Abstract
Protein S is a vitamin K-dependent anticoagulant protein. It functions as a cofactor of activated protein C to inactivate activated factor V (FVa) and activated factor VIII (FVIIIa). Its deficiency is a rare condition and can lead to deep vein thrombosis, pulmonary embolism or stroke. It is often treated with long-term anti-coagulant therapy. Protein S deficiency may be hereditary or acquired; the latter is usually due to hepatic diseases or a vitamin K deficiency. Protein S deficiency manifests as an autosomal dominant trait; manifestations of thrombosis are observed in both heterozygous and homozygous genetic deficiencies of protein S. This case report is of DVT due to Protein S deficiency in a 53 year old male. Venous Doppler was used to diagnose DVT and free Protein S level measured by ELISA. IVC filter was placed on the third day of admission.
Highlights
Protein S (PS) deficiency is an autosomal-dominant inherited disorder of coagulation, either homozygous or heterozygous
Protein S deficiency was first described in 1984.3 The association of protein S deficiency with arterial thrombosis appears coincidental or weak at best.[4]
An inferior vena cava (IVC) filter was placed in the patient to prevent any pulmonary thromboembolism as the clot was massive which is similar to a case report with placement of IVC filter in a case of pulmonary and deep venous thrombosis.[8]
Summary
Protein S (PS) deficiency is an autosomal-dominant inherited disorder of coagulation, either homozygous or heterozygous. 2-5% in patients with deep venous thrombosis (DVT) or pulmonary embolism (PE). This is as prevalent as protein C deficiency (5-8%) but less common than antithrombin III deficiency (12-15%).[1] Patients with phenotypic PS deficiency have a 50% chance of developing recurrent thrombosis before age 45.2 In homozygous individuals, a severe life threatening form of thrombosis called purpura fulminans can result in early infancy.
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