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Hypercoagulability states in upper-extremity deep venous thrombosis
F W Leebeek1, N A Stadhouders, D van Stein
1University Hospital Rotterdam "Dijkzigt", Department of Hematology, Rotterdam, The Netherlands. leebeek@haed.azr.nl
American Journal of Hematology
|April 3, 2001
Summary
Deep venous upper extremity thrombosis (DVTUE) is rare. Antiphospholipid antibodies are common causes, while Factor V Leiden and prothrombin gene variants are not significant factors in DVTUE.
Area of Science:
- Hematology
- Vascular Medicine
- Thrombosis Research
Background:
- Deep venous thrombosis of the upper extremity (DVTUE) is an uncommon condition.
- Predisposing factors include central venous catheters, malignancy, and exercise.
- The role of hypercoagulable states in DVTUE pathogenesis is not well understood.
Purpose of the Study:
- To investigate the prevalence of genetic and acquired thrombophilia in patients with DVTUE.
- To determine the contribution of various coagulation disorders to DVTUE.
- To compare coagulation abnormalities in spontaneous versus secondary DVTUE.
Main Methods:
- Consecutive patients with DVTUE were evaluated.
- Genetic thrombophilia screening included Factor V Leiden mutation, prothrombin G20210A gene variant, and deficiencies in antithrombin, protein C, and protein S.
- Acquired thrombophilia assessment included lupus anticoagulant and anticardiolipin antibodies.
Main Results:
- A hypercoagulable state was identified in 32% of patients.
- Antiphospholipid antibodies (lupus anticoagulant or anticardiolipin) were the most frequent abnormality, found in 27% of patients.
- Factor V Leiden mutation was present in two patients, antithrombin deficiency in one; other tested genetic factors were absent. No significant difference in coagulation abnormalities was observed between spontaneous and secondary DVTUE subgroups.
Conclusions:
- Antiphospholipid antibodies are frequently implicated in the pathogenesis of DVTUE.
- Factor V Leiden mutation, prothrombin G20210A gene variant, protein C deficiency, and protein S deficiency do not appear to be major contributors to DVTUE.