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Angiology
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Paget-Schroetter Syndrome Associated with FV:Q506 and Prothrombin 20210A

A Case Report

Nilgün Sayinalp, MD

Departments of Hematology, Eser Sitesi B-3 /10 Bahçelievler Ankara 06490 Turkey

Osman Ilhami Özcebe, MD

Departments of Hematology, Hacettepe University Medical School, Ankara 06490 Turkey

Serafettin Kirazli

Departments of Hematology, Hacettepe University Medical School, Ankara 06490 Turkey

Riza Dogan, MD

Departments of Cardiovascular Surgery, Hacettepe University Medical School, Ankara, Turkey

Semra V. Dündar, MD

Departments of Hematology, Hacettepe University Medical School, Ankara 06490 Turkey

Aytemiz Gürgey, MD

Departments of Cardiovascular Surgery, Hacettepe University Medical School, Ankara, Turkey

Effort thrombosis of the axillary-subclavian vein (Paget-Schroetter syndrome) develops usually secondary to heavy arm exertion. An underlying chronic venous compressive anomaly at the thoracic outlet or intimal damage of the axillary vein following forceful hyperabduction, external rotation of the shoulder joint has been proposed to explain the pathophysiology of this thrombosis. This condition is usually not attributed to an under lying hypercoagulability such as deficiency of natural coagulation inhibitors. Here, the authors present a case with thrombosis of the axillary-subclavian vein following an effort, with factor V Leiden and prothrombin 20210A mutations. Both factor V Leiden and the genetic variant in the prothrombin gene have been shown to confer an increased risk for venous thrombosis. Although rare, effort thrombosis may develop in a patient with hereditary thrombophilia, so laboratory evaluation should include the common causes of thrombosis.

Angiology, Vol. 50, No. 8, 689-692 (1999)
DOI: 10.1177/000331979905000811


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