Activated protein C resistance in patients with peripheral vascular disease

Sampram, Ellis S.K.; Lindblad, Bengt; Dahlbäck, Björn

doi:10.1016/s0741-5214(98)70086-2

Cited by 37 publications

(26 citation statements)

References 24 publications

(51 reference statements)

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“…Depending on which APC resistance assay is used and what patient population is studied, up to 37% of patients with an abnormal APC resistance test do not have factor V Leiden [4]. An abnormal APC resistance test can also be due to a lupus anticoagulant and other, yet unknown, causes, and should, therefore, always be followed by the genetic test [5].…”

Section: Clinical Relevancementioning

confidence: 99%

“…3 Probably reliable, but limited data in literature. 4 Test often positive or elevated at time of acute thrombosis, but subsequently negative [47]. 5 While many test kits used for lupus anticoagulant testing contain a heparin neutralizer that inactivates unfractionated heparin (UF) and possibly low molecular weight heparin (LMWH) thus making these tests reliable on UF and LMWH, clinicians needs to inquire with their laboratory how their individual test kit performs in samples with UF and LMW H. 6 No indication for testing in the acute setting provide education and support, advocate for those who are affected by, or at risk for blood clots, and to foster research.…”

Section: Patient Education Materials and Resourcesmentioning

confidence: 99%

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Thrombophilias—Practical Implications and Testing Caveats

Moll

2006

J Thromb Thrombolysis

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This review summarizes recent information about the major thrombophilic conditions, their clinical relevance, and practical aspects pertaining to testing for these thrombophilias, such as when to test and what assays are appropriate. Conditions covered include factor V Leiden, prothrombin 20210 mutation, proteins C and S, antithrombin, antiphospholipid antibodies, homocysteine, and methylene-tetrahydrofolate-reductase enzyme mutation. Additional comments focus on education of patients and educational resources for patients, such as the National Alliance for Thrombosis and Thrombophilia (www.nattinfo.org).

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Section: Clinical Relevancementioning

confidence: 99%

Section: Patient Education Materials and Resourcesmentioning

confidence: 99%

Thrombophilias—Practical Implications and Testing Caveats

Moll

2006

J Thromb Thrombolysis

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“…11 12 Three studies have examined the role of factor V Leiden in patients with peripheral vascular disease. [13][14][15] The prevalence of factor V Leiden was found to be increased in all three studies in patients with peripheral vascular disease but, when based on APC resistance measurements, the prevalence varied between 11.6% and 41% of patients with aortoiliac disease using DNA analysis. A small study from Bristol concluded that factor V Leiden was not an important factor in the outcome of infrainguinal bypass grafting.…”

Section: Factor V Leidenmentioning

confidence: 82%

Thrombophilia, polymorphisms, and vascular disease

Sykes

2000

Molecular Pathology

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“…2) enhances protein C activation and also can translocate APC to the cell nucleus, where it presumably could con- 31 tribute to anti-inflammatory signalling [see Esmon,this issue,and ref. 24].…”

Section: Antithrombotic Protein C Pathwaymentioning

confidence: 99%

Causes of Thrombophilia Yet to Be Discovered: A Personal View

Griffin¹,

Deguchi²,

Fernández³

2000

Pathophysiol Haemos Thromb

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Prediction of genetic risk factors for venous thrombosis might best be left for only wise soothsayers. Nonetheless, based on the principle that hypercoagulability, either systemic or vascular-bed-specific, predisposes to thrombosis, we venture some speculations. Hyperactivity of platelets could be caused by elevated numbers of surface glycoproteins or defective signal transduction pathways. The reported efficacy of aspirin for prevention of venous thrombosis is consistent with the prediction that certain platelet defects may increase the risk of venous thrombosis. Hyperlipidaemia is associated with hypercoagulability, and lipoproteins exhibit procoagulant (e.g. triglyceride-rich particles and oxidized low-density lipoprotein) or anticoagulant (e.g. high-density-lipoprotein’s cofactor activity for activated protein C/protein S) activities. This leads to the prediction that defects in lipids and/or lipoproteins may increase the risk for venous thrombosis. Interestingly, statins were recently reported to prevent the occurrence of venous thrombosis in the HERS (Heart and Estrogen/Progestin Replacement) trial. We also predict that new defects in the protein C pathway (e.g. defective endothelial protein C receptor or novel cofactors for activated protein C/protein S) will be discovered. Risk factors affecting the majority of patients will likely in- volve new single nucleotide polymorphisms (SNPs) like the factor V nt G1691A or prothrombin nt G20210A SNPs. The Human Genome Project will soon accelerate discovery of new SNPs that are risk factors for venous thrombosis.

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Activated protein C resistance in patients with peripheral vascular disease

Cited by 37 publications

References 24 publications

Thrombophilias—Practical Implications and Testing Caveats

Thrombophilias—Practical Implications and Testing Caveats

Thrombophilia, polymorphisms, and vascular disease

Causes of Thrombophilia Yet to Be Discovered: A Personal View

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