, a protein responsible for the formation of clots (thrombi) in blood vessels.
D-dimers and FDPs are present and measurable, albeit in very low concentration, even in perfectly healthy subjects, since the various pro-coagulant and anti-coagulant factors are in a condition of perfect homeostatic equilibrium.
On the two plates of this scale we find on the one hand the activation of coagulation mechanisms, with consequent formation of fibrin, and on the other, the lysis of stabilized fibrin and the inhibition of circulating thrombin (necessary for the activation of fibrinogen into fibrin).
Unfortunately, in various conditions, pathological or otherwise, this balance is lost and - depending on whether the balance hangs on the side of the first or second plate - there may be thrombotic diseases (excessive blood coagulability) or hemorrhagic (insufficient blood coagulability). In the first case, the body tries to compensate for the problem by increasing the fibrinolytic phenomena (degradation of fibrin), with a consequent increase in the D-dimers present in the blood.
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In the clinical setting, the determination of the D-dimer in the blood is part of the diagnostic process of deep vein thrombosis and pulmonary embolism. This test is therefore particularly useful in the study of pathologies related to excessive or inappropriate coagulation.
D-dimers and FDPs are present and measurable, albeit in very low concentration, even in perfectly healthy subjects, since the various pro-coagulant and anti-coagulant factors are in a condition of perfect homeostatic equilibrium.
On the two plates of this scale we find on the one hand the activation of coagulation mechanisms, with consequent formation of fibrin, and on the other, the lysis of stabilized fibrin and the inhibition of circulating thrombin (necessary for the activation of fibrinogen into fibrin).
Unfortunately, in various conditions, pathological or otherwise, this balance is lost and - depending on whether the balance hangs on the side of the first or second plate - there may be thrombotic diseases (excessive blood coagulability) or hemorrhagic (insufficient blood coagulability). In the first case, the body tries to compensate for the problem by increasing the fibrinolytic phenomena (degradation of fibrin), with a consequent increase in the D-dimers present in the blood.
In summary, the presence of D-dimer in the blood is the consequence of a triple mechanism:
- Activation of coagulation with the formation of fibrin;
- Stabilization by action of factor XIII (activated by thrombin);
- Subsequent proteolysis by the fibrinolytic system (plasmin).
