scholarly journals Minor Events and the Risk of Deep Venous Thrombosis

2000 ◽  
Vol 83 (03) ◽  
pp. 408-411 ◽  
Author(s):  
E. M. W. Eekhoff ◽  
J. P. Vandenbroucke ◽  
F. R. Rosendaal
Keyword(s):  
Risk Factors ◽  
Confidence Interval ◽  
Venous Thrombosis ◽  
Deep Venous Thrombosis ◽  
Odds Ratio ◽  
Factor V Leiden ◽  
Common Disease ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Synergy Index

SummaryBackground Deep venous thrombosis is a common disease, with genetic and acquired risk factors. Many patients have a history of minor events (short periods of immobilisation such as prolonged travel, short illness, minor surgery or injuries) before onset of venous thrombosis. However, the role of these minor events has received little formal study. Also, we do not know how minor events might interact with the presence of genetic prothrombotic defects (factor V Leiden mutation, factor II mutation, protein C, S and antithrombin deficiency). Patients and Methods On the basis of case-control data from a thrombosis service in the Netherlands, we added a follow-up period for a casecross-over analysis of minor events as risk factors, and a case-only analysis for the interaction with factor V Leiden. A total of 187 patients with first, objectively diagnosed venous thrombosis of the legs, aged 15–70, without underlying malignancies and without major acquired risk factors entered the study. For the analysis of minor events in the case-cross-over analysis, we used a matched odds ratio; in the caseonly analysis, we used the multiplicative synergy index. Results In 32.6% of the 187 patients with deep venous thrombosis who did not have major acquired risk factors, minor events were the only external risk factors. Minor events increased the risk of thrombosis about 3-fold, as estimated in the case-cross-over analysis (odds ratio 2.9, 95% confidence interval 1.5–5.4). The synergy index between minor events and factor V Leiden mutation in the case-only analysis was 0.7 (95% confidence interval 0.3–1.5). Therefore, persons with factor V Leiden mutation who experience a minor event will have an estimated risk increase of about 17-fold, which exceeds the sum of the individual risk factors. Conclusions Minor events are likely to play an important role in the development of deep venous thrombosis, especially in the presence of genetic prothrombotic conditions.

Combined Factor V Leiden (R506Q) and prothrombin G20210A genotyping in young patients presenting with deep venous thrombosis

2006 ◽  
Vol 21 (1) ◽  
pp. 24-27 ◽  
Author(s):  
A Mansilha ◽  
F Araújo ◽  
M Severo ◽  
S M Sampaio ◽  
T Toledo ◽  
...  
Keyword(s):  
Risk Factor ◽  
Young People ◽  
Venous Thrombosis ◽  
Deep Venous Thrombosis ◽  
Young Patients ◽  
Factor V Leiden ◽  
First Episode ◽  
Control Group ◽  
Factor V ◽  
Factor V Leiden Mutation

Objective: To evaluate the association between the Factor V Leiden (FV R506Q) and prothrombin gene (FII G20210A) mutations and deep venous thrombosis (DVT) in young people. Methods: Blood samples were drawn from 199 subjects: 100 healthy controls and 99 unselected patients, with an objectively documented first episode of DVT under 40 years old. DNA analysis was performed using the polymerase chain reaction. Results: The mean age in the patient cohort was 27 years (range 16–40) and 68 (68.7%) were women. Patient prevalences were 20.6% and 10.1% for FV R506Q and FII G20210A, respectively. In the control group, carrier frequencies were 2% and 5%, respectively. We found an increased overall relative risk of DVT with statistical significance for FV R506Q carriers (OR: 12.8; 95% CI: 2.9–56.7; P < 0.001), but not for FII G20210A mutation (OR: 2.1; 95% CI: 0.7–6.5; P = 0.19). Conclusions: Our results suggest a possible increase in DVT risk for the young G20210A allele carriers, which can be more expressed in the presence of a circumstantial risk factor. There is extremely strong evidence that the Factor V Leiden mutation is an important risk factor in the development of a first episode of DVT in young people.

High Prevalence of Factor V Leiden Mutation among Healthy Individuals and Patients with Deep Venous Thrombosis in Lebanon:

2001 ◽  
Vol 86 (08) ◽  
pp. 723-724 ◽  
Author(s):  
Ali Taher ◽  
Ismail Khalil ◽  
Ali Shamseddine ◽  
Fadi El-Ahdab ◽  
Ali Bazarbachi
Keyword(s):  
Venous Thrombosis ◽  
Deep Venous Thrombosis ◽  
Factor V Leiden ◽  
Factor V ◽  
Healthy Individuals ◽  
Factor V Leiden Mutation ◽  
High Prevalence

A low rate of factor V Leiden mutation among Sudanese women with deep venous thrombosis during pregnancy and puerperium

2017 ◽  
Vol 37 (7) ◽  
pp. 963-964 ◽  
Author(s):  
Abass Awad-Elkareem ◽  
Salaheldein G. Elzaki ◽  
Hanan Khalid ◽  
Mual S. Abdallah ◽  
Ishag Adam
Keyword(s):  
Venous Thrombosis ◽  
Deep Venous Thrombosis ◽  
Factor V Leiden ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Low Rate

A Reduced Sensitivity for Activated Protein C in the Absence of Factor V Leiden Increases the Risk of Venous Thrombosis

Blood ◽  
1999 ◽  
Vol 93 (4) ◽  
pp. 1271-1276 ◽  
Author(s):  
Marieke C.H. de Visser ◽  
Frits R. Rosendaal ◽  
Rogier M. Bertina
Keyword(s):  
Risk Factor ◽  
Confidence Interval ◽  
Venous Thrombosis ◽  
Protein C ◽  
Activated Protein C ◽  
Factor V Leiden ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Apc Resistance ◽  
Increased Risk

Abstract Activated protein C (APC) resistance caused by the factor V Leiden mutation is associated with an increased risk of venous thrombosis. We investigated whether a reduced response to APC, not due to the factor V point mutation, is also a risk factor for venous thrombosis. For this analysis, we used the Leiden Thrombophilia Study (LETS), a case-control study for venous thrombosis including 474 patients with a first deep-vein thrombosis and 474 age- and sex-matched controls. All carriers of the factor V Leiden mutation were excluded. A dose-response relationship was observed between the sensitivity for APC and the risk of thrombosis: the lower the normalized APC sensitivity ratio, the higher the associated risk. The risk for the lowest quartile of normalized APC-SR (&lt;0.92), which included 16.5% of the healthy controls, compared with the highest quartile (normalized APC-SR &gt; 1.05) was greater than fourfold increased (OR = 4.4; 95% confidence interval, 2.9 to 6.6). We adjusted for VIII:C levels, which appeared to affect our APC resistance test. The adjusted (age, sex, FVIII:C) odds ratio for the lowest quartile was 2.5 (95% confidence interval, 1.5 to 4.2). So, after adjustment for factor VIII levels, a reduced response to APC remained a risk factor. Our results show that a reduced sensitivity for APC, not caused by the factor V Leiden mutation, is a risk factor for venous thrombosis.

Follow-up von Patienten mit persistierender APC-Resistenz ohne Faktor V Leiden

VASA ◽  
2001 ◽  
Vol 30 (1) ◽  
pp. 24-27 ◽  
Author(s):  
T. Schwarz ◽  
G. Siegert ◽  
U. Mikulin ◽  
S. Gehrisch ◽  
E. Runge ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Deep Venous Thrombosis ◽  
Genetic Defect ◽  
Factor V Leiden ◽  
Arterial Disease ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Thrombotic Risk ◽  
Apc Resistance

Background: Activated protein C (APC) resistance and factor V Leiden mutation are major risk factors for deep venous thrombosis. Previous work has led to the view that the coagulation phenotype and the genetic defect are associated in almost all patients. It has been reported about single APC-resistant patients without associated factor V Leiden, but significance and thrombotic risk of this constellation have not yet been established. Patients and methods: We tested 486 consecutive patients with deep venous thrombosis, arterial disease or other than vascular disease for APC-resistance with a factor VIII based assay. Results: 149 patients (31%) showed a pathological APC-ratio. Sensitivity and specificity for detection of factor V Leiden were 100% and 40%, respectively. At 6 months follow-up APC-ratio returned to normal in 55% of the patients with initial pathological APC-resistance. At 12 months follow-up 91% of the patients with persistent APC-resistance showed a pathological ratio as well. Conclusions: Patients with APC-resistance not due to factor V Leiden can be attributed to one subset with reversible APC-resistance – possibly due to a hypercoagulable state in an acute thrombotic situation, and to another with persistent APC-resistance.

scholarly journals Thrombophilia in Klinefelter Syndrome With Deep Venous Thrombosis, Pulmonary Embolism, and Mesenteric Artery Thrombosis on Testosterone Therapy: A Pilot Study

2016 ◽  
Vol 23 (8) ◽  
pp. 973-979 ◽  
Author(s):  
Charles J. Glueck ◽  
Vybhav Jetty ◽  
Naila Goldenberg ◽  
Parth Shah ◽  
Ping Wang
Keyword(s):  
Venous Thrombosis ◽  
Deep Venous Thrombosis ◽  
Mesenteric Artery ◽  
Klinefelter Syndrome ◽  
Factor V Leiden ◽  
Testosterone Replacement Therapy ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Artery Thrombosis ◽  
Increased Risk

We compared thrombophilia and hypofibrinolysis in 6 men with Klinefelter syndrome (KS), without previously known familial thrombophilia, who had sustained deep venous thrombosis (DVT)–pulmonary emboli (PE) or mesenteric artery thrombosis on testosterone replacement therapy (TRT). After the diagnosis of KS, TRT had been started in the 6 men at ages 11, 12, 13, 13, 19, and 48 years. After starting TRT, DVT-PE or mesenteric artery thrombosis was developed in 6 months, 1, 11, 11, 12, and 49 years. Of the 6 men, 4 had high (>150%) factor VIII (177%, 192%, 263%, and 293%), 3 had high (>150%) factor XI (165%, 181%, and 193%), 1 was heterozygous for the factor V Leiden mutation, and 1 was heterozygous for the G20210A prothrombin gene mutation. None of the 6 men had a precipitating event before their DVT-PE. We speculate that the previously known increased rate of DVT-PE and other thrombi in KS reflects an interaction between prothrombotic, long-term TRT with previously undiagnosed familial thrombophilia. Thrombophilia screening in men with KS before starting TRT would identify a cohort at increased risk for subsequent DVT-PE, providing an optimally informed estimate of the risk/benefit ratio of TRT.

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