The blood flowing through our bodies typically maintains a fine balance between the mechanism that causes the blood that escapes outside the vessels to clot (hemostasis), the mechanism that prevents the blood flowing inside our vessels from clotting (coagulation inhibition), and the mechanism dissolving blood clots (fibrinolysis) and returning them to their original liquid state. An imbalance between these functions can lead to conditions in which the blood does not clot, as in hemophilia.1 Alternatively, conditions can emerge as a result of blocked blood vessels, such as cerebral infarction and deep vein thrombosis.

Hemophilia is classified into two varieties—hemophilia A and hemophilia B—depending on the type of coagulation factor that is deficient. Hemophilia A is a hemorrhagic disease that occurs due to a reduced hemostatic function stemming from a lack of coagulation factor VIII in the blood. Diagnosing hemophilia A involves quantitative testing for coagulation factor VIII. This testing is also conducted to monitor the disease after coagulation factor VIII drugs have been administered.

Quantitative testing for coagulation factor VIII mainly uses either the coagulation one-stage assay (using an APTT reagent) or the chromogenic assay. To date, the coagulation one-stage assay has been used more widely. However, with this method, measurement values are known to deviate, depending on the type of reagent used.

For this reason, the chromogenic assay is commonplace in Europe, and the Council of Europe publication European Pharmacopoeia requires the titer of all coagulation factor drugs to be measured with the chromogenic assay. In Japan as well, the Japanese Society on Thrombosis and Hemostasis calls for the introduction of factor VIII assay testing using the chromogenic assay.2