Reported causes of thrombophilia in HIV-infected subjects include antiphospholipid syndrome , increased platelet activation , elevated homocysteinemia , elevated plasma factor VII activity , lupus anticoagulant , activated protein C resistance , 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).
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.
Primary hypercoagulable states involve specific abnormalities of hemostasis and include antithrombin III deficiency, protein C deficiency, protein S deficiency, lupus anticoagulant, disorders of fibrinolytic system (eg, disorders of tissue plasminogen activator, abnormal plasminogen and hypoplasminogenemia), dysfibrinogenemia factor XII deficiency, and anticardiolipin antibody syndrome.
Protein S deficiency is the most frequent cause of idiopathic venous thrombosis, accounting for about 5% to 8% of cases.
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.