D-dimer

[2] Since its introduction in the 1990s, it has become an important test performed in people with suspected thrombotic disorders, such as venous thromboembolism.

[1][3] A four-fold increase in the protein is an indicator of poor prognosis in people hospitalized with COVID-19.

Both pathways lead to the generation of thrombin, an enzyme that turns the soluble blood protein fibrinogen into fibrin, which aggregates into protofibrils.

[1] D-dimer testing is of clinical use when there is a suspicion of deep venous thrombosis (DVTl), pulmonary embolism (PE) or disseminated intravascular coagulation (DIC).

It has therefore been suggested to use a cutoff equal to patient’s age in years × 10 μg/L (or x 0.056 nmol/L) for patients aged over 50 years for the suspicion of venous thromboembolism (VTE), as it decreases the false positive rate without substantially increasing the false negative rate.

For hospitalized patients, one study found the specificity to be about 50% (related to false positive rate) in the diagnosis of thrombotic disease.

[23][24] D-dimer was originally identified, described and named in the 1970s (Fibrinolysis, Dr P J Gaffney) and found its diagnostic application in the 1990s.

D-dimer formation. Shown are fibrinogen , with its one E domain and two D domains, acted upon in cascade, by the following enzymes : Thrombin , to create a mesh of fibrin protofibrils; Factor XIII to crosslink the fibrin mesh (linking protofibril D domains), the scaffold for clot formation; Plasmin , whose action in fibrinolysis produces fibrin degradation products ( FDPs ), the smallest of which are D-dimers , protein fragments with one E and two crosslinked D domains from an original fibrinogen. [ 1 ] [ 5 ]