40,912 research outputs found
Increased warfarin consumption and residual fibrin turnover in thrombotic patients with primary antiphospholipid syndrome.
No full textSymptomatic venous thromboembolism and thrombophilic status in adult acute leukemia: a single-center experience of 114 patients at diagnosis
No full textOccurrence of the JAK2 V617F mutation in the Budd–Chiari Syndrome
No full textMyeloproliferative diseases represent a major risk factor for Budd-Chiari syndrome. In 32 patients with Budd-Chiari syndrome, the JAK2 V617F mutation was detected, in heterozygous state, in 11 individuals (34.4%; 95% confidence interval: 18.6-53.2). Eight patients with (72.7%; 95% confidence interval: 39.0-94.0) and six without (28.6%; 95% confidence interval: 11.3-52.2) the JAK2 V617F mutation had a diagnosis of myeloproliferative diseases before or at the occurrence of the venous thrombotic event. In three patients carrying the JAK2 V617F mutation, a myeloproliferative disease was not detected. Determination of the JAK2 V617F mutation may be useful to recognize patients with Budd-Chiari syndrome with or at risk for the subsequent development of overt myeloproliferative diseases
Fibrinogen plasma levels in an apparently healthy general population. Relation to environmental and genetic determinants. Thromb Haemost 1998, 80:805-810
No full textA new JAK2 gene mutation in patients with polycythemia vera and splanchnic vein thrombosis.
No full textOutcome of patients with splanchnic venous thrombosis presenting without overt MPN: a role for the JAK2 V617F mutation re-evaluation.
No full textMeasurement of the branching fractions for B--> D(*)+pi(-)l(-)(nu)over-bar(l) and (B)over-bar(0)-> D-(*)0 pi(+)l(-)(nu)over-bar(l)
No full textWe report on a measurement of the branching fractions for B- --> D(*)+ pi(-)l(-)(nu) over bar (l) and (B) over bar (0) --> D-(*)0 pi(+)l(-)(nu) over bar (l) with 275 x 10(6) B (B) over bar events collected at the Y(4S) resonance with the Belle detector at KEKB. Events are tagged by fully reconstructing one of the B mesons in hadronic modes. We obtain B(B- --> D(+)pi(-)l(-)(nu) over bar (l)) = (0.54 +/- 0.07 (stat) +/- 0.07(syst) +/- 0.06(BR)) x 10(-2), B(B- --> D*+pi(-) l(-) (nu) over bar (l)) (0.67 +/- 0.11 (stat) +/- 0.09(syst) +/- 0.03(BR)) x 10(-2), B((B) over bar (0) --> D(0)pi(+)l(-) (nu) over bar (l)) = (0.33 +/- 0.06(stat) +/- 0.06(syst) +/- 0.03(BR)) x 10(-2), B((B) over bar (0) -->D(*0)pi(+)l(-)(nu) over bar (l)) = (0.65 +/- 0.12(stat) +/- 0.08(syst) +/- 0.05(BR)) x 10(-2), where the third error comes from the error on (B) over bar --> D((*))l(-)(nu) over bar (l) decays. Contributions from B-0 --> D(*+)l(-)(nu) over bar (l) decays are excluded in the measurement of (B) over bar (0) --> D(0)pi(+)l-(nu) over bar (l).Astronomy & AstrophysicsPhysics, Particles & FieldsSCI(E)0ARTICLE5null7
Gain-of-function gene mutations and venous thromboembolism: distinct roles in different clinical settings
No full textObjective To calculate the prevalence of common gain of function gene mutations in patients with different clinical manifestations of venous thromboembolism
Design Case-control study
Setting Two hospitals in Italy
Participants 387 patients with venous thromboembolism and 286 controls
Main measures factor V Leiden, factor II A20210, and JAK2 V617F mutations
Main results Among patients with deep vein thrombosis in one leg, 23 (20.9%) carried factor V Leiden and factor II A20210 mutations. Similar figures were observed in patients with cerebral vein thrombosis (n=9; 20.0%) and among patients presenting with splanchnic vein thrombosis (n=26; 18.7%). A lower prevalence was obtained in patients with retinal vein thrombosis (n=11; 11.8%). The JAK2 F617 mutant allele was found in 27 patients with splanchnic venous thrombosis (21.1%), and in none of the patients with a thrombotic event in different districts. Thirteen of the 27 JAK2 V617F-positive subjects with splanchnic venous thrombosis were previously known to have a myeloproliferative disease. Three other patients had a diagnosis of myeloproliferative disease after the occurrence of the thrombotic event
Conclusion Carriership of factor V Leiden or factor II A20210 mutations identifies an at-risk condition for venous thrombosis in the lower extremities, splanchnic or cerebral vein thrombosis. In patients with splanchnic venous thrombosis, screening for the JAK2 V617F mutation may be useful to recognize patients who should be carefully observed for the subsequent development of overt myeloproliferative disease. Thus, genetic tests may play a different role, various clinical manifestations of venous thromboembolism being associated with distinct risk profiles
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