject><subject>Humans</subject><subject>Integrin alpha2 - genetics</subject><subject>Lupus</subject><subject>Lupus Erythematosus, Systemic - blood</subject><subject>Lupus Erythematosus, Systemic - complications</subject><subject>Lupus Erythematosus, Systemic - genetics</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Patients</subject><subject>Platelet Glycoprotein GPIIb-IIIa Complex - genetics</subject><subject>Platelet Membrane Glycoproteins - genetics</subject><subject>Polymorphism, Genetic</subject><subject>Risk Factors</subject><subject>Studies</subject><subject>Thrombosis</subject><subject>Thrombosis - blood</subject><subject>Thrombosis - complications</subject><subject>Thrombosis - genetics</subject><subject>Ultrasonography</subject><subject>Womens health</subject><issn>0003-4967</issn><issn>1468-2060</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkd-L1DAQx4so3nr67JsEBB-E7iZNm7aPsrpn4VAQf4AvIW3Ta9a06WVStP6n_jfOXhcFX3wIyUw-851hvlH0lNEtY1zslG-3CaX5luY5T9i9aMNSUcQJFfR-tKGU8jgtRX4RPQI4YkgLVjyMLlieJwVPyk3067Wba6tJr4P27udy48CEhUzOLoPzU29gANI5TyargrY6kBu7NG7yLmgzAqnUrqoUUWNLqqrGNwZmbLxWoIEoj6pGWRJ674YateEOXfMOGotNT0kzkkkFo8cA5LsJPRZoJIOZegd4rJlMS2AZW9TRBOe5o2CBoAfTEDtPMxDtF6wbVHAww-PoQacs6Cfn-zL6dHjzcf82vn5_Ve1fXcc1L0WIu1IVddkkLMtKXhQdBnWSZHWr6rJsuOCd6Nom7ZKM5TzTlIqGMZGm-K3Tggl-Gb1YdXEnt7OGIAcDjbZWjdrNIEWZ0JLnJ_D5P-DRzX7E2ST6kReZoJwitVupBjcDXndy8mZQfpGMypPnEj2XJ8_l6jlWPDvrzvWg27_82WQE4hUwuK0ff_6V_yZFzvNMvvu8lwf24Sr5wr_KA_IvV74ejv_t_hvHu8rF</recordid><startdate>20080601</startdate><enddate>20080601</enddate><creator>Jiménez, S</creator><creator>Tàssies, D</creator><creator>Espinosa, G</creator><creator>García-Criado, Á</creator><creator>Plaza, J</creator><creator>Monteagudo, J</creator><creator>Cervera, R</creator><creator>Reverter, J C</creator><general>BMJ Publishing Group Ltd and European League Against Rheumatism</general><general>BMJ Publishing Group 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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>LK8</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20080601</creationdate><title>Double heterozygosity polymorphisms for platelet glycoproteins Ia/IIa and IIb/IIIa increases arterial thrombosis and arteriosclerosis in patients with the antiphospholipid syndrome or with systemic lupus erythematosus</title><author>Jiménez, S ; Tàssies, D ; Espinosa, G ; García-Criado, Á ; Plaza, J ; Monteagudo, J ; Cervera, R ; Reverter, J C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b396t-f9a8b9c21559388f8b9b225bdab99c363f6fdc4f251735e006c11644ab9e48163</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adult</topic><topic>Analysis of Variance</topic><topic>Antiphospholipid Syndrome - blood</topic><topic>Antiphospholipid Syndrome - complications</topic><topic>Antiphospholipid Syndrome - genetics</topic><topic>Arteriosclerosis - blood</topic><topic>Arteriosclerosis - complications</topic><topic>Arteriosclerosis - genetics</topic><topic>Atherosclerosis</topic><topic>Autoimmune diseases</topic><topic>Blood platelets</topic><topic>Carotid Arteries - diagnostic imaging</topic><topic>Case-Control Studies</topic><topic>Chi-Square Distribution</topic><topic>Disease</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>Hemophilia</topic><topic>Heterozygote</topic><topic>Humans</topic><topic>Integrin alpha2 - genetics</topic><topic>Lupus</topic><topic>Lupus Erythematosus, Systemic - blood</topic><topic>Lupus Erythematosus, Systemic - complications</topic><topic>Lupus Erythematosus, Systemic - genetics</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Patients</topic><topic>Platelet Glycoprotein GPIIb-IIIa Complex - genetics</topic><topic>Platelet Membrane Glycoproteins - genetics</topic><topic>Polymorphism, Genetic</topic><topic>Risk Factors</topic><topic>Studies</topic><topic>Thrombosis</topic><topic>Thrombosis - blood</topic><topic>Thrombosis - complications</topic><topic>Thrombosis - genetics</topic><topic>Ultrasonography</topic><topic>Womens health</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiménez, S</creatorcontrib><creatorcontrib>Tàssies, D</creatorcontrib><creatorcontrib>Espinosa, G</creatorcontrib><creatorcontrib>García-Criado, Á</creatorcontrib><creatorcontrib>Plaza, J</creatorcontrib><creatorcontrib>Monteagudo, J</creatorcontrib><creatorcontrib>Cervera, R</creatorcontrib><creatorcontrib>Reverter, J C</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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Annals of the rheumatic diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiménez, S</au><au>Tàssies, D</au><au>Espinosa, G</au><au>García-Criado, Á</au><au>Plaza, J</au><au>Monteagudo, J</au><au>Cervera, R</au><au>Reverter, J C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Double heterozygosity polymorphisms for platelet glycoproteins Ia/IIa and IIb/IIIa increases arterial thrombosis and arteriosclerosis in patients with the antiphospholipid syndrome or with systemic lupus erythematosus</atitle><jtitle>Annals of the rheumatic diseases</jtitle><addtitle>Ann Rheum Dis</addtitle><date>2008-06-01</date><risdate>2008</risdate><volume>67</volume><issue>6</issue><spage>835</spage><epage>840</epage><pages>835-840</pages><issn>0003-4967</issn><eissn>1468-2060</eissn><coden>ARDIAO</coden><abstract>Objective:We analysed the genetic polymorphisms in platelet glycoproteins (GP) Ib-α, Ia/IIa and IIb/IIIa and their correlation with the development of arterial thrombosis and preclinical arteriosclerosis in patients with antiphospholipid syndrome (APS) or with systemic lupus erythematosus (SLE).Methods:We included 131 patients with APS (86 with primary APS and 45 with APS associated with SLE), 102 patients with SLE and 160 healthy controls. GP Ib-α VNTR polymorphism, GP Ia/IIa 807 C/T polymorphism and GP IIb/IIIa PlA1/2 polymorphism were determined by polymerase chain reaction. Thrombotic events were assessed clinically and confirmed by objective methods. The presence of preclinical arteriosclerosis was evaluated by a carotid ultrasound study in a subgroup of 70 patients with SLE measuring the intima-media wall thickness and the presence of arteriosclerotic plaque.Results:A total of 50 episodes of arterial thrombosis in 36 patients with APS have been registered. We found a significant correlation between the 807 T/T genotype of GP Ia/IIa and arterial thrombosis (22% vs 7%, p = 0.04; OR 3.59, 95% CI 1.20 to 10.79). The VNTR Ib-α and P1A1/2 IIb/IIIa polymorphisms were not associated with arterial thrombosis in patients with APS when individually analysed. The coexistence of both 807 T and PlA2 alleles increased the arterial thrombosis risk (28% vs 7%, p = 0.005; OR 4.84, 95% CI 1.67 to 13.96). In patients with SLE, no relationship was found between the presence of carotid arteriosclerotic plaque and separate polymorphisms of platelet GP. The coexistence of alleles 807 T of GP Ia/IIa and PlA2 of GP IIb/IIIa was associated with the presence of carotid plaque (35% vs 4%, p = 0.002; OR 12.92, 95% CI 2.39 to 69.81).Conclusions:The T/T genotype of 807 C/T polymorphism of GP Ia/IIa may be an additional risk for the development of arterial thrombosis in APS. The coexistence of both 807 T and PlA2 alleles increased the arterial thrombosis risk in patients with APS and preclinical arteriosclerosis in patients with SLE.</abstract><cop>England</cop><pub>BMJ Publishing Group Ltd and European League Against Rheumatism</pub><pmid>17728329</pmid><doi>10.1136/ard.2007.077321</doi><tpages>6</tpages></addata></record> |
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| ispartof | Annals of the rheumatic diseases, 2008-06, Vol.67 (6), p.835-840 |
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| subjects | Adult Analysis of Variance Antiphospholipid Syndrome - blood Antiphospholipid Syndrome - complications Antiphospholipid Syndrome - genetics Arteriosclerosis - blood Arteriosclerosis - complications Arteriosclerosis - genetics Atherosclerosis Autoimmune diseases Blood platelets Carotid Arteries - diagnostic imaging Case-Control Studies Chi-Square Distribution Disease Female Genetic Predisposition to Disease Hemophilia Heterozygote Humans Integrin alpha2 - genetics Lupus Lupus Erythematosus, Systemic - blood Lupus Erythematosus, Systemic - complications Lupus Erythematosus, Systemic - genetics Male Middle Aged Patients Platelet Glycoprotein GPIIb-IIIa Complex - genetics Platelet Membrane Glycoproteins - genetics Polymorphism, Genetic Risk Factors Studies Thrombosis Thrombosis - blood Thrombosis - complications Thrombosis - genetics Ultrasonography Womens health |
| title | Double heterozygosity polymorphisms for platelet glycoproteins Ia/IIa and IIb/IIIa increases arterial thrombosis and arteriosclerosis in patients with the antiphospholipid syndrome or with systemic lupus erythematosus |
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