Why the study?
Patients with low levels of antithrombin III are at an increased risk of developing arteriovenous thromboembolic disease.
Does rivaroxaban improve thrombus resolution in a patient with antithrombin III deficiency complicated by deep vein thrombosis and pulmonary embolism?
Does rivaroxaban improve thrombus resolution in a patient with antithrombin III deficiency complicated by deep vein thrombosis and pulmonary embolism?
Direct factor Xa inhibition with rivaroxaban provides an effective alternative for anticoagulation in patients with antithrombin III deficiency who may be heparin-resistant.
May support rivaroxaban in antithrombin III deficiency; hypothesis-generating and should not change practice.
BACKGROUND: Patients with low levels of antithrombin III (AT III) are at an increased risk of developing arteriovenous thromboembolic disease. CASE SUMMARY: We report a case of a 28-year-old woman who presented with a 1-week history of spontaneous right calf pain and swelling. A heterozygous AT III deficiency, phenotypically expressed as deep vein thrombosis, was reported in the patient's mother and sister. Blood workup revealed residual AT III activity at 58% with normal protein C and protein S levels. Computed tomographic angiography (CTA) revealed subsegmental bilateral pulmonary embolism (PE) and deep vein thrombosis in the right leg extending into the inferior vena cava up to the confluence of the left renal vein. Placement of an inferior vena cava filter was not considered. Given the patient's haemodynamic stability, anticoagulant therapy with 15 mg of rivaroxaban twice a day was initiated instead. Echocardiography after 10 days of treatment revealed complete resolution of the thrombus located in the inferior vena cava, while CTA revealed complete resolution of the PE. DISCUSSION: Patients with AT III deficiency are likely to be heparin-resistant and will require higher heparin doses or the administration of AT III replacement therapy for the treatment of thrombosis, both of which are associated with an increased risk for haemorrhagic complications. Direct factor Xa inhibition by rivaroxaban provided an alternative mechanism for anticoagulation, which was found to be particularly useful in this patient with familial AT III deficiency, deep vein thrombosis, and PE.
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Appignani et al. (2019) studied this question.
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