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Bob Siegerink - One of the best experts on this subject based on the ideXlab platform.
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Intrinsic Coagulation pathway history of headache and risk of ischemic stroke
Stroke, 2019Co-Authors: Hendrikus J A Van Os, Marieke J H Wermer, Frits R Rosendaal, Jose W P Goversriemslag, Ale Algra, Bob SiegerinkAbstract:Background and Purpose- Hypercoagulable states in migraine patients may play a role in the pathophysiology underlying the association between migraine and ischemic stroke. This study aims to provide more insight into the potential association of headache, ischemic stroke, and the Intrinsic Coagulation pathway. Methods- We included patients from the RATIO study (Risk of Arterial Thrombosis in Relation to Oral Contraceptives), a Dutch population-based case-control study including young women (age <50) with ischemic stroke and healthy controls. We defined a headache group based on a questionnaire on headache history. Intrinsic Coagulation proteins were measured through both antigen levels (FXII, FXI, prekallikrein, HK [high molecular weight kininogen]) and protein activation, determined by measuring activated protein complex with C1esterase-inhibitor (FXIIa-C1-INH, FXIa-C1-INH, Kallikrein-C1-INH) or antitrypsin-inhibitor (FXIa-AT-INH). We calculated adjusted odds ratios and performed an interaction analysis assessing the increase in stroke risk associated with high levels of Intrinsic Coagulation and history of headache. Results- We included 113 ischemic stroke cases and 598 healthy controls. In total, 134 (19%) patients had a history of headache, of whom 38 were cases and 96 controls. The combination of headache and high Intrinsic Coagulation protein levels (all but FXII antigen level and both FXIa-inhibitors) was associated with an increase in ischemic stroke risk higher than was expected based on their individual effects (adjusted odds ratio FXI antigen level alone: 1.7, 95% CI, 1.0-2.9; adjusted odds ratio headache alone: 2.0, 95% CI, 1.1-3.7; combination: 5.2, 95% CI, 2.3-11.6) Conclusions- Headache and high Intrinsic Coagulation protein levels may biologically interact, increasing risk for ischemic stroke.
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Intrinsic Coagulation Pathway, History of Headache, and Risk of Ischemic Stroke
Stroke, 2019Co-Authors: Hendrikus J A Van Os, Marieke J H Wermer, Frits R Rosendaal, Ale Algra, José W. P. Govers-riemslag, Bob SiegerinkAbstract:Background and Purpose- Hypercoagulable states in migraine patients may play a role in the pathophysiology underlying the association between migraine and ischemic stroke. This study aims to provide more insight into the potential association of headache, ischemic stroke, and the Intrinsic Coagulation pathway. Methods- We included patients from the RATIO study (Risk of Arterial Thrombosis in Relation to Oral Contraceptives), a Dutch population-based case-control study including young women (age
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Intrinsic Coagulation activation and the risk of arterial thrombosis in young women results from the risk of arterial thrombosis in relation to oral contraceptives ratio case control study
Circulation, 2010Co-Authors: Bob Siegerink, Frits R Rosendaal, Jose W P Goversriemslag, Ten H Cate, A. AlgraAbstract:Background—Classically, Intrinsic Coagulation proteins are thought to have a minor role in hemostasis. Recently, these proteins, especially FXII, were implicated as possible key players in the pathogenesis of arterial thrombosis. This study aims to determine the risks of arterial thrombosis conferred by increased activation of Intrinsic Coagulation proteins in young women and the effect of oral contraceptive use on this association. Methods and Results—The Risk of Arterial Thrombosis In relation to Oral contraceptives (RATIO) study is a population-based case-control study including young women (age 18 to 50 years) with myocardial infarction (n=205) and ischemic stroke (n=175) and 638 healthy controls. Intrinsic Coagulation protein activation was determined by measuring activated protein-inhibitor complexes. This complex is with C1 esterase inhibitor (FXIIa-C1-INH, FXIa-C1-INH, Kallikrein-C1-INH) or antitrypsin inhibitor (FXIa-AT-INH). Odds ratios (ORs) and corresponding confidence intervals (95% CIs) were...
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Intrinsic Coagulation Activation and the Risk of Arterial Thrombosis in Young Women Results From the Risk of Arterial Thrombosis in Relation to Oral Contraceptives (RATIO) Case-Control Study
Circulation, 2010Co-Authors: Bob Siegerink, Frits R Rosendaal, José W. P. Govers-riemslag, H. Ten Cate, A. AlgraAbstract:BACKGROUND: Classically Intrinsic Coagulation proteins are thought to have a minor role in hemostasis. Recently these proteins especially FXII were implicated as possible key players in the pathogenesis of arterial thrombosis. This study aims to determine the risks of arterial thrombosis conferred by increased activation of Intrinsic Coagulation proteins in young women and the effect of oral contraceptive use on this association. Methods and Results-The Risk of Arterial Thrombosis In relation to Oral contraceptives (RATIO) study is a population-based case-control study including young women (age 18 to 50 years) with myocardial infarction (n=205) and ischemic stroke (n=175) and 638 healthy controls. Intrinsic Coagulation protein activation was determined by measuring activated protein-inhibitor complexes. This complex is with C1 esterase inhibitor (FXIIa-C1-INH FXIa-C1-INH Kallikrein-C1-INH) or antitrypsin inhibitor (FXIa-AT-INH). Odds ratios (ORs) and corresponding confidence intervals (95% CIs) were calculated with logistic regression. High levels of protein activation (>90th percentile of controls) showed an increased risk of ischemic stroke: FXIIa-C1-INH (OR 2.1; 95% CI 1.3 to 3.5) FXIa-C1-INH (OR 2.8; 95% CI 1.6 to 4.7) FXIa-AT-INH (OR 2.3; 95% CI 1.4 to 4.0) and Kallikrein-C1 (OR 4.3; 95% CI 2.6 to 7.2). If anything myocardial infarction risk was only increased by Kallikrein-C1-INH (OR 1.5; 95% CI 0.9 to 2.5). Oral contraceptive use further increased the risks. Conclusions-High levels of activated proteins of the Intrinsic Coagulation system are associated with arterial thrombosis whereas the strength of these associations differs for myocardial infarction and ischemic stroke. This contradicts similar analyses among men in the Northwick Park Heart Study. Together with the finding that oral contraceptive use further increases the risks the question of whether the role of Intrinsic Coagulation proteins in the pathogenesis of arterial thrombosis is sex-specific is raised.
Anders Hamsten - One of the best experts on this subject based on the ideXlab platform.
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in vivo demonstration in humans that large postprandial triglyceride rich lipoproteins activate Coagulation factor vii through the Intrinsic Coagulation pathway
Arteriosclerosis Thrombosis and Vascular Biology, 1996Co-Authors: Angela Silveira, Fredrik Karpe, Hans Johnsson, Kenneth A. Bauer, Anders HamstenAbstract:In vitro studies in purified plasma systems have suggested that triglyceride-rich lipoproteins such as chylomicrons, very low density lipoproteins, and their remnants promote activation of factor VII through activated factor XII (XIIa) and the Intrinsic Coagulation pathway. We specifically examined the roles of factors XII, XI, and IX in activation of factor VII during alimentary lipemia in vivo in humans and addressed the issue of whether generation of activated factor VII (VIIa) is accompanied by increased thrombin production. For this purpose XIIa, factor IX activation peptide (IXP), VIIa, prothrombin fragment 1+2 (F1+2), and thrombin-antithrombin complex (TAT) were determined in plasma samples taken before and 3, 6, and 9 hours after intake of a mixed meal type of oral fat load in 24 healthy men. The VIIa response to fat intake was also determined in 7 patients with single Coagulation–factor deficiency, of whom 2 were deficient in factor XII, 2 in factor XI, and 3 in factor IX. Postprandial activation of factors IX and VII occurred in the healthy individuals, whereas the plasma levels of XIIa did not change in response to the test meal. Of note, plasma concentrations of F1+2 were unaltered during alimentary lipemia, and TAT levels showed a small decrease ( P <.05) in the 3-hour sample compared with the fasting level, indicating that thrombin generation is not stimulated in the postprandial state, despite the generation of activated factor IX (IXa) and VIIa. Factor VIIa increased in the postprandial period in the 2 factor XII–deficient patients who underwent the oral fat tolerance test but appeared to remain unchanged in the factor XI– and factor IX–deficient patients. Therefore, the current concept that activation of factor XII plays a pivotal role in initiating the sequence of events linking postprandial lipemia to activation of factor VII is contradicted by the present study. Whether activation of factor XI by triglyceride-rich lipoproteins initiates these reactions needs to be demonstrated in future studies.
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In Vivo Demonstration in Humans That Large Postprandial Triglyceride-Rich Lipoproteins Activate Coagulation Factor VII Through the Intrinsic Coagulation Pathway
Arteriosclerosis thrombosis and vascular biology, 1996Co-Authors: Angela Silveira, Fredrik Karpe, Hans Johnsson, Kenneth A. Bauer, Anders HamstenAbstract:In vitro studies in purified plasma systems have suggested that triglyceride-rich lipoproteins such as chylomicrons, very low density lipoproteins, and their remnants promote activation of factor VII through activated factor XII (XIIa) and the Intrinsic Coagulation pathway. We specifically examined the roles of factors XII, XI, and IX in activation of factor VII during alimentary lipemia in vivo in humans and addressed the issue of whether generation of activated factor VII (VIIa) is accompanied by increased thrombin production. For this purpose XIIa, factor IX activation peptide (IXP), VIIa, prothrombin fragment 1+2 (F1+2), and thrombin-antithrombin complex (TAT) were determined in plasma samples taken before and 3, 6, and 9 hours after intake of a mixed meal type of oral fat load in 24 healthy men. The VIIa response to fat intake was also determined in 7 patients with single Coagulation–factor deficiency, of whom 2 were deficient in factor XII, 2 in factor XI, and 3 in factor IX. Postprandial activation of factors IX and VII occurred in the healthy individuals, whereas the plasma levels of XIIa did not change in response to the test meal. Of note, plasma concentrations of F1+2 were unaltered during alimentary lipemia, and TAT levels showed a small decrease ( P
Frits R Rosendaal - One of the best experts on this subject based on the ideXlab platform.
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Intrinsic Coagulation pathway history of headache and risk of ischemic stroke
Stroke, 2019Co-Authors: Hendrikus J A Van Os, Marieke J H Wermer, Frits R Rosendaal, Jose W P Goversriemslag, Ale Algra, Bob SiegerinkAbstract:Background and Purpose- Hypercoagulable states in migraine patients may play a role in the pathophysiology underlying the association between migraine and ischemic stroke. This study aims to provide more insight into the potential association of headache, ischemic stroke, and the Intrinsic Coagulation pathway. Methods- We included patients from the RATIO study (Risk of Arterial Thrombosis in Relation to Oral Contraceptives), a Dutch population-based case-control study including young women (age <50) with ischemic stroke and healthy controls. We defined a headache group based on a questionnaire on headache history. Intrinsic Coagulation proteins were measured through both antigen levels (FXII, FXI, prekallikrein, HK [high molecular weight kininogen]) and protein activation, determined by measuring activated protein complex with C1esterase-inhibitor (FXIIa-C1-INH, FXIa-C1-INH, Kallikrein-C1-INH) or antitrypsin-inhibitor (FXIa-AT-INH). We calculated adjusted odds ratios and performed an interaction analysis assessing the increase in stroke risk associated with high levels of Intrinsic Coagulation and history of headache. Results- We included 113 ischemic stroke cases and 598 healthy controls. In total, 134 (19%) patients had a history of headache, of whom 38 were cases and 96 controls. The combination of headache and high Intrinsic Coagulation protein levels (all but FXII antigen level and both FXIa-inhibitors) was associated with an increase in ischemic stroke risk higher than was expected based on their individual effects (adjusted odds ratio FXI antigen level alone: 1.7, 95% CI, 1.0-2.9; adjusted odds ratio headache alone: 2.0, 95% CI, 1.1-3.7; combination: 5.2, 95% CI, 2.3-11.6) Conclusions- Headache and high Intrinsic Coagulation protein levels may biologically interact, increasing risk for ischemic stroke.
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Intrinsic Coagulation Pathway, History of Headache, and Risk of Ischemic Stroke
Stroke, 2019Co-Authors: Hendrikus J A Van Os, Marieke J H Wermer, Frits R Rosendaal, Ale Algra, José W. P. Govers-riemslag, Bob SiegerinkAbstract:Background and Purpose- Hypercoagulable states in migraine patients may play a role in the pathophysiology underlying the association between migraine and ischemic stroke. This study aims to provide more insight into the potential association of headache, ischemic stroke, and the Intrinsic Coagulation pathway. Methods- We included patients from the RATIO study (Risk of Arterial Thrombosis in Relation to Oral Contraceptives), a Dutch population-based case-control study including young women (age
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Intrinsic Coagulation activation and the risk of arterial thrombosis in young women results from the risk of arterial thrombosis in relation to oral contraceptives ratio case control study
Circulation, 2010Co-Authors: Bob Siegerink, Frits R Rosendaal, Jose W P Goversriemslag, Ten H Cate, A. AlgraAbstract:Background—Classically, Intrinsic Coagulation proteins are thought to have a minor role in hemostasis. Recently, these proteins, especially FXII, were implicated as possible key players in the pathogenesis of arterial thrombosis. This study aims to determine the risks of arterial thrombosis conferred by increased activation of Intrinsic Coagulation proteins in young women and the effect of oral contraceptive use on this association. Methods and Results—The Risk of Arterial Thrombosis In relation to Oral contraceptives (RATIO) study is a population-based case-control study including young women (age 18 to 50 years) with myocardial infarction (n=205) and ischemic stroke (n=175) and 638 healthy controls. Intrinsic Coagulation protein activation was determined by measuring activated protein-inhibitor complexes. This complex is with C1 esterase inhibitor (FXIIa-C1-INH, FXIa-C1-INH, Kallikrein-C1-INH) or antitrypsin inhibitor (FXIa-AT-INH). Odds ratios (ORs) and corresponding confidence intervals (95% CIs) were...
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Intrinsic Coagulation Activation and the Risk of Arterial Thrombosis in Young Women Results From the Risk of Arterial Thrombosis in Relation to Oral Contraceptives (RATIO) Case-Control Study
Circulation, 2010Co-Authors: Bob Siegerink, Frits R Rosendaal, José W. P. Govers-riemslag, H. Ten Cate, A. AlgraAbstract:BACKGROUND: Classically Intrinsic Coagulation proteins are thought to have a minor role in hemostasis. Recently these proteins especially FXII were implicated as possible key players in the pathogenesis of arterial thrombosis. This study aims to determine the risks of arterial thrombosis conferred by increased activation of Intrinsic Coagulation proteins in young women and the effect of oral contraceptive use on this association. Methods and Results-The Risk of Arterial Thrombosis In relation to Oral contraceptives (RATIO) study is a population-based case-control study including young women (age 18 to 50 years) with myocardial infarction (n=205) and ischemic stroke (n=175) and 638 healthy controls. Intrinsic Coagulation protein activation was determined by measuring activated protein-inhibitor complexes. This complex is with C1 esterase inhibitor (FXIIa-C1-INH FXIa-C1-INH Kallikrein-C1-INH) or antitrypsin inhibitor (FXIa-AT-INH). Odds ratios (ORs) and corresponding confidence intervals (95% CIs) were calculated with logistic regression. High levels of protein activation (>90th percentile of controls) showed an increased risk of ischemic stroke: FXIIa-C1-INH (OR 2.1; 95% CI 1.3 to 3.5) FXIa-C1-INH (OR 2.8; 95% CI 1.6 to 4.7) FXIa-AT-INH (OR 2.3; 95% CI 1.4 to 4.0) and Kallikrein-C1 (OR 4.3; 95% CI 2.6 to 7.2). If anything myocardial infarction risk was only increased by Kallikrein-C1-INH (OR 1.5; 95% CI 0.9 to 2.5). Oral contraceptive use further increased the risks. Conclusions-High levels of activated proteins of the Intrinsic Coagulation system are associated with arterial thrombosis whereas the strength of these associations differs for myocardial infarction and ischemic stroke. This contradicts similar analyses among men in the Northwick Park Heart Study. Together with the finding that oral contraceptive use further increases the risks the question of whether the role of Intrinsic Coagulation proteins in the pathogenesis of arterial thrombosis is sex-specific is raised.
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Levels of Intrinsic Coagulation factors and the risk of myocardial infarction among men: Opposite and synergistic effects of factors XI and XII.
Blood, 2006Co-Authors: Catharina Jacoba Maria Doggen, Frits R Rosendaal, Joost C M MeijersAbstract:The role of the Intrinsic Coagulation system on the risk of myocardial infarction is unclear. In the Study of Myocardial Infarctions Leiden (SMILE) that included 560 men younger than age 70 with a first myocardial infarction and 646 control subjects, we investigated the risk of myocardial infarction for levels of factor XI (factor XIc) and factor XII (factor XIIc). Furthermore, the risks for factor VIII activity (factor VIIIc) and factor IX activity (factor IXc) were assessed. Factor XIc was 113.0% in patients compared with 109.8% in control subjects (difference, 3.2%; 95% CI, 1.1%-5.4%). The risk of myocardial infarction adjusted for age for men in the highest quintile compared with those in the lowest quintile was 1.8-fold increased (ORadj, 1.8; 95% CI, 1.2-2.7). In contrast, factor XIIc among patients with myocardial infarction was lower than in control subjects, respectively, 93.0% and 98.6% (difference, 5.6%; 95% CI, 3.3%-7.9%). The odds ratio of myocardial infarction for men in the highest quintile versus those in the lowest quintile was 0.4 (ORadj, 0.4; 95% CI, 0.2-0.5). The highest risk was found among men with both high factor XIc and low factor XIIc (analyses in tertiles: ORadj, 6.4; 95% CI, 2.2-18.0). Factor VIIIc increased the risk of myocardial infarction although not dose dependently. Factor IXc increased the risk; odds ratio of myocardial infarction for men in the highest quintile versus those in the lowest quintile was 3.2 (ORadj, 3.2; 95% CI, 2.0-5.1). Thus, factors XIc and XIIc have opposite and synergistic effects on the risk of myocardial infarction in men; factor VIIIc and factor IXc increase the risk.
A. Algra - One of the best experts on this subject based on the ideXlab platform.
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Intrinsic Coagulation activation and the risk of arterial thrombosis in young women results from the risk of arterial thrombosis in relation to oral contraceptives ratio case control study
Circulation, 2010Co-Authors: Bob Siegerink, Frits R Rosendaal, Jose W P Goversriemslag, Ten H Cate, A. AlgraAbstract:Background—Classically, Intrinsic Coagulation proteins are thought to have a minor role in hemostasis. Recently, these proteins, especially FXII, were implicated as possible key players in the pathogenesis of arterial thrombosis. This study aims to determine the risks of arterial thrombosis conferred by increased activation of Intrinsic Coagulation proteins in young women and the effect of oral contraceptive use on this association. Methods and Results—The Risk of Arterial Thrombosis In relation to Oral contraceptives (RATIO) study is a population-based case-control study including young women (age 18 to 50 years) with myocardial infarction (n=205) and ischemic stroke (n=175) and 638 healthy controls. Intrinsic Coagulation protein activation was determined by measuring activated protein-inhibitor complexes. This complex is with C1 esterase inhibitor (FXIIa-C1-INH, FXIa-C1-INH, Kallikrein-C1-INH) or antitrypsin inhibitor (FXIa-AT-INH). Odds ratios (ORs) and corresponding confidence intervals (95% CIs) were...
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Intrinsic Coagulation Activation and the Risk of Arterial Thrombosis in Young Women Results From the Risk of Arterial Thrombosis in Relation to Oral Contraceptives (RATIO) Case-Control Study
Circulation, 2010Co-Authors: Bob Siegerink, Frits R Rosendaal, José W. P. Govers-riemslag, H. Ten Cate, A. AlgraAbstract:BACKGROUND: Classically Intrinsic Coagulation proteins are thought to have a minor role in hemostasis. Recently these proteins especially FXII were implicated as possible key players in the pathogenesis of arterial thrombosis. This study aims to determine the risks of arterial thrombosis conferred by increased activation of Intrinsic Coagulation proteins in young women and the effect of oral contraceptive use on this association. Methods and Results-The Risk of Arterial Thrombosis In relation to Oral contraceptives (RATIO) study is a population-based case-control study including young women (age 18 to 50 years) with myocardial infarction (n=205) and ischemic stroke (n=175) and 638 healthy controls. Intrinsic Coagulation protein activation was determined by measuring activated protein-inhibitor complexes. This complex is with C1 esterase inhibitor (FXIIa-C1-INH FXIa-C1-INH Kallikrein-C1-INH) or antitrypsin inhibitor (FXIa-AT-INH). Odds ratios (ORs) and corresponding confidence intervals (95% CIs) were calculated with logistic regression. High levels of protein activation (>90th percentile of controls) showed an increased risk of ischemic stroke: FXIIa-C1-INH (OR 2.1; 95% CI 1.3 to 3.5) FXIa-C1-INH (OR 2.8; 95% CI 1.6 to 4.7) FXIa-AT-INH (OR 2.3; 95% CI 1.4 to 4.0) and Kallikrein-C1 (OR 4.3; 95% CI 2.6 to 7.2). If anything myocardial infarction risk was only increased by Kallikrein-C1-INH (OR 1.5; 95% CI 0.9 to 2.5). Oral contraceptive use further increased the risks. Conclusions-High levels of activated proteins of the Intrinsic Coagulation system are associated with arterial thrombosis whereas the strength of these associations differs for myocardial infarction and ischemic stroke. This contradicts similar analyses among men in the Northwick Park Heart Study. Together with the finding that oral contraceptive use further increases the risks the question of whether the role of Intrinsic Coagulation proteins in the pathogenesis of arterial thrombosis is sex-specific is raised.
Angela Silveira - One of the best experts on this subject based on the ideXlab platform.
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in vivo demonstration in humans that large postprandial triglyceride rich lipoproteins activate Coagulation factor vii through the Intrinsic Coagulation pathway
Arteriosclerosis Thrombosis and Vascular Biology, 1996Co-Authors: Angela Silveira, Fredrik Karpe, Hans Johnsson, Kenneth A. Bauer, Anders HamstenAbstract:In vitro studies in purified plasma systems have suggested that triglyceride-rich lipoproteins such as chylomicrons, very low density lipoproteins, and their remnants promote activation of factor VII through activated factor XII (XIIa) and the Intrinsic Coagulation pathway. We specifically examined the roles of factors XII, XI, and IX in activation of factor VII during alimentary lipemia in vivo in humans and addressed the issue of whether generation of activated factor VII (VIIa) is accompanied by increased thrombin production. For this purpose XIIa, factor IX activation peptide (IXP), VIIa, prothrombin fragment 1+2 (F1+2), and thrombin-antithrombin complex (TAT) were determined in plasma samples taken before and 3, 6, and 9 hours after intake of a mixed meal type of oral fat load in 24 healthy men. The VIIa response to fat intake was also determined in 7 patients with single Coagulation–factor deficiency, of whom 2 were deficient in factor XII, 2 in factor XI, and 3 in factor IX. Postprandial activation of factors IX and VII occurred in the healthy individuals, whereas the plasma levels of XIIa did not change in response to the test meal. Of note, plasma concentrations of F1+2 were unaltered during alimentary lipemia, and TAT levels showed a small decrease ( P <.05) in the 3-hour sample compared with the fasting level, indicating that thrombin generation is not stimulated in the postprandial state, despite the generation of activated factor IX (IXa) and VIIa. Factor VIIa increased in the postprandial period in the 2 factor XII–deficient patients who underwent the oral fat tolerance test but appeared to remain unchanged in the factor XI– and factor IX–deficient patients. Therefore, the current concept that activation of factor XII plays a pivotal role in initiating the sequence of events linking postprandial lipemia to activation of factor VII is contradicted by the present study. Whether activation of factor XI by triglyceride-rich lipoproteins initiates these reactions needs to be demonstrated in future studies.
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In Vivo Demonstration in Humans That Large Postprandial Triglyceride-Rich Lipoproteins Activate Coagulation Factor VII Through the Intrinsic Coagulation Pathway
Arteriosclerosis thrombosis and vascular biology, 1996Co-Authors: Angela Silveira, Fredrik Karpe, Hans Johnsson, Kenneth A. Bauer, Anders HamstenAbstract:In vitro studies in purified plasma systems have suggested that triglyceride-rich lipoproteins such as chylomicrons, very low density lipoproteins, and their remnants promote activation of factor VII through activated factor XII (XIIa) and the Intrinsic Coagulation pathway. We specifically examined the roles of factors XII, XI, and IX in activation of factor VII during alimentary lipemia in vivo in humans and addressed the issue of whether generation of activated factor VII (VIIa) is accompanied by increased thrombin production. For this purpose XIIa, factor IX activation peptide (IXP), VIIa, prothrombin fragment 1+2 (F1+2), and thrombin-antithrombin complex (TAT) were determined in plasma samples taken before and 3, 6, and 9 hours after intake of a mixed meal type of oral fat load in 24 healthy men. The VIIa response to fat intake was also determined in 7 patients with single Coagulation–factor deficiency, of whom 2 were deficient in factor XII, 2 in factor XI, and 3 in factor IX. Postprandial activation of factors IX and VII occurred in the healthy individuals, whereas the plasma levels of XIIa did not change in response to the test meal. Of note, plasma concentrations of F1+2 were unaltered during alimentary lipemia, and TAT levels showed a small decrease ( P
