Factor XII, also known as Hageman factor, is indicated when factor XII deficiency is suspected.
The reference range of factor XII is 60-150% of normal. 
Decreased factor XII levels are associated with congenital deficiency. No bleeding diathesis is associated with its deficiency.
Collection and Panels
Container: Blue-top vacuum tube
Collection method: Routine venipuncture
Other instructions: All samples must be sent in a sealed, leak-proof container marked with a biohazard sticker to comply with Occupational Safety and Health Administration (OSHA) safety standards
Panels: Quantitative functional assays of coagulation factors
Quantitative functional assays of coagulation factors
Factor XII is synthesized in the liver. Factor XII, factor XI, high–molecular-weight kininogen (HK), and prekallikrein (PK) are referred to as the contact factors.
The gene for factor XII is located on chromosome 5.
Factor XII is responsible for the contact activation of blood coagulation as seen in the activated partial thromboplastin time test (aPTT). In this clinical test, plasma is mixed with a reagent such as kaolin, glass, or celite, which provides a negatively charged surface. Contact activation involves both protein-protein and protein-surface interactions that activates factor XII.
Factor XIIa activates factor XI, which in turn leads to the activation of factor IX. Factor XII, HK, and PK are necessary for a normal aPTT, but they do not appear to be required for normal hemostasis.  This is reflected in the fact that individuals who are deficient in any of these factors do not have a hemorrhagic diathesis, even after significant trauma or surgery. However, factor XII, HK, PK and complement factor C1q participate in inflammatory responses that involve blood coagulation, fibrinolysis, and generation of kinins. [3, 4]
Targeted deletion of factor XII in a mouse model does not impair hemostasis but does result in reduced generation of inflammatory mediators. 
Factor XII deficiency is associated with an increased tendency toward thrombosis in animal models  and perhaps in humans.  Therefore, activation of the contact factors plays a much bigger role in thrombosis than hemostasis. The contact system usually works on the surface of endothelial cells. Kallikrein activates factor XII, which, then initiates fibrinolysis by causing activation urokinase. Therefore, activation of the contact system on cell surfaces differs mechanistically from activation on a charged surface in the aPTT. The kallikrein/kinin system has been theorized as a functional counterbalance to the renin–angiotensin system by preventing thrombosis and lowering blood pressure in vivo. [2, 8]
Factor XII testing is indicated when factor XII deficiency is suspected.
No hemorrhagic diathesis is associated with congenital factor XII deficiency.
Potential limitations of the factor XII test include partially clotted specimens owing to a poor mixture of anticoagulant (3:2 sodium citrate as per manufacturer’s blue-topped tube), overfilled or underfilled test tubes (altering the ratio of blood to anticoagulant [9:1]), improperly stored plasma, contamination with heparin, dilution of the collected sample if indwelling catheters are used, or analytical errors such as lipemic, icteric, or hemolyzed plasma, which may interfere with photoelectric measuring instruments.