protein S deficiency


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protein S deficiency

Hematology An AD condition clinically and therapeutically similar to heterozygous protein C deficiency, characterized by pulmonary thrombosis, DVT, thrombophlebitis
References in periodicals archive ?
Reported causes of thrombophilia in HIV-infected subjects include antiphospholipid syndrome [1], increased platelet activation [1], elevated homocysteinemia [2], elevated plasma factor VII activity [2], lupus anticoagulant [3], activated protein C resistance [3], protein C deficiency [3,4], and acquired protein S deficiency [4-10].
Twelve HIV-seropositive with laboratory-confirmed protein S deficiency were identified, and their clinical features are summarized (Table 1).
But HIV is also associated with a variety of acquired coagulopathies that increase the incidence of venous and arterial thrombosis, including antiphospholipid-anticardoplipin antibodies, increased platelet activation, elevated serum homocysteine levels, lupus anticoagulant, elevated plasma factor VII activity, activated protein C resistance, protein C deficiency, and protein S deficiency [1-10].
These protein deficiencies/abnormalities are genetic and include entities such as antithrombin deficiency, protein C deficiency, protein S deficiency, Factor V Leiden mutation, prothrombin 20210, and dysfibrinogenemia, among others.
The search for risk factors for central retinal vein occlusion in this young patient revealed protein S deficiency and a history of iron deficiency.
Key Words: central retinal vein occlusion, protein S deficiency, sickle cell disease
Acquired Protein S deficiency may be seen during pregnancy, oral contraceptive or oral anticoagulant therapy, liver disease, diabetes mellitus, postoperative complications, septicemia and various inflammatory syndromes.
Because the new Corgenix test utilizes a monoclonal antibody specific for Free Protein S, it provides a more specific method for laboratory diagnosis of Protein S deficiency.
Protein S deficiency was first described in 1984 by Comp et al.
Hopefully these new insights will result in the near future in new recommendations for the laboratory diagnosis of protein S deficiency.
In addition to the significantly differing median NRs observed between healthy donors and thrombophilia patients without FV Leiden, protein C, or protein S deficiency (PWD), the difference becomes obvious in the ROC curve analysis either with the PWD group or the healthy donor group as negative control group (Fig.
Clinical studies have clearly shown the relevance of hereditary protein S deficiency for the development of thromboembolism [1, 4].