Chromogenic substrate (S-2238) prothrombin assay in prothrombin deficiencies and abnormalities. Lack of identity with clotting assays in congenital dysprothrombinemias.

Prothrombin was assayed using chromogenic substrate of S-2238 for patients who were being treated with coumarin, for patients who had liver disease, and for patients who had congenital hypoprothrombinemias and dysprothrombinemias. In coumarin therapy and in patients with liver disease the levels found correlated well with the one-stage clotting methods. The same was true for heterozygous and homozygous "true" prothrombin deficiency.

Factor VII survival studies in factor VII Padua abnormality.

Two patients with factor VII Padua abnormality were studied during prophylactic administration of factor VII concentrates for tooth extractions. The amounts administered were 15.8 and 17.

Factor VII Padua 2: another factor VII abnormality with defective ox brain thromboplastin activation and a complex hereditary pattern.

A new factor VII abnormality is presented. The propositus was a 9-yr-old child who presented a mild bleeding tendency characterized by epistaxis and easy bruising. The parents were not consanguineous, but they came from the same area.

Short heparin thrombin clotting time, increased fibrinogen and platelet aggregates count in coronary disease: a probable hypercoagulable state.

Several indices of plasmatic and platelet coagulability (H.T.C.