Answer
D-dimer is the degradation product of crosslinked fibrin; therefore, it reflects ongoing activation of the hemostatic system. Since there is constant minimal physiologic fibrin formation and degradation in vivo, healthy individuals have a minimal D-dimer level.
Elevated D-dimer levels reflect ongoing activation of the hemostatic and thrombolytic system, providing clinical utility in the following:
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Evaluation of thrombus formation
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Ruling out DVT (discussed further below)
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Monitoring anticoagulative treatment (a decreasing value indicates effective treatment)
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Snake venom poisoning
Additionally, D-dimer levels may be elevated in the setting of pregnancy, inflammation, malignancy, trauma, postsurgical treatment, liver disease (decreased clearance), and heart disease. [2, 3] It is also frequently high in hospitalized patients. [4]
Lipemia, a high triglyceride level, an elevated bilirubin level, an elevated serum rheumatoid factor level, or hemolysis may falsely increase the D-dimer level.
Keep in mind that the D-dimer level in individuals with factor XIII deficiency remains low (eventually zero in homozygous factor XIII deficiency), even in the presence of a large clot formation, owing to the inability of crosslink formation. Consequently, if these individuals develop thrombosis, they present with increased fibrin degradation products but undetectable plasma D-dimer levels.
Also keep in mind that the D-dimer level increases naturally with age.
