scholarly journals New Prothrombin Mutation (Arg596Trp, Prothrombin Padua 2) Associated With Venous Thromboembolism

2016 ◽  
Vol 36 (5) ◽  
pp. 1022-1029 ◽  
Author(s):  
Cristiana Bulato ◽  
Claudia Maria Radu ◽  
Elena Campello ◽  
Sabrina Gavasso ◽  
Luca Spiezia ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Prothrombin Mutation

Plasma fibrin clot properties in the G20210A prothrombin mutation carriers following venous thromboembolism: the effect of rivaroxaban

2017 ◽  
Vol 117 (09) ◽  
pp. 1739-1749 ◽  
Author(s):  
Agnieszka Janion-Sadowska ◽  
Joanna Natorska ◽  
Jakub Siudut ◽  
Michal Zabczyk ◽  
Andrzej Stanisz ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Fibrin Clot ◽  
Clot Lysis ◽  
Mutation Carriers ◽  
Lysis Time ◽  
Prothrombin Mutation ◽  
Fibrinolysis Inhibitor ◽  
Heterozygous Carriers ◽  
Mutation Group ◽  
Clot Structure

SummaryWe sought to investigate whether the G20210A prothrombin mutation modifies plasma fibrin clot properties in patients after venous thromboembolism (VTE) and how rivaroxaban treatment affects these alterations. We studied 34 prothrombin mutation heterozygous carriers and sex- and age-matched 34 non-carriers, all at least three months since the first VTE episode, before and during treatment with rivaroxaban. Clot permeability (Ks) and clot lysis time (CLT) with or without elimination of thrombin activatable fibrinolysis inhibitor (TAFI) were assessed at baseline, 2–6 hours (h) after and 20–25 h after intake of rivaroxaban (20 mg/day). At baseline, the prothrombin mutation group formed denser clots (Ks −12 %, p=0.0006) and had impaired fibrinolysis (CLT +14 %, p=0.004, and CLT-TAFI +13 %, p=0.03) compared with the no mutation group and were similar to those observed in 15 healthy unrelated prothrombin mutation carriers. The G20210A prothrombin mutation was the independent predictor for Ks and CLT before rivaroxaban intake. At 2–6 h after rivaroxaban intake, clot properties improved in both G20210A carriers and non-carriers (Ks +38 %, and +37 %, CLT −25 % and −25 %, CLT-TAFI −20 % and −24 %, respectively, all p<0.001), but those parameters were worse in the prothrombin mutation group (Ks −12.8 %, CLT +17 %, CLT-TAFI +13 %, all p<0.001). Rivaroxaban concentration correlated with fibrin clot properties. After 20–25 h since rivaroxaban intake most clot properties returned to baseline. Rivaroxaban-related differences in clot structure were confirmed by scanning electron microscopy images. In conclusion, rivaroxaban treatment, though improves fibrin clot properties, cannot abolish more prothrombotic fibrin clot phenotype observed in prothrombin mutation carriers following VTE.

Inherited Thrombophilia and First Venous Thromboembolism during Pregnancy and Puerperium

2002 ◽  
Vol 87 (05) ◽  
pp. 791-795 ◽  
Author(s):  
Valerio De Stefano ◽  
Emanuela Taioli ◽  
Katia Paciaroni ◽  
Elena Rossi ◽  
Mannucci Pier ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Factor V Leiden ◽  
Protein S ◽  
First Episode ◽  
Factor V ◽  
Inherited Thrombophilia ◽  
Vein Thrombosis ◽  
Increased Risk ◽  
Prothrombin Mutation ◽  
Heterozygous Carriers

SummaryVenous thromboembolism is a rare but threatening complication of pregnancy. Little conclusive information is available on the actual risk of venous thromboembolism during pregnancy or puerperium in women with inherited thrombophilia, particularly in carriers of factor V Leiden and of the G20210A prothrombin gene mutation. To determine the pregnancy-related and puerperium-related risk of venous thromboembolism in women with inherited thrombophilia, we performed a case-control study on 119 women who had a first episode of deep vein thrombosis and/or pulmonary embolism during pregnancy or puerperium and 232 healthy women who had at least one pregnancy without thrombosis. Inherited thrombophilia was diagnosed in 47 patients (39.5%) and 15 controls (6.5%). The relative risk of venous thromboembolism was 10.6 (95% CI, 5.6-20.4) for heterozygous carriers of factor V Leiden, 2.9 (95% CI, 1.0-8.6) for heterozygous carriers of the prothrombin mutation and 13.1 (95% CI, 5.0-34.2) for those with antithrombin, protein C or protein S deficiency taken together. Sixty-eight of the 119 women (57%) had thrombosis after delivery, confirming the puerperium as a particularly high-risk period. When women were divided into two groups of those with antenatal or postnatal thrombosis, the relative risks associated with each type of inherited thrombophilia were of similar magnitude. In conclusion, women with inherited thrombophilia have an increased risk of venous thromboembolism during pregnancy. Among thrombophilic abnormalities, the prothrombin mutation was the weakest risk factor. Thrombosis occurred more frequently in puerperium than in pregnancy, whether or not thrombophilia was diagnosed.

Allele 4G of gene PAI-1 associated with prothrombin mutation G20210A increases the risk for venous thrombosis

2003 ◽  
Vol 90 (12) ◽  
pp. 1061-1064 ◽  
Author(s):  
Doris Barcellona ◽  
Lara Fenu ◽  
Cristiana Cauli ◽  
Giulia Pisu ◽  
Francesco Marongiu
Keyword(s):  
Risk Factor ◽  
Venous Thromboembolism ◽  
Odds Ratio ◽  
Final Conclusion ◽  
Thrombotic Risk ◽  
G20210a Mutation ◽  
Increased Risk ◽  
Prothrombin Mutation ◽  
Pai 1

SummarySeveral studies have tried to clarify the role of polymorphism 4G/5G of the PAI-1 gene in venous thromboembolism without reaching any final conclusion. It has been demonstrated that this polymorphism may induce an increased risk for venous thromboembolism (VTE) in patients with thrombophilic defects. We studied the association of prothrombin mutation G20210A with 4G/5G polymorphism in 402 VTE patients and 466 healthy controls. Patients affected by prothrombin mutation G20210A, with or without the concomitant presence of allele 4G, had a 3.7 thrombotic risk (C.I. 95% 2.3–6.0; p<0.0001). Moreover, genotype 4G/4G is a mild risk factor for VTE, irrespectively of whether the prothrombin mutation was present.Logistic regression analysis showed that patients carrying the G20210A prothrombin mutation with allele 4G gave an odds ratio for VTE of 6.1 (C.I. 95% 3.2 – 11.4; p<0.001). The risk increased up to 13.0 (C.I. 95% 3.0 – 60.4; p<0.001) when we considered the association of the prothrombin mutation with genotype 4G/4G. The G20210A mutation without allele 4G (5G/5G) was not a risk factor for VTE. In conclusion, we believe that patients affected by VTE with concomitant presence of the G20210A prothrombin mutation could be tested for genotype 4G/4G to better define their thrombotic risk.

German S3 guideline for the prevention of venous thromboembolism updated Comment on Vasa Supplement 92

VASA ◽  
2016 ◽  
Vol 45 (5) ◽  
pp. 347-348 ◽  
Author(s):  
Sylvia Haas ◽  
Albrecht Encke ◽  
Ina Kopp
Keyword(s):  
Venous Thromboembolism ◽  
S3 Guideline

Venous thromboembolism in a general hospital. An update with low molecular weight heparin prophylaxis

VASA ◽  
2007 ◽  
Vol 36 (1) ◽  
pp. 17-22
Author(s):  
Schulz ◽  
Kesselring ◽  
Seeberger ◽  
Andresen
Keyword(s):  
Molecular Weight ◽  
Pulmonary Embolism ◽  
Venous Thromboembolism ◽  
Low Molecular Weight ◽  
Trauma Patients ◽  
Vte Prophylaxis ◽  
Vein Thrombosis ◽  
Patients At Risk ◽  
Hospital Stays ◽  
Event Rates

Background: Patients admitted to hospital for surgery or acute medical illnesses have a high risk for venous thromboembolism (VTE). Today’s widespread use of low molecular weight heparins (LMWH) for VTE prophylaxis is supposed to have reduced VTE rates substantially. However, data concerning the overall effectiveness of LMWH prophylaxis is sparse. Patients and methods: We prospectively studied all patients with symptomatic and objectively confirmed VTE seen in our hospital over a three year period. Event rates in different wards were analysed and compared. VTE prophylaxis with Enoxaparin was given to all patients at risk during their hospital stay. Results: A total of 50 464 inpatients were treated during the study period. 461 examinations were carried out for symptoms suggestive of VTE and yielded 89 positive results in 85 patients. Seventy eight patients were found to have deep vein thrombosis, 7 had pulmonary embolism, and 4 had both deep venous thrombosis and pulmonary embolism. The overall in hospital VTE event rate was 0.17%. The rate decreased during the study period from 0.22 in year one to 0,16 in year two and 0.13 % in year three. It ranged highest in neurologic and trauma patients (0.32%) and lowest (0.08%) in gynecology-obstetrics. Conclusions: With a simple and strictly applied regimen of prophylaxis with LMWH the overall rate of symptomatic VTE was very low in our hospitalized patients. Beside LMWH prophylaxis, shortening hospital stays and substantial improvements in surgical and anasthesia techniques achieved during the last decades probably play an essential role in decreasing VTE rates.

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