Markers of<i>In Vivo</i>Activation of Coagulation:<i>Interrelationships Change With Intensity of Oral Anticoagulation</i>

Solymoss, Susan; Bovill, Edwin G.

doi:10.1093/ajcp/105.3.293

Cited by 8 publications

(3 citation statements)

References 10 publications

(13 reference statements)

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“…The prothrombin activation fragment F 1+2 is an index of in vivo thrombin generation; one molecule of F1+2 is released with the generation of each thrombin molecule [11][12][13][14] . Anticoagulation suppresses the F1+2 level in a dose-response fashion [15][16][17] .It has been demonstrated that CU patients showed high blood coagulation state with F1+2 levels were higher than normal [18] . The mechanism may be: excessive activation of mast cells in patients with (CU).…”

Section: Discssionmentioning

confidence: 99%

Relation between Autoimmunity Chronic Urticaria and the Levels of Plasma Prothrombin F1+2

Liu¹,

Wanxiang²,

Khalaf³

et al. 2007

American J. of Applied Sciences

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A number of recent epidemiologic and experimental studies have enhanced our knowledge of the etiology and pathogenesis of chronic urticaria (CU), a disease that imposes profound impairment on patients quality of life. Our study was performed to explore the relation between autoimmunity (CU) and the levels of plasma prothrombin F1+2. Thirty four (CU) patients with positive autologous serum skin test (APST) their F1+2 were measured by ELISA at pre and post therapy. The levels of F1+2 in autoimmunity (CU) patients have been decreased obviously after treatment (3.34±2.87vs 0.94±0.58, p<0.001). Before treatment, the levels of treatment group was significantly higher than that of control group (3.34±2.87vs 0.72±0.36,p<0.001). After treatment, they have no significant difference (0.94±0.58vs 0.72±0.36, p>0.05)

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Section: Discssionmentioning

confidence: 99%

Relation between Autoimmunity Chronic Urticaria and the Levels of Plasma Prothrombin F1+2

Liu¹,

Wanxiang²,

Khalaf³

et al. 2007

American J. of Applied Sciences

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“…A second possibility is that capture antibodies are not very specific for F 1+2 and this is likely to become more evident at the lowest F 1+2 levels which accompanies the higher degrees of anticoagulation. Whatever the reason(s), these and other similar observations (18,19) indicate that the measurement of F 1+2 is not a suitable laboratory tool to monitor oral anticoagulants. Methods suitable to this goal must be responsive to anticoagulation both at low and high intensity of treatment.…”

Section: Discussionmentioning

confidence: 91%

Changes of Prothrombin Fragment 1+2 (F 1+2) as a Function of Increasing Intensity of Oral Anticoagulation

et al. 1998

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SummaryPlasma F 1+2 levels, the activation peptide originating from the factor Xa-mediated activation of prothrombin, increase in many clinical conditions associated with hypercoagulability and decrease in patients on oral anticoagulant treatment (OAT). However, the usefulness of F 1+2 measurement to monitor OAT has not yet been investigated in clinical studies. Before those studies are attempted, the plausibility of its implementation in the laboratory control of OAT should be evaluated. In this respect, a thorough investigation of the pattern of changes of F 1+2 as a function of increased intensity of anticoagulation expressed as International Normalized Ratio is essential. One hundred and thirty-two patients on long-term warfarin treatment were recruited to cover 8 ranges of anticoagulation from <1.5 to 9.0 INR. F 1+2 was measured in batch on frozen plasma and INR was determined on fresh plasma. The relationship of F 1+2 vs. INR showed a hyperbolic pattern with F 1+2 levels decreasing progressively and significantly as a function of increasing INR up to 3.0. A further decrease in F 1+2 levels observed at INR up to 4.0 was not statistically significant. At INR greater than 4.0, F 1+2 reached a plateau, with mean levels not significantly different for patients at increasing INR up to 9.0. Since the risk of bleeding increases at INR greater than 4.5, our results suggest that F 1+2 is of little value to assess the hemorrhagic risk in patients on OAT.

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“…36,37 An approach that suggests the use of biological markers as therapeutic indicators has already been proposed, with determination of F 1.2 levels to monitor anticoagulant treatment and response to therapy in patients with nonvalvular atrial fibrillation. 38,39 A substudy of an ongoing randomized trial 40 is also currently looking at the potential value of F 1.2 as a guide to the use of antithrombotic therapy, which may include either aspirin or warfarin in the prevention of stroke recurrence after a first noncardiogenic cerebral infarction.…”

Section: Côté Et Al Hemostasis and Cerebral Ischemia 1859mentioning

confidence: 99%

Hemostatic Markers in Patients at Risk of Cerebral Ischemia

Côté

Wolfson

Solymoss

et al. 2000

Stroke

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Background-Increased levels of markers of hemostasis may assist in the determination of the extent of carotid occlusive disease and the identification of neurologically intact individuals at increased risk of ischemic events. Methods-We conducted a prospective study of 304 subjects, including 82 with a recent (Յ7 days) transient ischemic attack (TIA), 157 asymptomatic individuals with a cervical bruit, and 65 control subjects. Baseline evaluation included a neurological assessment, ECG, cervical ultrasonography, and cerebral CT and/or MRI. Levels of markers of coagulation and fibrinolytic activity were also determined. Results were analyzed in relation to the degree of carotid disease and the subsequent occurrence of cerebral and cardiac ischemic events. Results-Over a mean follow-up period of 2.8 years (SD, 1.3 years), 114 ischemic events occurred. Survival analyses showed that prothrombin fragment 1.2 (F 1.2 ) was a predictor of time to cerebral and cardiac ischemic events in the combined TIA and asymptomatic bruit group (relative risk [RR], 1.46; 95% CI, 1.18 to 1.81) as well as in the asymptomatic bruit group separately (RR, 1.70; 95% CI, 1.14 to 2.53). In the TIA group, both F 1.2 (RR, 2.36; 95% CI, 1.19 to 4.68) and severe (Ն80%) carotid stenosis (RR, 3.53; 95% CI, 1.19 to 10.51) were predictive of time to ischemic stroke, myocardial infarction, or vascular death. Conclusions-In patients with TIAs and in asymptomatic individuals with cervical bruits, F 1.2 levels were found to be independent predictors of subsequent cerebral and cardiac ischemic events. Our results are consistent with an active role of the coagulation system through upregulation of thrombin in carotid disease progression and in the pathogenesis of

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Markers ofIn VivoActivation of Coagulation:Interrelationships Change With Intensity of Oral Anticoagulation

Cited by 8 publications

References 10 publications

Relation between Autoimmunity Chronic Urticaria and the Levels of Plasma Prothrombin F1+2

Relation between Autoimmunity Chronic Urticaria and the Levels of Plasma Prothrombin F1+2

Changes of Prothrombin Fragment 1+2 (F 1+2) as a Function of Increasing Intensity of Oral Anticoagulation

Hemostatic Markers in Patients at Risk of Cerebral Ischemia

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