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Reviews |
1 Angelo Bianchi Bonomi Hemophilia and Thrombosis Center, Department of Internal Medicine, University and IRCCS Maggiore Hospital, 20122 Milan, Italy
aAddress correspondence to this author at: Hemophilia and Thrombosis Centre, Via Pace 9, 20122 Milan, Italy. Fax 39-02-5516093; e-mail armando.tripodi{at}unimi.it.
Until recently, laboratory diagnosis of thrombophilia was based on investigation of the plasmatic anticoagulant pathways to detect antithrombin, protein C, and protein S deficiencies and on the search for dysfibrinogenemia and anti-phospholipid antibodies/lupus anticoagulants. More recently, laboratory investigations have been expanded to include activated protein C (APC) resistance, attributable or not to the presence of the factor V Leiden mutation; hyperprothrombinemia attributable to the presence of the prothrombin gene mutation G20210A; and hyperhomocysteinemia attributable to impairment of the relevant metabolic pathway because of enzymatic and/or vitamin deficiencies. All of the above are established congenital or acquired conditions associated with an increased risk of venous and, more rarely, arterial thrombosis.
Testing is recommended for patients who have a history of venous thrombosis and should be extended to their first-degree family members. Because most of the tests are not reliable during anticoagulation, it is preferable to postpone laboratory testing until after discontinuation of treatment.
Whenever possible, testing should be performed by means of functional assays. DNA analysis is required for the prothrombin gene mutation G20210A. Laboratory diagnosis for anti-phospholipid antibodies/lupus anticoagulant should be performed by a combination of tests, including phospholipid-dependent clotting assays and solid-phase anti-cardiolipin antibodies. Hyperhomocysteinemia can be diagnosed by HPLC methods or by fluorescence polarization immunoassays.
The following articles in journals at HighWire Press have cited this article:
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  C. Infante-Rivard and C. R. Weinberg Parent-of-Origin Transmission of Thrombophilic Alleles to Intrauterine Growth-Restricted Newborns and Transmission-Ratio Distortion in Unaffected Newborns Am. J. Epidemiol., November 1, 2005; 162(9): 891 - 897. [Abstract] [Full Text] [PDF]
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 G. A. Knoll, P. S. Wells, D. Young, S. L. Perkins, R. M. Pilkey, J. J. Clinch, and M. A. Rodger Thrombophilia and the Risk for Hemodialysis Vascular Access Thrombosis J. Am. Soc. Nephrol., April 1, 2005; 16(4): 1108 - 1114. [Abstract] [Full Text] [PDF]
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 C. M. Johnson, L. Mureebe, and D. Silver Hypercoagulable States: A Review Vascular and Endovascular Surgery, March 1, 2005; 39(2): 123 - 133. [Abstract] [PDF]
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 A. Tripodi, V. Chantarangkul, I. Martinelli, P. Bucciarelli, and P. M. Mannucci A shortened activated partial thromboplastin time is associated with the risk of venous thromboembolism Blood, December 1, 2004; 104(12): 3631 - 3634. [Abstract] [Full Text] [PDF]
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Z. K. Baldwin, A. J. Comerota, and L. B. Schwartz Catheter-Directed Thrombolysis for Deep Venous Thrombosis Vascular and Endovascular Surgery, January 1, 2004; 38(1): 1 - 9. [Abstract] [PDF]
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 A. Tripodi, A. Biasiolo, V. Chantarangkul, and V. Pengo Lupus Anticoagulant (LA) Testing: Performance of Clinical Laboratories Assessed by a National Survey Using Lyophilized Affinity-purified Immunoglobulin with LA Activity Clin. Chem., October 1, 2003; 49(10): 1608 - 1614. [Abstract] [Full Text] [PDF]
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G. Podda, E. M. Faioni, M. L. Zighetti, and M. Cattaneo No effect of fasting plasma total homocysteine on protein C activity in vitro Blood, March 15, 2003; 101(6): 2446 - 2446. [Full Text] [PDF]
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K. G. Mann and M. Kalafatis Factor V: a combination of Dr Jekyll and Mr Hyde Blood, January 1, 2003; 101(1): 20 - 30. [Full Text] [PDF]
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