The complex mechanism of the factors concerned in blood coagulation has been investigated in many ways, not least among these being a study of such factors during anticoagulant therapy, and by the use of plasma from patients treated with anticoagulant drugs in cross mixture experiments with plasma from patients having congenital coagulation defects. Earlier results from such investigations indicated a simple deficiency of prothrombin and VII. It is now known, however, that Christmas factor (Douglas, 1955; Biggs, 1956; Naeye, 1957), plasma thromboplastin antecedent (Naeye, 1957), and Prower-Stuart factor (Telfer, Denson, and Wright, 1956; Hougie, Barrow, and Graham, 1957; Denson, 1958) are all reduced. Factor X* (Duckert, Fliickiger, Matter, and Koller, 1955) is also reduced early in therapy. The existence of the latter factor as a separate entity, however, has not been estab lished, and it is probably an intermediate product of thromboplastin formation. Horder (1958) studied levels of factor VII, Prower Stuart factor, and prothrombin, together with the partial thromboplastin time, and thromboplastin generation in one case receiving anticoagulant therapy with the coumarin derivative phenprocoumon ( marcoumar; 4-hydroxy-3-(1-phenylpropyl)coumarin). Hicks and Bonnin (1959) compared the reduction in plasma thromboplastic factors, the one-stage prothrombin time, and the two-stage prothrombin levels in several cases receiving anticoagulant therapy with different drugs, and concluded that the one-stage assay provided an adequate measure of the reduction in thromboplastic factors.
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K. W. E. Denson (1961) studied this question.
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