D-Dimer Test

Excerpt

D-dimer is a byproduct of the blood clotting and breakdown process, serving as a marker of ongoing coagulation and fibrinolysis. Circulating fibrinogen consists of 3 paired polypeptide chains—Aα, Bβ, and γ. At the site of vascular injury, thrombin cleaves fibrinopeptides from fibrinogen Aα and Bβ that polymerize into fibrin monomers. Factor XIII, activated by thrombin, then binds the interspersed γ units to form a fibrin net, stabilizing the clot.

Under normal physiological conditions, the balance between clot formation and destruction prevents excess bleeding and ensures proper blood flow after blood vessel healing. When a clot is no longer needed, tissue-type plasminogen activator and urokinase plasminogen activator activate plasminogen, a component of the fibrinolytic system. This activation leads to the formation of plasmin, an enzyme that dissolves the clot through lytic action. Clot breakdown produces fibrin degradation products, one of which is D-dimer. Specifically, if 2 D-domains of the original fibrinopeptides link the polymers, D-dimer forms upon degradation. A combination of proteases and the mononuclear phagocytic system, primarily in the liver, clears most fibrin degradation products. However, the kidneys and reticuloendothelial system primarily clear D-dimer, which has a plasma half-life of 6 to 8 hours.

The D-dimer test has high sensitivity but low specificity, resulting in a high negative predictive value, which makes it helpful for excluding diagnoses such as deep vein thrombosis, pulmonary embolism, and disseminated intravascular coagulation in the appropriate clinical setting. Clinicians must take into account that pregnancy, trauma, malignancy, surgery, and liver disease can all cause elevations of the D-dimer.