The Risk of Recurrent Venous Thromboembolism in Patients with and without Factor V Leiden

1997 ◽  
Vol 77 (04) ◽  
pp. 624-628 ◽  
Author(s):  
Sabine Eichinger ◽  
Ingrid Pabinger ◽  
Andreas Stümpfien ◽  
Mirko Hirschl ◽  
Christine Bialonczyk ◽  
...  
Keyword(s):  
Oral Anticoagulant Therapy ◽  
Oral Anticoagulants ◽  
Factor V Leiden ◽  
Multicenter Trial ◽  
Observation Time ◽  
Antiphospholipid Antibody ◽  
Antiphospholipid Antibody Syndrome ◽  
Factor V ◽  
Increased Risk ◽  
Recurrent Vte

SummaryThromboprophylaxis with oral anticoagulants up to six months is established in patients after a first venous thromboembolic event (VTE). The risk of recurrent VTE is still considerable thereafter, and it is uncertain whether some patients might benefit from extended anticoagulation. We performed a prospective, multicenter trial (4 thrombosis centers) and evaluated in 380 patients with a first or recurrent VTE (patients with a deficiency of antithrombin, protein C, protein S or plasminogen; cancer; or an antiphospholipid antibody syndrome were excluded) the risk of recurrence after discontinuation of secondary thromboprophylaxis with oral anticoagulants. It was the aim of the study to evaluate whether patients with factor V Leiden are at an increased risk of recurrent VTE. 112 (29.5%) patients were carriers of factor V Leiden (26.9% heterozygous, 2.6% homozygous). After a median observation time of 19.3 months the overall recurrence rate of VTE was 9.9%. Recurrent deep vein thrombosis and/or pulmonary embolism occurred in 26 of 268 patients without factor V Leiden (9.7%) and in 10 of 112 patients with factor V Leiden (8.9%). The probability of recurrent VTE two years after discontinuation of oral anticoagulants was 12.4% (95% Cl 7.8-17) in patients without factor V Leiden and was 10.6% (95% Cl 3.8-17.4) in carriers of the mutation. This difference was statistically not significant. Patients with factor V Leiden are not at a higher risk of recurrent VTE within two years after discontinuation of oral anticoagulants than patients without factor V Leiden. Balancing the risk of recurrent VTE and bleeding from oral. anticoagulants, patients with factor V Leiden are not likely to benefit from oral anticoagulant therapy extended beyond six months.

"ProC Global": A functional screening test that predicts recurrent venous thromboembolism

2005 ◽  
Vol 93 (03) ◽  
pp. 600-604 ◽  
Author(s):  
Shannon Bates ◽  
Marilyn Johnston ◽  
Simon McRae ◽  
Jeffrey Ginsberg ◽  
Anne Grand’Maison
Keyword(s):  
Venous Thromboembolism ◽  
Protein C ◽  
Specific Inhibitor ◽  
Factor V Leiden ◽  
First Episode ◽  
Functional Screening ◽  
Factor V ◽  
Increased Risk ◽  
Global Result ◽  
Recurrent Vte

SummaryAbnormalities of the Protein C (PC) pathway are found in the majority of patients with thrombophilia. ProC Global is a coagulation assay that reflects the net effect of the PC pathway by measuring the activated partial thromboplastin time (APTT) of patient and control plasma, before and after activation of endogenous PC by Protac, a snake venom. Previous studies have suggested that abnormalities in this test are associated with an increased risk of venous thromboembolism (VTE). A retrospective analysis was performed using frozen plasma samples from 140 patients with confirmed VTE to determine whether an abnormal ProC Global result (in the presence and in the absence of known abnormalities in the PC pathway) is a predictor of initial and recurrent VTE. Patients were tested for the presence of activated protein C resistance, Factor V Leiden, PC and protein S (PS) deficiency, and non-specific inhibitor positivity. Mean ProC Global results were significantly lower in patients with recurrent VTE than in patients without recurrent VTE. The association between abnormal ProC Global result and recurrent VTE showed a strong trend, before (odds ratio, OR 3.6) and after (OR 3.1) exclusion of known thrombophilic abnormalities. Patients with a first episode of idiopathic VTE also expressed significant lower ProC Global results than those with secondary VTE. After exclusion of known PC pathway abnormalities, there was a statistically significant association between abnormal ProC Global and initial idiopathic VTE (p=0.04). These results suggest that ProC Global may serve as a predictor of recurrent VTE and potentially for first episode of idiopathic VTE. ProC Global may help identify patients at increased risk of initial and recurrent VTE.

Influence of thrombophilia on risk of recurrent venous thromboembolism while on warfarin: results from a randomized trial

Blood ◽  
2008 ◽  
Vol 112 (12) ◽  
pp. 4432-4436 ◽  
Author(s):  
Clive Kearon ◽  
Jim A. Julian ◽  
Michael J. Kovacs ◽  
David R. Anderson ◽  
Philip Wells ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Warfarin Therapy ◽  
Factor V Leiden ◽  
International Normalized Ratio ◽  
Antiphospholipid Antibody ◽  
Factor V ◽  
Antithrombin Deficiency ◽  
Recurrent Venous Thromboembolism ◽  
Prothrombin Gene Mutation ◽  
Recurrent Vte

Abstract We sought to determine whether thrombophilic defects increase recurrent venous thromboembolism (VTE) during warfarin therapy. Six hundred sixty-one patients with unprovoked VTE who were randomized to extended low-intensity (international normalized ratio [INR], 1.5-1.9) or conventional-intensity (INR, 2.0-3.0) anticoagulant therapy were tested for thrombophilia and followed for a mean of 2.3 years. One or more thrombophilic defects were present in 42% of patients. The overall rate of recurrent VTE was 0.9% per patient-year. Recurrent VTE was not increased in the presence of factor V Leiden (hazard ratio [HR], 0.7; 95% CI, 0.2-2.6); the 20210G>A prothrombin gene mutation (HR, 0); antithrombin deficiency (HR, 0); elevated factor VIII (HR, 0.7; 95% CI, 0.1-5.4); elevated factor XI (HR, 0.7; 95% CI, 0.1-5.0), or elevated homocysteine (HR, 0.7; 95% CI, 0.1-5.3), but showed a trend to an increase with an antiphospholipid antibody (HR, 2.9; 95% CI, 0.8-10.5). Compared with patients with no thrombophilic defects, the rate of recurrence was not increased in the presence of one (HR, 0.7; 95% CI, 0.2-2.3) or more than one (HR, 0.7; 95% CI, 0.2-3.4) defect. We conclude that single or multiple thrombophilic defects are not associated with a higher risk of recurrent VTE during warfarin therapy.

scholarly journals Venous Thromboembolism: A Survey of Oral Anticoagulant Preferences in the Treatment of Challenging Patient Populations

2018 ◽  
Vol 24 (9_suppl) ◽  
pp. 209S-216S ◽  
Author(s):  
Genevieve Claire Moyer ◽  
Bethany Samuelson Bannow ◽  
Courtney Thornburg ◽  
Rachel Rosovsky ◽  
Tzu-Fei Wang ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Oral Anticoagulant ◽  
Oral Anticoagulants ◽  
Direct Oral Anticoagulants ◽  
Treatment Options ◽  
Antiphospholipid Antibody ◽  
Antiphospholipid Antibody Syndrome ◽  
Oral Anticoagulant Treatment ◽  
Increased Risk ◽  
Altered Metabolism

Venous thromboembolism (VTE) is a highly morbid condition with several available oral anticoagulant treatment options. Numerous studies have been published comparing warfarin to direct oral anticoagulants; however, several populations remain underrepresented in these reports. We surveyed members of The Venous ThromboEmbolism Network U.S. working group regarding their oral anticoagulant preferences for the treatment of VTE in different and challenging populations. In individuals with VTE and no other medical comorbidities, respondents preferred either rivaroxaban (48.7%) or apixaban (48.7%). Apixaban (53.3%) was preferred in elderly individuals with an increased risk of bleeding. Warfarin was preferred in individuals with liver or kidney dysfunction (42% and 47%), altered metabolism (>55%), and antiphospholipid antibody syndrome (84.2%). Low-molecular-weight heparin was preferred in individuals with malignancy (56.6%), followed by edoxaban (23.7%). These findings may help guide clinicians when choosing an anticoagulant in these challenging situations and demonstrate the urgent need for additional study in these groups.

Danger of false negative (exclusion) or false positive (diagnosis) for ‘congenital thrombophilia’ in the age of anticoagulants

2019 ◽  
Vol 57 (6) ◽  
pp. 873-882 ◽  
Author(s):  
Emmanuel J. Favaloro
Keyword(s):  
False Positive ◽  
Ex Vivo ◽  
Oral Anticoagulants ◽  
Direct Oral Anticoagulants ◽  
False Negative ◽  
Factor V Leiden ◽  
Protein S ◽  
Factor V ◽  
Increased Risk

Abstract Background Most guidelines and experts recommend against performance of thrombophilia testing in general, and specifically against testing patients on pharmacological anticoagulants, due to substantially increased risk of false positive identification. For example, vitamin K antagonist (VKA) therapy affects protein C (PC) and protein S (PS), as well as some clotting assays (e.g. as used to investigate activated PC resistance [APCR]). Although heparin may also affect clotting assays, most commercial methods contain neutralisers to make them ‘insensitive’ to therapeutic levels. Direct oral anticoagulants (DOACs) also affect a wide variety of thrombophilia assays, although most reported data has employed artificial in vitro spiked samples. Methods In the current report, data from our facility for the past 2.5 years has been assessed for all ‘congenital thrombophilia’ related tests, as evaluated against patient anticoagulant status. We processed 10,571 ‘thrombophilia’ related test requests, including antithrombin (AT; n=3470), PC (n=3569), PS (n=3585), APCR (n=2359), factor V Leiden (FVL; n=2659), and prothrombin gene mutation (PGM; n=2103). Results As expected, VKA therapy affected PC and PS, and despite manufacturer claims, also APCR. Most assays, as suggested by manufacturers, were largely resistant to heparin therapy. DOACs’ use was associated with falsely low APCR ratios (i.e. FVL-like effect) and somewhat unexpectedly, anti-Xa agents apixaban and rivaroxaban were also associated with lower AT and higher PS values. Conclusions It is concluded that ex-vivo data appears to confirm the potential for both false positive and false negative ‘thrombophilia’ events in patients on anticoagulant (including DOAC) treatment.

Heritable and Acquired Thrombophilias in Clinical Practice

2019 ◽  
Author(s):  
Hanny Al-Samkari ◽  
Nathan T. Connell
Keyword(s):  
Clinical Practice ◽  
Venous Thromboembolism ◽  
Gene Mutation ◽  
Protein C ◽  
Factor V Leiden ◽  
Protein S ◽  
Antiphospholipid Antibody ◽  
Antiphospholipid Antibody Syndrome ◽  
Factor V ◽  
Thrombophilia Testing

Thrombosis is common in clinical practice. Venous thromboembolism in particular raises questions of a possible underlying hereditary or acquired thrombophilic state. Despite considerable data describing the impact of various thrombophilic states on risks of initial and recurrent thromboembolic events, thrombophilia testing is not standardized. An understanding of the utility and pitfalls of clinical thrombophilia testing is necessary to employ this testing properly. When utilized appropriately, thrombophilia testing can be vital in informing an individual patient’s thrombosis risk and pursuing optimal anticoagulant management. Hereditary thrombophilia testing involves investigation for factor V Leiden, the prothrombin G202010A gene mutation, and deficiencies of the natural anticoagulants protein C, protein S, and antithrombin. Assessment for acquired thrombophilias is perhaps even more important, recognizing the possibility for myeloproliferative neoplasms, antiphospholipid antibody syndrome, occult malignancy and other important acquired thrombotic predispositions. Timing of thrombophilia testing in relation to anticoagulation, acute thrombosis, and use of hormonal agents or pregnancy is critical to ensure accurate diagnosis. This review describes each of the most important hereditary and acquired thrombophilias, explains their relationship to venous and arterial thrombosis, delineates evidence-based indications for thrombophilia testing, identifies potential testing pitfalls, and synthesizes the key points in outlining algorithms for thrombophilia testing in clinical practice. This review contains 4 figures, 4 tables, and 48 references. Key words: thrombophilia, venous thromboembolism, pulmonary embolus, deep vein thrombosis, factor V Leiden, prothrombin gene mutation, protein C deficiency, protein S deficiency, antiphospholipid antibody syndrome, hypercoagulability of malignancy

Safety and Efficacy of Direct Oral Anticoagulant Therapy in Patients With Cancer

2019 ◽  
pp. 089719001989650
Author(s):  
Lindsey M. Fovel ◽  
Robert W. Seabury ◽  
Christopher D. Miller ◽  
William Darko ◽  
Luke A. Probst ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Oral Anticoagulant Therapy ◽  
Oral Anticoagulants ◽  
Direct Oral Anticoagulants ◽  
Antiphospholipid Antibody ◽  
Antiphospholipid Antibody Syndrome ◽  
Minor Bleeding ◽  
Safety And Efficacy ◽  
Patients With Cancer ◽  
Significant Difference

Background: Venous thromboembolism (VTE) is the second leading cause of death in patients with malignancy. The currently available guidelines have shown greater support for utilization of low-molecular-weight heparin (LMWH) over direct oral anticoagulants (DOACs) in cancer-associated VTE. Current data on the safety and efficacy of DOAC therapy in patients with cancer are lacking. Objective: To evaluate the safety and efficacy of the use of DOACs compared to LMWH in patients with cancer. Methods: A retrospective review of outpatient records was completed to identify patients with documented cancer diagnosis and either a DOAC or LMWH as a listed medication. Patients were excluded if they had atrial fibrillation, valvular disease, antiphospholipid antibody syndrome, current pregnancy, body mass index (BMI) >40 kg/m2 or weight >120 kg, severe renal or hepatic impairment, or were on concomitant therapy with a significant interacting medication. The primary outcome was frequency of VTE recurrence, and secondary outcomes included the frequency of major and minor bleeding and other thrombotic events. Results: One hundred fifty-six patients were included in the study population, 78 in both the DOAC and LMWH groups. Venous thromboembolism recurrence occurred in 5 (6.4%) patients in the DOAC group and 8 (10.3%) patients in the LMWH group ( P = .39). There was no significant difference in major or minor bleeding or other thrombotic events between the 2 groups. Conclusion: The frequency of VTE recurrence was similar between DOACs and LMWH in patients with cancer. DOACs may be an alternative agent to LMWH for the prevention of recurrent VTE in patients with cancer.

Heritable and Acquired Thrombophilias in Clinical Practice

2019 ◽  
Author(s):  
Hanny Al-Samkari ◽  
Nathan T. Connell
Keyword(s):  
Clinical Practice ◽  
Venous Thromboembolism ◽  
Gene Mutation ◽  
Protein C ◽  
Factor V Leiden ◽  
Protein S ◽  
Antiphospholipid Antibody ◽  
Antiphospholipid Antibody Syndrome ◽  
Factor V ◽  
Thrombophilia Testing

Thrombosis is common in clinical practice. Venous thromboembolism in particular raises questions of a possible underlying hereditary or acquired thrombophilic state. Despite considerable data describing the impact of various thrombophilic states on risks of initial and recurrent thromboembolic events, thrombophilia testing is not standardized. An understanding of the utility and pitfalls of clinical thrombophilia testing is necessary to employ this testing properly. When utilized appropriately, thrombophilia testing can be vital in informing an individual patient’s thrombosis risk and pursuing optimal anticoagulant management. Hereditary thrombophilia testing involves investigation for factor V Leiden, the prothrombin G202010A gene mutation, and deficiencies of the natural anticoagulants protein C, protein S, and antithrombin. Assessment for acquired thrombophilias is perhaps even more important, recognizing the possibility for myeloproliferative neoplasms, antiphospholipid antibody syndrome, occult malignancy and other important acquired thrombotic predispositions. Timing of thrombophilia testing in relation to anticoagulation, acute thrombosis, and use of hormonal agents or pregnancy is critical to ensure accurate diagnosis. This review describes each of the most important hereditary and acquired thrombophilias, explains their relationship to venous and arterial thrombosis, delineates evidence-based indications for thrombophilia testing, identifies potential testing pitfalls, and synthesizes the key points in outlining algorithms for thrombophilia testing in clinical practice. This review contains 4 figures, 4 tables, and 48 references. Key words: thrombophilia, venous thromboembolism, pulmonary embolus, deep vein thrombosis, factor V Leiden, prothrombin gene mutation, protein C deficiency, protein S deficiency, antiphospholipid antibody syndrome, hypercoagulability of malignancy

scholarly journals The Risk of Early Recurrent Venous Thromboembolism after Oral Anticoagulant Therapy in Patients with the G20210A Transition in the Prothrombin Gene

1999 ◽  
Vol 81 (01) ◽  
pp. 14-17 ◽  
Author(s):  
Erich Minar ◽  
Mirko Hirschl ◽  
Christine Bialonczyk ◽  
Milena Stain ◽  
Christine Mannhalter ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Venous Thrombosis ◽  
Oral Anticoagulant Therapy ◽  
Oral Anticoagulants ◽  
Multicenter Trial ◽  
Observation Time ◽  
G20210a Mutation ◽  
Recurrent Venous Thromboembolism ◽  
Prothrombin Gene ◽  
Recurrent Venous Thrombosis

SummaryA G20210A transition in the prothrombin gene is a common risk factor of venous thrombosis. The risk of recurrent venous thrombo-embolism in carriers of the 20210A allele is unknown and guidelines for secondary thromboprophylaxis in these patients are not available.In a prospective multicenter trial, 492 patients with a history of objectively documented venous thromboembolism were followed for a mean observation time of 24 ± 16 months after discontinuation of oral anticoagulants. Forty-two patients (8.5%) were carriers of the 20210A allele. Three of the 42 patients with the G20210A mutation (7%) and 54 of 450 patients without the mutation (12%) experienced recurrent venous thrombosis. At 24 months, the probability of recurrence was 8% (95% CI 0-16.7) in patients with the mutation and was 12.2% (95% CI 8.8-15.6) in patients without the mutation.In conclusion, the risk of early recurrent venous thromboembolism is not higher in patients with the G20210A mutation than in those without the mutation. Therefore, long-term secondary thromboprophylaxis with oral anticoagulants in heterozygous carriers of the 20210A allele is not justified.

scholarly journals Predisposition to Budd-Chiari Syndrome: A Single-Center Case Series of a Rare Subset of Venous Thromboembolism

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 4719-4719
Author(s):  
Krishna Gundabolu ◽  
Vijaya R. Bhatt ◽  
Lori J. Maness ◽  
Catalina C Amador ◽  
Marco Olivera ◽  
...  
Keyword(s):  
Liver Transplant ◽  
Factor V Leiden ◽  
Smoking History ◽  
Antiphospholipid Antibody ◽  
Antiphospholipid Antibody Syndrome ◽  
Factor V ◽  
Budd Chiari Syndrome ◽  
Chiari Syndrome ◽  
The One ◽  
L 14

Abstract Introduction: Budd-Chiari Syndrome (BCS) is a consequence of obstruction of hepatic venous outflow tract leading to increased sinusoidal pressure, portal hypertension and hepatic necrosis. The true incidence and ideal management strategy including the duration of anticoagulation is not fully clear due to the rarity of the event in general population. Many associations like hypercoagulablestates, tumors, infections, and auto immune diseases are described. We intend to describe the patient population diagnosed with BCS and following up in our thrombosis clinic. Methods: We identified 9 patients diagnosed with from 2010-2015. We evaluated various demographics, laboratory data, identifiable etiology of BCS, Child-Pugh score (CP), Model of End stage Liver Disease score (MELD), presence of esophageal varices, anticoagulation used and duration of therapy. Results: Characteristics of the study population included a median age of 36 years (28-58 y), 55% females and 77% whites (Table 1). Following anticoagulants used: Warfarin (n=7), Heparin switched to Bivalirudin due to heparin induced thrombocytopenia (n=1), None (n=1) and those 7 remained on indefinite anticoagulation. The one treated with Heparin-Bivalirudin died soon from diagnosis and the one with no identifiable thrombophilia was non compliant and did not receive anticoagulation. Of those 7 on Warfarin only one experienced anticoagulation failure with recurrence of thrombosis needing a change in anticoagulant. At diagnosis median INR was 1.5 (1-2.4), median Anti thrombin (AT) activity of 68% (39-111%) (Ref range 80-120%) in 8 evaluated patients, Protein C was 62% (65-145%) in 3 patients tested, Protein S was 90% (71-170%) in 3 tested patients. Other tests were positive for heterozygous factor V Leiden (FVL) mutation (11%) and Antiphospholipid antibody syndrome (APS) (11%) but not for Prothrombin G20210A mutation. Median Creatinine was 1.04 mg/dL (0.5-2.2 mg/dL), bilirubin 2.8 mg/dL (0.3-6.4 mg/dL), Albumin 3.3 gm/dL (2.3-3.4 gm/dL), Alkaline phosphatase 163 U/L (86-275 U/L), AST 135 U/L (14-1037 U/L), ALT 236 U/L (18-1694 U/L), Hemoglobin 15.8 gm/dL (9.9-20 gm/dL), Platelet count of 335 x 10E3/cmm (70-971 x 10E3/cmm). 2 of the 5 women were on OC pills (One >6 month and one patient <6 months duration). 8 of 9 had ascites, 2 of 9 had alcohol abuse, 4 of 9 had cirrhosis. Median MELD score was 11 (6-28) and Child-Pugh score of 9 (8-13), 3 of 9 patients did not have varices, 3 of 9 had smoking history. Median BMI is 30 (18-38), 3 of 9 underwent liver transplant and 1 of 9 underwent TIPS but died before liver transplant. Etiologies include Myeloproliferative Neoplasms (67%), APS (11%), Sarcoidosis(11%) and none (11%). Conclusions: The incidence of Myeloprolifeartive neoplasms was very high (67%) in our cohort and indicates that such disorders be ruled out in patients with BCS at diagnosis. The most common familial thrombophilia including Factor V Leiden and Prothrombingene mutations appear to be less frequent than reported previously. Acquired AT deficiency is not uncommon. Proper evaluation of the underlying etiology may help identify important disorders and may guide anticoagulant management. APS-Antiphospholipid antibody syndrome, AT-Antithrombin activity, ET-Essential thrombocythemia, MPN-MyeloprolifeativeNeoplasms, NA-Not available, PV-Polycythemia Vera Table.Age/SexAT%FVLPT G20210AMELDCP scoreThrombophilia/etiologySmokingBMI30/F70NANA89JAK2+ETNo1828/F59NANA119APSNo2440/F111NN66SarcoidosisNo3036/M63NN1612JAK2+PVNo3029/M66NN118JAK2+ETYes3750/FNANANA2813JAK2+PVNo3846/F39NN1611JAK2+PVYes2858/M90HeteroN88CALR+MPNYes3829/M89NN98NoneNo26 Disclosures No relevant conflicts of interest to declare.

The Risk Of Recurrence In Women With Venous Thromboembolism While Using Estrogens: A Prospective Observational Cohort Study

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 1123-1123
Author(s):  
Paul A Kyrle ◽  
Lisbeth Eischer ◽  
Sabine Eichinger
Keyword(s):  
Venous Thromboembolism ◽  
Conflicts Of Interest ◽  
Oral Anticoagulants ◽  
Hormone Replacement ◽  
Factor V Leiden ◽  
Recurrence Risk ◽  
Cumulative Probability ◽  
Carrier Status ◽  
Factor V ◽  
Recurrent Vte

Abstract Objective Because of the high recurrence risk, guidelines recommend indefinite anticoagulation in women with a first unprovoked proximal deep-vein thrombosis (DVT) and/or pulmonary embolism (PE). The optimal duration of anticoagulation in women who had venous thromboembolism (VTE) while using estrogens is unknown. We therefore compared the risk of recurrent VTE between women who used estrogens at the time of first VTE and women who did not. Methods This analysis was performed within the frame of the Austrian Study on Recurrent Venous Thromboembolism (AUREC), an on-going prospective observational study. Patients with a first objectively confirmed DVT of the leg and/or PE who had received anticoagulants for 3 to 18 months were included. Exclusion criteria were: age < 18 years; VTE associated with surgery, trauma, cancer or pregnancy; long-term anticoagulation; natural inhibitor deficiency; lupus anticoagulant; homozygosity or double heterozygosity for factor V Leiden and/or the prothrombin mutation. Women were advised to refrain from further estrogen use and were excluded in case of non-adherence. The study end point was recurrent symptomatic DVT and/or PE verified by imaging. The local ethics committee approved the study and all patients gave written informed consent. Results We followed 630 women (mean age 46 +/- 17 years) who had been treated with oral anticoagulants for 7 (+/- 3) months for an average of 69 (+/- 52) months. Recurrent VTE was recorded in 71 patients (11%). Recurrent VTE occurred in 22 (7%) of 333 estrogen users and in 49 (17%) of 297 non-users. After 1, 2 and 5 years, the cumulative probability of recurrence was 1% (95% CI 0-2), 1% (95% CI 0-2) and 6% (95% CI 3-9) among estrogen users and 5% (95% CI 2-7), 9% (95% CI 6-13) and 17% (95% CI 12-22) among non-users, respectively (p < 0.001, Figure). Compared to non-users, estrogen users had a relative risk (RR) of recurrent VTE of 0.4 (95% CI 0.2-0.8) after adjustment for age, site of first VTE and factor V Leiden carrier status. Compared to non-users in the respective age groups, the RR of recurrent VTE was 0.4 (95% CI 0.2-0.8) among estrogen containing contraceptive users and was 0.7 (95% CI 0.3-1.5) among women using estrogen containing hormone replacement therapy. Conclusion Women who had their first VTE while using estrogens have a low risk of recurrent VTE. The recurrence risk is particularly low in estrogen containing contraceptive users. We therefore propose that these women should receive anticoagulant therapy for no longer than 3 months. Disclosures: No relevant conflicts of interest to declare.

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