However, for any given DIC stimulus, more than one activation pathway may be involved (see Table 4).[6,7] When endothelial cells are damaged, the exposed collagen activates FXII, which stimulates the intrinsic pathway and converts
prekallikrein to kallikrein to activate fibrinolysis.
Basically, aPTT is affected by the activities of clotting factors XII, XI, X, IX, VIII, V, II, and I, as well as by high molecular weight kininogen and
prekallikrein. Measuring the PT and the thrombin time (TT) can efficiently narrow the number of required analyses.
Activated factor XII converts
prekallikrein into kallikrein, and the latter cleaves high-molecular-weight kininogen into bradykinin, which mediates many of the biologic effects of this system.
An isolated result showing aPTT prolongation suggests a deficiency or inhibitor of one or more of the intrinsic pathway clotting factors (
prekallikrein, high molecular weight kininogen, factors XII, XI, IX, and VIII).
Fibrinogen Vitamin K-dependent Contact Fibrinogen Factor II Factor XII Factor V Factor VII HMWKa Factor VIII Factor IX
Prekallikrein (b) Factor XIII Factor X Factor XI (a) HMWK, high-molecular weight kininogen, also known as Fitzgerald factor.