A Comparison of Six Weeks with Six Months of Oral Anticoagulant Therapy after a First Episode of Venous Thromboembolism

Schulman, Sam; Rhedin, Ann-Sofie; Lindmarker, Per; Carlsson, Anders; Lärfars, Gerd; Nicol, Peter; Loogna, Enno; Svensson, Else; Ljungberg, Bengt; Walter, Hans; Viering, Stanka; Nordlander, S; Leijd, Barbro; Jönsson, Klas; Hjorth, Martin; Linder, Olle; Boberg, J.

doi:10.1056/nejm199506223322501

Cited by 823 publications

(184 citation statements)

References 18 publications

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“…As our control group was only tested for the presence or absence of the C677T mutation in the MTHFR gene, we were unable to determine such a gene–gene interaction in our study. If such an interaction between identifiable inherited hypercoagulable states is highly probable [25], it is also remarkable that: (1) the risk of recurrent VTE in patients with idiopathic VTE is higher than that of those with secondary VTE [26, 27, 28], the former having or not having, an identifiable hypercoagulable state [22], and (2) in patients who developed an acute episode of idiopathic VTE in association with inherited thrombophilia, only one biochemical abnormality is found in most of them [22]. These observations indirectly suggest that an underlying persistent prothrombotic condition (i.e.…”

Section: Discussionmentioning

confidence: 99%

Methylenetetrahydrofolate Reductase C677T Genotype and Venous Thromboembolic Disease

Couturaud

Oger

Abalain³

et al. 2000

Respiration

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Background: Many studies have suggested an increased risk of venous thromboembolism (VTE) in patients with mild hyperhomocysteinemia. The C677T mutation in the MTHFR gene has recently been described as a cause of mild hyperhomocysteinemia.Objectives: To investigate the potential of the C677T mutation in the MTHFR gene in its homozygous state as a risk factor for VTE. Methods: Case-control study design. The presence of the mutation was determined in all consecutive patients referred from July 1994 to September 1997 and in whom the diagnosis was duly confirmed. Analysis was carried out in a subgroup of VTE patients free from both acquired and genetic risk factors (factor-V mutation and/or prothrombin gene mutation). A control group consisted of 105 volunteer blood donors. Results: In the 366 patients with a confirmed VTE, 253 presented acquired risk factors and 58 were carriers of the factor-V Leiden mutation and/or G20210A mutation of the prothrombin gene. In the remaining 55 patients, VTE was considered as ’unexplained’, and the frequency of the C677T mutation MTHFR was 21.8% in its homozygous state and 34.5% in its heterozygous state. In the control group, 9.5% were found homozygous and 34.3% heterozygous. The odds ratio for having VTE in the presence of the mutation in its homozygous state was 2.9 (95% CI 1.0–8.6). Conclusion: This study suggests that the homozygous C677T mutation in the MTHFR gene might be a risk factor of VTE in patients with spontaneous events and without other common genetic risk factors.

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Section: Discussionmentioning

confidence: 99%

Methylenetetrahydrofolate Reductase C677T Genotype and Venous Thromboembolic Disease

Couturaud

Oger

Abalain³

et al. 2000

Respiration

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“…These investigators used data analyzed retrospectively from the Duration of Anticoagulation Trial, the so-called DURAC study, which was designed to compare prospectively the efficacy of 6 weeks and 6 months of oral anticoagulation therapy [25]. The data analysis in the DURAC study regarding incidence of cancer in the two groups suffers from some of the same limitations discussed above for retrospective studies (e.g.…”

Section: Occult Malignancy In Patients With Vtementioning

confidence: 99%

Epidemiology of Thrombosis in Cancer

2001

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We have utilized epidemiological data to address three questions in patients with cancer and venous thromboembolism (VTE): (1) What is the risk for occult cancer in patients with idiopathic versus secondary VTE? (2) What is the risk for thrombosis in patients with cancer (vs. noncancer patients)? (3) What is the risk of recurrent VTE in cancer patients with an initial episode of VTE compared to noncancer patients? The risk for a new cancer diagnosis within 6–12 months of the diagnosis of idiopathic VTE (including pulmonary embolism) is well supported by retrospective analyses of large numbers of unselected patients, population-based retrospective cohort analyses from large registries and prospective studies. The odds ratios for these studies are in the range of 4- to 7-fold increased risk. In surgical patients with known cancer the odds ratio for an episode of postoperative VTE is approximately 2, when compared to a control group of noncancer patients subjected to the same procedures. A similar odds ratio of approximately 2 exists for the relative risk for recurrence of VTE in the first 3 months after an initial episode in cancer patients treated with heparin and warfarin (Coumadin^®) compared to noncancer patients. Therefore, patients with idiopathic VTE are at increased risk for occult cancer and cancer patients are at increased risk for VTE. Appropriate studies are underway to determine the best strategies for anticoagulant management of these patients.

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“…This practice is now questioned as accumulating evidence suggests that the duration of treatment should be adjusted depending on the presence or absence of ongoing thrombotic risk factors [22, 23, 24]. In a patient with idiopathic venous thromboembolism, a longer course of anticoagulant therapy (6 months or longer) is associated with a lower risk of recurrent thromboembolism than shorter courses (3 months or less) [22, 23, 24]. In a patient with a transient risk factor, e.g.…”

Section: Long-term Anticoagulant Therapymentioning

confidence: 99%

Treatment of Venous Thrombosis in the Cancer Patient

Levine

Lee²

2001

Acta Haematol

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Venous thromboembolism is a common complication in patients with cancer. The management of deep vein thrombosis and pulmonary embolism can be a considerable challenge in patients with cancer. The cancer itself and associated treatments contribute to an ongoing thrombogenic stimulus, while cancer patients are thought to be at increased risk for anticoagulant-induced bleeding. Initial treatment of acute thromboembolism is with intravenous unfractionated heparin or subcutaneous low molecular weight heparin. Treatment at home with low molecular weight heparin is an attractive option in patients with malignant disease. Long-term treatment of acute venous thromboembolism has traditionally been with oral anticoagulants. However, the inconvenience and narrow therapeutic window of oral anticoagulants make such therapy unattractive and problematic in cancer patients. Low molecular weight heparins are being evaluated as an alternative for long-term therapy because their anticoagulant effects are more predictable and laboratory monitoring is unnecessary. Although many clinical issues remain unresolved in the treatment of cancer patients with venous thromboembolism, the future holds much promise as new antithrombotic agents, including factor Xa antagonists and oral thrombin inhibitors, are being tested in clinical trials.

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A Comparison of Six Weeks with Six Months of Oral Anticoagulant Therapy after a First Episode of Venous Thromboembolism

Cited by 823 publications

References 18 publications

Methylenetetrahydrofolate Reductase C677T Genotype and Venous Thromboembolic Disease

Methylenetetrahydrofolate Reductase C677T Genotype and Venous Thromboembolic Disease

Epidemiology of Thrombosis in Cancer

Treatment of Venous Thrombosis in the Cancer Patient

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