protein s deficiency/protease

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Protein S Deficiency

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Protein S deficiency is a rare disorder, characterized by reduced activity of protein S, a plasma serine protease with complex roles in coagulation, inflammation, and apoptosis.[1] A deficiency in protein S characteristically demonstrates the inability to control coagulation, resulting in the

Protein Z/Z-dependent protease inhibitor (PZ/ZPI) anticoagulant system and thrombosis.

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A new anticoagulant system involving a serpin has been recently characterised. The protein Z/Z-dependent protease inhibitor (PZ/ZPI) system inhibits activated factors X, XI and IX by different mechanisms. By homology with other anticoagulant systems (antithrombin or the protein C/protein S),

Portal vein thrombosis in a patient with HIV treated with a protease inhibitor-containing regimen.

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We report a case of an HIV seropositive female patient treated with a protease inhibitor-containing regimen who developed recurrent severe life-threathening episodes of haematemesis over time, caused by ruptured oesophageal varices as a consequence of a portal vein thrombosis. Coagulation tests

Preliminary Data From the Study of Coagulative Profile of HIV Infected Individuals Suggest a Role For Point Mutations in the Gene in Protein S Deficiency in Individuals Undergoing Highly Antiretroviral Therapy.

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UNASSIGNED HIV infection is a known prothrombotic condition but factors involved are still controversial. A role for antiretrovirals, especially protease inhibitors, was advocated. UNASSIGNED The study aimed to analyze the levels of anticoagulant proteins in virally suppressed HIV-infected subjects

Characterization of endoplasmic reticulum-associated degradation of a protein S mutant identified in a family of quantitative protein S deficiency.

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BACKGROUND Misfolded and unassembled glycoproteins are eliminated from the endoplasmic reticulum (ER) lumen by the ER-associated degradation (ERAD). We previously identified a Tyr595Cys (Y595C) mutation of protein S (PS) in a family of a quantitative PS deficiency. The mutation causes intracellular

[Protein C, protein S].

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Protein C is a potent inhibitor of blood coagulation, and, in addition, appears to be a profibrinolytic agent. In a first step, protein C must be converted to a serine protease. This activation is catalyzed by a complex formed between thrombin and thrombomodulin, an endothelial cell surface protein.

Anticoagulant protein C pathway defective in majority of thrombophilic patients.

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A defect involving poor anticoagulant response to activated protein C (APC), an anticoagulant serine protease known to inactivate factors Va and VIIIa in plasma, was recently reported and the existence of a novel APC cofactor was suggested. To define the frequency of this defect among 25 venous

Familial thrombophilia due to a previously unrecognized mechanism characterized by poor anticoagulant response to activated protein C: prediction of a cofactor to activated protein C.

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Although patients with thromboembolic disease frequently have family histories of thrombosis, well-defined defects such as inherited deficiencies of anticoagulant proteins are found only in a minority of cases. Based on the hypothesis that a poor anticoagulant response to activated protein C (APC)

HIV-Associated Venous Thromboembolism.

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HIV infection has been recognized as a prothrombotic condition and this association has now been proven by a large number of studies with a reported VTE frequency among HIV-infected patients ranging from 0.19% to 7,63 %/year. HIV infection is associated with a two to tenfold increased risk of venous

Venous thrombosis among patients with AIDS.

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Thrombosis has been considered an uncommon complication in patients with AIDS. In a 42-month period, 28 adult male homosexuals with AIDS experienced 34 thrombotic events. All but three received HAART regimen, two a successful round of double nucleoside analog therapy, and one patient received no

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