Saphenous vein thrombophlebitis (SVT): A deceptively benign disease
Autor: | Marcel Scheinman, Anil Hingorani, William Yorkovich, Elke Lorensen, Patrick DePippo, Enrico Ascher, Judith N. Hanson |
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Rok vydání: | 1998 |
Předmět: |
Male
Deep vein Thrombophlebitis Gastroenterology Protein S Ambulatory Care Ultrasonography Doppler Duplex biology Incidence Antithrombin Anti-Inflammatory Agents Non-Steroidal Factor V Blood Coagulation Disorders Middle Aged Thrombosis medicine.anatomical_structure Treatment Outcome Female Prothrombin medicine.symptom Cardiology and Cardiovascular Medicine medicine.drug Adult medicine.medical_specialty Serine Proteinase Inhibitors Antithrombin III Postphlebitic Syndrome Varicose Veins Fibrinolytic Agents Internal medicine Varicose veins medicine Humans Saphenous Vein Antigens Aged business.industry Vascular disease Heparin Anticoagulants DNA Femoral Vein medicine.disease Surgery Hemostasis Factor X Mutation biology.protein Warfarin business Phlebitis Follow-Up Studies Protein C |
Zdroj: | Journal of Vascular Surgery. 27(4):677-680 |
ISSN: | 0741-5214 |
DOI: | 10.1016/s0741-5214(98)70233-2 |
Popis: | Purpose: The association between deep vein thrombosis (DVT) and the hypercoagulable state is a well-established entity. However, the association between saphenous vein thrombophlebitis and coagulation abnormalities has not been investigated. Although thrombosis of varicose veins typically runs a benign course, phlebitis of the saphenous system may propagate to the deep system or saphenofemoral junction that requires more aggressive therapy. Given the potential similarity in clinical outcome between saphenous vein thrombophlebitis (SVT) and DVT, we have investigated the coagulation profile of patients presenting with isolated SVT. Methods: Seventeen consecutive patients who presented to our vascular laboratory with isolated SVT had a coagulation profile performed that included antithrombin III (AT III), protein C (PC), protein S (PS) antigen and activity levels, activated protein C (APC) resistance, factor V DNA mutation, and coagulation factors II and X. All patients had duplex scans performed on both the superficial and deep venous systems. Patients with SVT only were treated with nonsteroidal antiinflammatory drugs (NSAIDs) and warm soaks as outpatients, whereas those patients found to have DVT or a clot at the saphenofemoral junction were fully anticoagulated with heparin and coumadin therapy. All 17 patients had at least one repeat coagulation profile performed up to 5 months after their SVT occurrence to ensure that the results of hypercoagulability were not transient. Results: Ten (59%) of the 17 patients with SVT had abnormal coagulation profiles on initial presentation. All 10 patients who were hypercoagulable had repeat tests and 6 (35%) remained abnormal. Four patients who had abnormal results converted to normal values. Seven patients with normal coagulation profiles on initial presentation had repeat tests and all remained normal. Conclusion: The incidence of the hypercoagulable state in patients with SVT is high. Thirty-five percent of patients with isolated SVT had consistently abnormal coagulation profiles. Patients with SVT may be prone to the development of DVT or saphenofemoral junction thrombophlebitis and should be closely followed after the initial diagnosis of hypercoagulability. (J Vasc Surg 1998;27:677-80.) |
Databáze: | OpenAIRE |
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