Soluble P-selectin and vascular endothelial growth factor in steady state sickle cell disease: relationship to genotype
Abstract Sickle cell disease (SCD) is characterised by abnormal coagulopathy and angiogenesis although their relationships in two common genotypes, homozygous (HbSS) SCD and sickle-haemoglobin C disease (HbSC), are unexplored. We measured markers of platelet activation (soluble P-selectin [sP-select...
Ausführliche Beschreibung
Autor*in: |
Blann, A. D. [verfasserIn] Mohan, J. S. [verfasserIn] Bareford, D. [verfasserIn] Lip, G. Y. H. [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2007 |
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Schlagwörter: |
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Übergeordnetes Werk: |
Enthalten in: Journal of thrombosis and thrombolysis - Dordrecht [u.a.] : Springer Science + Business Media B.V, 1994, 25(2007), 2 vom: 14. Dez., Seite 185-189 |
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Übergeordnetes Werk: |
volume:25 ; year:2007 ; number:2 ; day:14 ; month:12 ; pages:185-189 |
Links: |
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DOI / URN: |
10.1007/s11239-007-0177-7 |
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Katalog-ID: |
SPR018009662 |
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520 | |a Abstract Sickle cell disease (SCD) is characterised by abnormal coagulopathy and angiogenesis although their relationships in two common genotypes, homozygous (HbSS) SCD and sickle-haemoglobin C disease (HbSC), are unexplored. We measured markers of platelet activation (soluble P-selectin [sP-selectin]), fibrinolysis (D-dimer) and angiogenesis (vascular endothelial growth factor [VEGF]) in 27 HbSS patients, 37 HbSC patients and in 42 age and race matched subjects with normal haemoglobin (AA). sP-selectin (P = 0.025) and D-dimers (P < 0.001) were higher in HbSS than in HbSC but there was no difference in VEGF. In HbSC, sPselectin correlated with VEGF (P = 0.012) and D-dimers (P = 0.021). There were no significant correlations in health or in HbSS. Platelet and coagulation activation, but not angiogenic activity, is elevated in HbSS disease compared to the clinically milder HbSC genotype. The correlation between sP-selectin and VEGF in SCD and HbSC disease is consistent with the view that VEGF is released from platelets during in vivo activation. | ||
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700 | 1 | |a Lip, G. Y. H. |e verfasserin |4 aut | |
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10.1007/s11239-007-0177-7 doi (DE-627)SPR018009662 (SPR)s11239-007-0177-7-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Blann, A. D. verfasserin aut Soluble P-selectin and vascular endothelial growth factor in steady state sickle cell disease: relationship to genotype 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Sickle cell disease (SCD) is characterised by abnormal coagulopathy and angiogenesis although their relationships in two common genotypes, homozygous (HbSS) SCD and sickle-haemoglobin C disease (HbSC), are unexplored. We measured markers of platelet activation (soluble P-selectin [sP-selectin]), fibrinolysis (D-dimer) and angiogenesis (vascular endothelial growth factor [VEGF]) in 27 HbSS patients, 37 HbSC patients and in 42 age and race matched subjects with normal haemoglobin (AA). sP-selectin (P = 0.025) and D-dimers (P < 0.001) were higher in HbSS than in HbSC but there was no difference in VEGF. In HbSC, sPselectin correlated with VEGF (P = 0.012) and D-dimers (P = 0.021). There were no significant correlations in health or in HbSS. Platelet and coagulation activation, but not angiogenic activity, is elevated in HbSS disease compared to the clinically milder HbSC genotype. The correlation between sP-selectin and VEGF in SCD and HbSC disease is consistent with the view that VEGF is released from platelets during in vivo activation. Soluble P-selectin (dpeaa)DE-He213 VEGF (dpeaa)DE-He213 D-dimers (dpeaa)DE-He213 Sickle cell disease (dpeaa)DE-He213 Mohan, J. S. verfasserin aut Bareford, D. verfasserin aut Lip, G. Y. H. verfasserin aut Enthalten in Journal of thrombosis and thrombolysis Dordrecht [u.a.] : Springer Science + Business Media B.V, 1994 25(2007), 2 vom: 14. Dez., Seite 185-189 (DE-627)320578445 (DE-600)2017305-2 1573-742X nnns volume:25 year:2007 number:2 day:14 month:12 pages:185-189 https://dx.doi.org/10.1007/s11239-007-0177-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.85 ASE AR 25 2007 2 14 12 185-189 |
spelling |
10.1007/s11239-007-0177-7 doi (DE-627)SPR018009662 (SPR)s11239-007-0177-7-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Blann, A. D. verfasserin aut Soluble P-selectin and vascular endothelial growth factor in steady state sickle cell disease: relationship to genotype 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Sickle cell disease (SCD) is characterised by abnormal coagulopathy and angiogenesis although their relationships in two common genotypes, homozygous (HbSS) SCD and sickle-haemoglobin C disease (HbSC), are unexplored. We measured markers of platelet activation (soluble P-selectin [sP-selectin]), fibrinolysis (D-dimer) and angiogenesis (vascular endothelial growth factor [VEGF]) in 27 HbSS patients, 37 HbSC patients and in 42 age and race matched subjects with normal haemoglobin (AA). sP-selectin (P = 0.025) and D-dimers (P < 0.001) were higher in HbSS than in HbSC but there was no difference in VEGF. In HbSC, sPselectin correlated with VEGF (P = 0.012) and D-dimers (P = 0.021). There were no significant correlations in health or in HbSS. Platelet and coagulation activation, but not angiogenic activity, is elevated in HbSS disease compared to the clinically milder HbSC genotype. The correlation between sP-selectin and VEGF in SCD and HbSC disease is consistent with the view that VEGF is released from platelets during in vivo activation. Soluble P-selectin (dpeaa)DE-He213 VEGF (dpeaa)DE-He213 D-dimers (dpeaa)DE-He213 Sickle cell disease (dpeaa)DE-He213 Mohan, J. S. verfasserin aut Bareford, D. verfasserin aut Lip, G. Y. H. verfasserin aut Enthalten in Journal of thrombosis and thrombolysis Dordrecht [u.a.] : Springer Science + Business Media B.V, 1994 25(2007), 2 vom: 14. Dez., Seite 185-189 (DE-627)320578445 (DE-600)2017305-2 1573-742X nnns volume:25 year:2007 number:2 day:14 month:12 pages:185-189 https://dx.doi.org/10.1007/s11239-007-0177-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.85 ASE AR 25 2007 2 14 12 185-189 |
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10.1007/s11239-007-0177-7 doi (DE-627)SPR018009662 (SPR)s11239-007-0177-7-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Blann, A. D. verfasserin aut Soluble P-selectin and vascular endothelial growth factor in steady state sickle cell disease: relationship to genotype 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Sickle cell disease (SCD) is characterised by abnormal coagulopathy and angiogenesis although their relationships in two common genotypes, homozygous (HbSS) SCD and sickle-haemoglobin C disease (HbSC), are unexplored. We measured markers of platelet activation (soluble P-selectin [sP-selectin]), fibrinolysis (D-dimer) and angiogenesis (vascular endothelial growth factor [VEGF]) in 27 HbSS patients, 37 HbSC patients and in 42 age and race matched subjects with normal haemoglobin (AA). sP-selectin (P = 0.025) and D-dimers (P < 0.001) were higher in HbSS than in HbSC but there was no difference in VEGF. In HbSC, sPselectin correlated with VEGF (P = 0.012) and D-dimers (P = 0.021). There were no significant correlations in health or in HbSS. Platelet and coagulation activation, but not angiogenic activity, is elevated in HbSS disease compared to the clinically milder HbSC genotype. The correlation between sP-selectin and VEGF in SCD and HbSC disease is consistent with the view that VEGF is released from platelets during in vivo activation. Soluble P-selectin (dpeaa)DE-He213 VEGF (dpeaa)DE-He213 D-dimers (dpeaa)DE-He213 Sickle cell disease (dpeaa)DE-He213 Mohan, J. S. verfasserin aut Bareford, D. verfasserin aut Lip, G. Y. H. verfasserin aut Enthalten in Journal of thrombosis and thrombolysis Dordrecht [u.a.] : Springer Science + Business Media B.V, 1994 25(2007), 2 vom: 14. Dez., Seite 185-189 (DE-627)320578445 (DE-600)2017305-2 1573-742X nnns volume:25 year:2007 number:2 day:14 month:12 pages:185-189 https://dx.doi.org/10.1007/s11239-007-0177-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.85 ASE AR 25 2007 2 14 12 185-189 |
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10.1007/s11239-007-0177-7 doi (DE-627)SPR018009662 (SPR)s11239-007-0177-7-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Blann, A. D. verfasserin aut Soluble P-selectin and vascular endothelial growth factor in steady state sickle cell disease: relationship to genotype 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Sickle cell disease (SCD) is characterised by abnormal coagulopathy and angiogenesis although their relationships in two common genotypes, homozygous (HbSS) SCD and sickle-haemoglobin C disease (HbSC), are unexplored. We measured markers of platelet activation (soluble P-selectin [sP-selectin]), fibrinolysis (D-dimer) and angiogenesis (vascular endothelial growth factor [VEGF]) in 27 HbSS patients, 37 HbSC patients and in 42 age and race matched subjects with normal haemoglobin (AA). sP-selectin (P = 0.025) and D-dimers (P < 0.001) were higher in HbSS than in HbSC but there was no difference in VEGF. In HbSC, sPselectin correlated with VEGF (P = 0.012) and D-dimers (P = 0.021). There were no significant correlations in health or in HbSS. Platelet and coagulation activation, but not angiogenic activity, is elevated in HbSS disease compared to the clinically milder HbSC genotype. The correlation between sP-selectin and VEGF in SCD and HbSC disease is consistent with the view that VEGF is released from platelets during in vivo activation. Soluble P-selectin (dpeaa)DE-He213 VEGF (dpeaa)DE-He213 D-dimers (dpeaa)DE-He213 Sickle cell disease (dpeaa)DE-He213 Mohan, J. S. verfasserin aut Bareford, D. verfasserin aut Lip, G. Y. H. verfasserin aut Enthalten in Journal of thrombosis and thrombolysis Dordrecht [u.a.] : Springer Science + Business Media B.V, 1994 25(2007), 2 vom: 14. Dez., Seite 185-189 (DE-627)320578445 (DE-600)2017305-2 1573-742X nnns volume:25 year:2007 number:2 day:14 month:12 pages:185-189 https://dx.doi.org/10.1007/s11239-007-0177-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.85 ASE AR 25 2007 2 14 12 185-189 |
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10.1007/s11239-007-0177-7 doi (DE-627)SPR018009662 (SPR)s11239-007-0177-7-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Blann, A. D. verfasserin aut Soluble P-selectin and vascular endothelial growth factor in steady state sickle cell disease: relationship to genotype 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Sickle cell disease (SCD) is characterised by abnormal coagulopathy and angiogenesis although their relationships in two common genotypes, homozygous (HbSS) SCD and sickle-haemoglobin C disease (HbSC), are unexplored. We measured markers of platelet activation (soluble P-selectin [sP-selectin]), fibrinolysis (D-dimer) and angiogenesis (vascular endothelial growth factor [VEGF]) in 27 HbSS patients, 37 HbSC patients and in 42 age and race matched subjects with normal haemoglobin (AA). sP-selectin (P = 0.025) and D-dimers (P < 0.001) were higher in HbSS than in HbSC but there was no difference in VEGF. In HbSC, sPselectin correlated with VEGF (P = 0.012) and D-dimers (P = 0.021). There were no significant correlations in health or in HbSS. Platelet and coagulation activation, but not angiogenic activity, is elevated in HbSS disease compared to the clinically milder HbSC genotype. The correlation between sP-selectin and VEGF in SCD and HbSC disease is consistent with the view that VEGF is released from platelets during in vivo activation. Soluble P-selectin (dpeaa)DE-He213 VEGF (dpeaa)DE-He213 D-dimers (dpeaa)DE-He213 Sickle cell disease (dpeaa)DE-He213 Mohan, J. S. verfasserin aut Bareford, D. verfasserin aut Lip, G. Y. H. verfasserin aut Enthalten in Journal of thrombosis and thrombolysis Dordrecht [u.a.] : Springer Science + Business Media B.V, 1994 25(2007), 2 vom: 14. Dez., Seite 185-189 (DE-627)320578445 (DE-600)2017305-2 1573-742X nnns volume:25 year:2007 number:2 day:14 month:12 pages:185-189 https://dx.doi.org/10.1007/s11239-007-0177-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.85 ASE AR 25 2007 2 14 12 185-189 |
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Enthalten in Journal of thrombosis and thrombolysis 25(2007), 2 vom: 14. Dez., Seite 185-189 volume:25 year:2007 number:2 day:14 month:12 pages:185-189 |
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Enthalten in Journal of thrombosis and thrombolysis 25(2007), 2 vom: 14. Dez., Seite 185-189 volume:25 year:2007 number:2 day:14 month:12 pages:185-189 |
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Blann, A. D. @@aut@@ Mohan, J. S. @@aut@@ Bareford, D. @@aut@@ Lip, G. Y. H. @@aut@@ |
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Blann, A. D. |
spellingShingle |
Blann, A. D. ddc 610 bkl 44.85 misc Soluble P-selectin misc VEGF misc D-dimers misc Sickle cell disease Soluble P-selectin and vascular endothelial growth factor in steady state sickle cell disease: relationship to genotype |
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610 ASE 44.85 bkl Soluble P-selectin and vascular endothelial growth factor in steady state sickle cell disease: relationship to genotype Soluble P-selectin (dpeaa)DE-He213 VEGF (dpeaa)DE-He213 D-dimers (dpeaa)DE-He213 Sickle cell disease (dpeaa)DE-He213 |
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ddc 610 bkl 44.85 misc Soluble P-selectin misc VEGF misc D-dimers misc Sickle cell disease |
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Soluble P-selectin and vascular endothelial growth factor in steady state sickle cell disease: relationship to genotype |
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Soluble P-selectin and vascular endothelial growth factor in steady state sickle cell disease: relationship to genotype |
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Blann, A. D. |
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Journal of thrombosis and thrombolysis |
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soluble p-selectin and vascular endothelial growth factor in steady state sickle cell disease: relationship to genotype |
title_auth |
Soluble P-selectin and vascular endothelial growth factor in steady state sickle cell disease: relationship to genotype |
abstract |
Abstract Sickle cell disease (SCD) is characterised by abnormal coagulopathy and angiogenesis although their relationships in two common genotypes, homozygous (HbSS) SCD and sickle-haemoglobin C disease (HbSC), are unexplored. We measured markers of platelet activation (soluble P-selectin [sP-selectin]), fibrinolysis (D-dimer) and angiogenesis (vascular endothelial growth factor [VEGF]) in 27 HbSS patients, 37 HbSC patients and in 42 age and race matched subjects with normal haemoglobin (AA). sP-selectin (P = 0.025) and D-dimers (P < 0.001) were higher in HbSS than in HbSC but there was no difference in VEGF. In HbSC, sPselectin correlated with VEGF (P = 0.012) and D-dimers (P = 0.021). There were no significant correlations in health or in HbSS. Platelet and coagulation activation, but not angiogenic activity, is elevated in HbSS disease compared to the clinically milder HbSC genotype. The correlation between sP-selectin and VEGF in SCD and HbSC disease is consistent with the view that VEGF is released from platelets during in vivo activation. |
abstractGer |
Abstract Sickle cell disease (SCD) is characterised by abnormal coagulopathy and angiogenesis although their relationships in two common genotypes, homozygous (HbSS) SCD and sickle-haemoglobin C disease (HbSC), are unexplored. We measured markers of platelet activation (soluble P-selectin [sP-selectin]), fibrinolysis (D-dimer) and angiogenesis (vascular endothelial growth factor [VEGF]) in 27 HbSS patients, 37 HbSC patients and in 42 age and race matched subjects with normal haemoglobin (AA). sP-selectin (P = 0.025) and D-dimers (P < 0.001) were higher in HbSS than in HbSC but there was no difference in VEGF. In HbSC, sPselectin correlated with VEGF (P = 0.012) and D-dimers (P = 0.021). There were no significant correlations in health or in HbSS. Platelet and coagulation activation, but not angiogenic activity, is elevated in HbSS disease compared to the clinically milder HbSC genotype. The correlation between sP-selectin and VEGF in SCD and HbSC disease is consistent with the view that VEGF is released from platelets during in vivo activation. |
abstract_unstemmed |
Abstract Sickle cell disease (SCD) is characterised by abnormal coagulopathy and angiogenesis although their relationships in two common genotypes, homozygous (HbSS) SCD and sickle-haemoglobin C disease (HbSC), are unexplored. We measured markers of platelet activation (soluble P-selectin [sP-selectin]), fibrinolysis (D-dimer) and angiogenesis (vascular endothelial growth factor [VEGF]) in 27 HbSS patients, 37 HbSC patients and in 42 age and race matched subjects with normal haemoglobin (AA). sP-selectin (P = 0.025) and D-dimers (P < 0.001) were higher in HbSS than in HbSC but there was no difference in VEGF. In HbSC, sPselectin correlated with VEGF (P = 0.012) and D-dimers (P = 0.021). There were no significant correlations in health or in HbSS. Platelet and coagulation activation, but not angiogenic activity, is elevated in HbSS disease compared to the clinically milder HbSC genotype. The correlation between sP-selectin and VEGF in SCD and HbSC disease is consistent with the view that VEGF is released from platelets during in vivo activation. |
collection_details |
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container_issue |
2 |
title_short |
Soluble P-selectin and vascular endothelial growth factor in steady state sickle cell disease: relationship to genotype |
url |
https://dx.doi.org/10.1007/s11239-007-0177-7 |
remote_bool |
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author2 |
Mohan, J. S. Bareford, D. Lip, G. Y. H. |
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Mohan, J. S. Bareford, D. Lip, G. Y. H. |
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doi_str |
10.1007/s11239-007-0177-7 |
up_date |
2024-07-03T16:40:36.868Z |
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score |
7.402935 |