Summary
After addition of a suspension of normal platelets the coagulation defect in Hageman plasma was corrected. The recalcification time became nearly normal and it was possible to activate the plasma by treatment with glass.
Hageman serum was unable to accelerate thromboplastin activation in normal plasma. After addition of a platelet suspension and exposure to glass the Hageman serum became as active as normal serum treated in the same way.
The results suggest that the Hageman trait might be caused by the presence of an excess of an inhibitor against glass activation and not by a deficiency in a clotting factor.
A study of previously published data on the Hageman trait shows that it is possible to explain many observations by the presence of such an inhibitor.
