HYPERCOAGUABLE STATE ASSOCIATED WITH A DEFICIENCY OF PROTEIN-C IN A THOROUGHBRED COLT

Protein C is a vitamin K-dependent serine protease with anticoagulant and profibrinolytic activity which is synthesized in the liver. Decrea sed protein C activity was detected in a Thoroughbred colt with clinic al and histopathologic evidence of recurrent venous thrombosis. Althou gh protein C activity was reduced, protein C antigen concentration was normal. Consumptive coagulopathies produce a decrease in both the fun ctional and antigenic concentrations of protein C, thus a defect in pr otein C synthesis was suspected. Inhibition of gamma-carboxylation sec ondary to vitamin K antagonism results in the synthesis of a protein C molecule with antigenicity, but without biological activity. However, there was no evidence of vitamin K antagonism. The hypercoaguable sta te resulting from the reduced activity of protein C in this colt was a ssociated with uncomplicated renal disease, rather than a protein C co nsumptive process such as endotoxemia. A primary hypercoaguable state due to a deficiency of protein C activity was diagnosed. Primary defic iencies of protein C activity have not been previously documented in h orses.