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Case Reports
. 1995 Sep;17(3):189-92.
doi: 10.1016/1054-139X(94)00188-K.

Antithrombin III deficiency, deep venous thrombosis, and oral contraceptive use

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Case Reports

Antithrombin III deficiency, deep venous thrombosis, and oral contraceptive use

M J Werner. J Adolesc Health. 1995 Sep.

Abstract

PIP: Oral contraceptive use is a risk factor for the development of deep venous thromboses in adolescents. Most patients with venous thromboses have no well-defined disorder of hemostasis. Identifying such abnormalities in some patients, however, will allow the best decisions to be made concerning contraceptive practices, the treatment of acute thromboses, and long-term prophylaxis. For example, studies have established a relationship between oral contraceptive use and changes in antithrombin III. A case is presented which highlights the multifaceted nature of venous thromboses and the need for clinicians to be aware of potential hypercoagulable states and their implications for patient care. A 16-year-old Black female had a five-day history of rapidly progressive left leg swelling and pain. Five weeks earlier she was diagnosed with dysfunctional uterine bleeding and placed upon a triphasic oral contraceptive. This patient had multiple risks for thrombosis including obesity, prolonged periods of bed rest, oral contraceptive use, and possibly hypercoagulability related to markedly decreased antithrombin III levels. The patient was initially felt to be at high risk for a congenital antithrombin III deficiency because of her profoundly low plasma level and thus treated with antithrombin III concentrates. Based on the subsequent normalization of her antithrombin III levels, however, it appears that her acquired deficiency resulted from either accelerated utilization associated with an extensive thrombus or oral contraceptive use or the combination of both. Decreases in antithrombin III of this magnitude have not been previously reported in association with either oral contraceptives or extensive thromboses. The clinical importance of acquired antithrombin III deficiency for an increased risk of venous thromboembolism remains uncertain.

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