Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (820 page)

   Prekallikrein: 55–207%

   High molecular weight kininogen: 59–135%

   Use

   Quantitation of clotting factors can be achieved through assays specific for each factor, whether chromogenic or, more commonly, automated clotting tests. A plasma deficient in each factor is purchased and used to find out whether it corrects the patient’s plasma. When there is correction, the patient’s defect has been identified and can be quantitated using a reference curve obtained with dilutions of normal pooled plasmas.

   A plasma deficient in any factor(s) active in the extrinsic and common pathway (VII, V, X, and II) results in a prolonged PT. These four factors are quantitated in assays that use PT reagents as activators. Plasma deficient in factors active in the intrinsic (and common) pathway (high molecular weight kininogen, prekallikrein, and factors XII, XI, IX, and VIII) prolongs the PTT and is assayed with PTT reagents.

   When to use clotting factor tests:

   When a discrete congenital clotting deficiency (most commonly factors VIII and IX) is suspected

   Occasionally, to separate the effect of oral anticoagulants (decrease in factors II, VII, IX, and X but not V or VIII) from liver disease (deficiencies of all these clotting factors, including factor V, but not factor VIII)

   To measure blood heparin (factor Xa inhibition) and possibly when therapeutic inhibitors of factor X are used therapeutically

   Interpretation

Increased In

   
Factor II:
The genetic mutation
G20210A
predisposes to thromboembolism.

   
Factor VII:
Pregnancy and oral contraceptive use. An increase in factor VII has been linked to thrombophilia in some studies.

   
Factor VIII:
Acute-phase reactant (acute inflammatory conditions), pregnancy, and the use of oral contraceptives. If markedly increased, it may predispose to thromboembolism.