Initial set of tests to investigate a hemostatic abnormalities include PT, aPTT and platelet counts to assess the major components of the hemostatic system. PT and aPTT may be extended in many situations and performing a battery of tests of coagulation is often needed to determine the cause of the hemostatic anomaly , one of these tests being  TT.

In vivo: thrombin binds to the central domain of fibrinogen and releases proteolytic  the A and B fibrinopeptides, resulting in the fibrin monomers; following their polymerization, the fibrin clot formation, whose resistance to degradation by plasmin is mainly influenced by the cross-linked with calcium mediated FXIIa.

In vitro: TT is a plasma clotting time required citrate, low platelets after addition of thrombin and Ca2 ions.

The pro-clotting enzyme waterfall (respectively the “intrinsic”, “extrinsic” and “common” clotting) is surpassed by adding exogenous thrombin. Thus TT mainly reflects the functions and interactions between the exogenous thrombin and the endogenous fibrinogen.

Recommendations for testing

– Investigate the cause of a prolonged PT or aPTT;

– CID diagnosis;

– Disfibrinogenemias , hypo- / afibrinogenemias;

– Monitoring of treatment with plasminogen activators (streptokinase and urokinase).

Reference values ​​- ≤21s.

Interpretation of results

Extension TT: hypo /dis / afibrinogenemias,  heparin therapy , argatroban, hirudin, CID, multiple myeloma (in this paraprotein) present in plasma of anti-thrombin (eg. In amyloidosis), presence of degradation products of fibrinogen / fibrin (PDF), uremia, severe liver disease, malignancy, treatment with plasminogen activators (streptokinase, urokinase, tissue plasminogen activator).

TT will be increased when the level of functional fibrinogen is <100 mg / dL.

An immeasurable prolonged TT is generally the result of the presence of  heparin or, more rarely, the presence of antithrombin antibodies or afibrinogenemia.