Starting warfarin therapy caused protein C antigen to decrease at a rate similar to factor VII, alongside the early appearance of an abnormal protein C with poor calcium-binding properties.
Observational (n=10)
Does warfarin alter protein C antigen levels and properties in patients starting oral anticoagulation?
The rapid decline of protein C, similar to factor VII, and the appearance of an abnormal protein C early in warfarin therapy may explain the initial poor antithrombotic efficacy and transient prothrombotic state.
Changes in protein C antigen (PC:Ag) have been compared with those in factor II, VII, IX and X antigens (II:Ag; VII:Ag; IX:Ag and X:Ag) in 10 patients starting on oral anticoagulant therapy with warfarin, monitored with thrombotest. Between days 0 and 3 of therapy, PC:Ag decreased at the same rate as VII:Ag, whilst IX:Ag, X:Ag and II:Ag decreased at progressively slower rates. On days 15 and 21, clotting proteins and PC:Ag did not differ significantly. Before and after warfarin, PC:Ag had the same mobility on crossed immunoelectrophoresis in Ca2+-free agarose gel; with Ca2+, a protein with faster anodal mobility appeared on day 1 and became maximal 5 d after warfarin was started. These findings indicate that the rate of PC decrease is closer to that of factor VII than those of factors IX, X and II, and that an abnormal PC with poor Ca2+-binding properties appears soon after treatment is started. The early decrease in the physiological inactivator (i.e. PC) might contribute to the poor antithrombotic efficacy of anticoagulant therapy during the first days.
Viganò et al. (Fri,) conducted a observational in Patients starting oral anticoagulant therapy (n=10). Warfarin vs. Baseline (before warfarin) was evaluated on Changes in protein C antigen (PC:Ag) compared with factor II, VII, IX and X antigens. Starting warfarin therapy caused protein C antigen to decrease at a rate similar to factor VII, alongside the early appearance of an abnormal protein C with poor calcium-binding properties.