scholarly journals Elevation of Blood Plasminogen Activator Inhibitor Level in Patients With Cerebral Venous Thrombosis

2018 ◽  
Vol 8 (1-2) ◽  
pp. 4-9
Author(s):  
Suzan Bindal ◽  
Ozlem Coskun ◽  
Bulent Alioglu ◽  
Levent E. Inan ◽  
Burc Esra Sahin ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Plasminogen Activator ◽  
Cerebral Venous Thrombosis ◽  
Plasminogen Activator Inhibitor ◽  
Inhibitor Level ◽  
Activator Inhibitor

scholarly journals Specific Polymorphism 4G/5G Gene for PAI-1 as a Possible Cause of Cerebral Venous Thrombosis: A Case Report

2017 ◽  
Vol 18 (2) ◽  
pp. 169-173
Author(s):  
Tatjana Boskovic Matic ◽  
Aleksandar Gavrilovic ◽  
Snezana Simovic ◽  
Dejan Aleksic ◽  
Katarina Vesic ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Plasminogen Activator ◽  
Cerebral Venous Thrombosis ◽  
Sinus Thrombosis ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activator Inhibitor 1 ◽  
Sagittal Sinus ◽  
Clinical Center ◽  
The Impact ◽  
Activator Inhibitor

AbstractThrombosis of veins and venous sinus (CVT) is the rare cerebral vascular disorder which makes less than 1% of all strokes. Thrombosis of veins and venous sinuses is picturesquely called “мајоr neurological forger” since it is characterized by very varied clinical picture. Among the various causes of CVT, which can be of infective or non-infective nature, the congenital hyper coagulations especially stand out, diagnosis is based on highly sophisticated diagnostic tests.We present the case of a female patient, 36 years old, who was hospitalized at the Clinic for Neurology in Clinical Center because of the diffuse headache she had for the last few days, with milder right-sided hemiparesis and one generalized tonic-clonic epileptic seizure. With nuclear magnetic resonance (MR/2D venography) the thrombosis of the upper and lower sagittal sinuses is confirmed. By appropriate laboratory tests, as well as by confirmatory immunological and genetic analyses, the impact of the most of the factors is excluded which can contribute to the occurrence of venous thrombosis. The only pathological findings which indicated the possible congenital thrombophilia as the cause of the sagittal sinus thrombosis was the determination of the specific polymorphism of the 4G/5G gene for plasminogen activator inhibitor 1.According to our knowledge, this is the first decribed case of the possible impact of the specific polymorphism of the 4G/5G gene for plasminogen activator inhibitor of 1 on the development of cerebral venous thrombosis.

REDUCED TISSUE PLASMINOGEN ACTIVATOR RELEASE AND NORMAL PLASMINOGEN ACTIVATOR INHIBITOR LEVEL IN A FAMILY WITH RECURRENT VENOUS THROMBOSES

1987 ◽  
Author(s):  
J Petäjä ◽  
G Myllylä ◽  
V Rasi ◽  
E Vahtera
Keyword(s):  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Protein S ◽  
Venous Occlusion ◽  
C Protein ◽  
Tissue Plasminogen ◽  
Inhibitor Level ◽  
Fast Acting ◽  
Activator Inhibitor

We have studied the fibrinolytic system in one asymptomatic and six symptomatic members of a family with recurrent DVTs in three generations. Tissue plasminogen activator activity (TPA) and fast acting inhibitor of TPA (PAI) were determined using chromogenic substrate and TPA antigen with ELISA. Measurements were made at rest and after 10 and 20 minutes of venous occlusion (VO). 17 healthy subjects served as controls. The mean TPA in the seven family members was significantly lower than in controls at 10 and 20 min VO (p< 0.01).TPA was below the lowest value of controls (<1.7 U/ml) in five of the six patients with DVT at 10 min VO and remained below the range of controls in three at 20 min VO (<3.3 U/ml). The lowered TPA activity was associated with impaired release of TPA antigen (mean level at 10 min VO 12.A ng/ml, controls 19.5 ng/ml, p<0.05; at 20 min VO 18.2 ng/ml, controls 43.2 ng/ml, p<0.01). Four .patients with and one without DVT had TPA antigen below the lowest level of controls at 10 and/or 20 min VO. The level of'PAI at rest was normal in all cases (from 0.6 to 1.7 U/ml, controls from 0 to 3.7 U/ml). In accordance with low release of TPA antigen PAI was consumed less during VO in patients than in controls (mean level at 20 min VO 0.9 U/ml, controls 0.4 U/ml, p<0.05). The levels of antithrombin III, protein C, protein S, plasminogen, fibrinogen, F V, F VIII:C, vWf:Ag, fibrinopeptide A and beta-thromboglobulin were normal . Circulating anticoagulant was not found. It is concluded that impaired release of TPA, independent of PAI, is associated with DVT in this family. The pattern of inheritance suggested autosomal dominant trait.

Association between the plasminogen activator inhibitor-1 4G/5G polymorphism and venous thrombosis

2007 ◽  
Vol 97 (06) ◽  
pp. 907-913 ◽  
Author(s):  
Argirios Tsantes ◽  
Pantelis Bagos ◽  
Evdoxia Rapti ◽  
Georgios Mantzios ◽  
Violeta Kapsimali ◽  
...  
Keyword(s):  
Risk Factor ◽  
Venous Thrombosis ◽  
Plasminogen Activator ◽  
Genetic Risk ◽  
Plasminogen Activator Inhibitor ◽  
Genetic Risk Factor ◽  
Published Data ◽  
Antiphospholipid Antibody ◽  
Plasminogen Activator Inhibitor 1 ◽  
Activator Inhibitor

SummaryThe effect of the 675 insertion/deletion (4G/5G) polymorphism of plasminogen activator inhibitor-1 (PAI-1) gene on the risk of venous thromboembolism (VTE) remains controversial. In this study, we performed a meta-analysis of published data regarding this issue. A comprehensive electronic search was carried out up until September 2006. A total of 22 articles were included in the analysis that was performed using random effects models. Eighteen papers, concerning patients without another known risk factor, comprised 2,644 cases and 3,739 controls. The alleles contrast (4G vs. 5G allele) yielded a statistically significant odds ratio (OR) of 1.153 (95% confidence interval [CI]: 1.068–1.246). In a sub-analysis of five studies that included 256 cases with another genetic risk factor and 147 controls, the combined per-allele OR was still significant (OR:1.833,95% CI:1.325–2.536). On the contrary, the analysis of five studies regarding cases with a non-genetic risk factor for VTE (antiphospholipid antibody syndrome, Behcet disease) provided insignificant results in all aspects. There was no evidence for heterogeneity and publication bias in all analyses. Based on our findings, the 4G allele appears to increase the risk of venous thrombosis, particularly in subjects with other genetic thrombophilic defects. Recommendation for detection of this polymorphism in evaluating thrombophilia in such patients might be considered.

The association between the 4G/5G polymorphism in the promoter of the plasminogen activator inhibitor-1 gene and deep venous thrombosis in young people

2005 ◽  
Vol 20 (1) ◽  
pp. 48-52 ◽  
Author(s):  
A Mansilha ◽  
F Araújo ◽  
M Severo ◽  
S M Sampaio ◽  
T Toledo ◽  
...  
Keyword(s):  
Young People ◽  
Venous Thrombosis ◽  
Deep Venous Thrombosis ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Control Group ◽  
Plasminogen Activator Inhibitor 1 ◽  
Increased Risk ◽  
Activator Inhibitor ◽  
Pai 1

Objective: To evaluate the association between the 4G/5G polymorphism in the promoter of the plasminogen activator inhibitor-1 (PAI-1) gene and deep venous thrombosis (DVT) in young people. Methods: Prevalence of the 4G/5G polymorphism was investigated using DNA analysis in a population of 81 consecutive and unrelated patients with an objectively documented first episode of DVT under 40 years old and in a control group of 88 healthy subjects. Results: The frequency of genotypes among patients was 0.27 4G/4G, 0.49 4G/5G and 0.23 5G/5G, corresponding to a frequency of 0.52 for the 4G allele. In the control group the results were, respectively, 0.24, 0.44 and 0.32, corresponding to a frequency of 0.46 for the 4G allele. The odds ratio (OR) for homozygous 4G genotype was 1.5 (95% confidence interval: 0.7–3.6), which was not statistically significant ( P = 0.51). Conclusion: In this study, the 4G/5G polymorphism in the promoter of the PAI-1 gene, including the homozygous 4G genotype, was not associated with a significantly increased risk of DVT in young people.

Incidence of increased plasminogen activator inhibitor in patients with deep venous thrombosis and/or pulmonary embolism

1989 ◽  
Vol 56 (4) ◽  
pp. 565-570 ◽  
Author(s):  
M.Dolores Tabernero ◽  
Amparo Estellés ◽  
Vicente Vicente ◽  
Ignacio Alberca ◽  
Justo Aznar
Keyword(s):  
Pulmonary Embolism ◽  
Venous Thrombosis ◽  
Deep Venous Thrombosis ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Activator Inhibitor

scholarly journals Protein C inhibitor (plasminogen activator inhibitor-3) and the risk of venous thrombosis

2002 ◽  
Vol 118 (2) ◽  
pp. 604-609 ◽  
Author(s):  
Joost C. M. Meijers ◽  
J. Arnoud Marquart ◽  
Rogier M. Bertina ◽  
Bonno N. Bouma ◽  
Frits R. Rosendaal
Keyword(s):  
Venous Thrombosis ◽  
Plasminogen Activator ◽  
Protein C ◽  
Plasminogen Activator Inhibitor ◽  
Protein C Inhibitor ◽  
Activator Inhibitor
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