Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary superior mesenteric venous thrombosis is sometimes preceded by peripheral thrombophlebitis. Inherited antithrombin-III deficiency is a recently recognized autosomal dominant trait, which is characterized by thrombophlebitis and pulmonary embolism. This case report illustrates many features of both entities and strongly suggest a causal relationship. While long-term therapy has yet to be established, prophylactic therapy is recommended when asymptomatic individuals with known antithrombin-III deficiency are at increased risk of thrombosis. The efficacy of heparin alone has been unreliable, whereas Coumadin has been encouraging. Antithrombin-III concentrates are being developed and theoretically should be helpful. Patients with thrombophlebitis or pulmonary embolism should be suspected of having antithrombin-III deficiency. Such individuals also represent one mechanism to explain "primary" mesenteric venous thrombosis.
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PMID:Inherited antithrombin-III deficiency causing mesenteric venous infarction: a new clinical entity. 113 28

Antithrombin-III activity was determined in 752 patients with a history of venous thrombosis and/or pulmonary embolism. 54 patients (7.18%) had an antithrombin-III activity below the normal range. Among these were 13 patients (1.73%) with proven hereditary deficiency. 14 patients were judged to have probable hereditary antithrombin-III deficiency, because they had a positive family history, but antithrombin-III deficiency could not be verified in other members of the family. In the 27 remaining patients (most of them with only slight deficiency) hereditary antithrombin-III deficiency was unlikely. The prevalence of hereditary antithrombin-III deficiency was higher in patients with recurrent venous thrombosis.
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PMID:The prevalence of hereditary antithrombin-III deficiency in patients with a history of venous thromboembolism. 408 8

We report a case of acute massive pulmonary embolism in a patient with antithrombin III deficiency. The patient was treated with rivaroxaban. The patient responded well to the therapy, and contrast-enhanced computed tomography showed nearly complete disappearance of the pulmonary embolism. Patients with low antithrombin III activity may have resistance to heparin therapy, leading to insufficient anticoagulation during the acute phase of thromboembolism. This case suggests that direct oral anticoagulants, such as rivaroxaban, may be effective first-line agents for treating venous thromboembolism in patients with antithrombin III deficiency. <Learning objective: Recently, direct oral anticoagulants represent a novel treatment option for venous thromboembolism with several practical advantages over conventional therapy. Antithrombin-III deficiency may lead to insufficient anticoagulation during the acute phase of thromboembolism. The present case suggests that rivaroxaban is a direct Factor Xa inhibitor and does not require cofactors such as antithrombin-III, thus it is suitable for anticoagulation therapy in patients with low antithrombin-III activity.>.
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PMID:Successful treatment of a massive pulmonary embolism using rivaroxaban in a patient with antithrombin III deficiency. 3027 20