British Journal of Haematology · 1984 · 106 citations · 30 references
MedicineHematologyImmunologyClinical BiochemistryClinical ImmunologyHemostasisAnticoagulant TherapyAnticoagulation TherapyAntithrombotic TherapyCoagulation AbnormalitiesCoagulation DisordersThrombosisAnticoagulant BiomarkersMonitoring Of Anticoagulant TherapyPlasma Anticoagulant ActivityProtein C Pathway ImpairmentProtein C SystemTherapeutic Anticoagulation
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.
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Deficiency of protein C in congenital thrombotic disease.
John H. Griffin, B. L. Evatt, T S Zimmerman et al. · Journal of Clinical Investigation · 1981 · 1.3K citations · Full text
Medicine, Genetics, Hematology +14
Walter Kisiel · Journal of Clinical Investigation · 1979 · 508 citations · Full text