D-dimer overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
D-dimer is a fibrin degradation product. D-dimer levels are elevated in the plasma after the acute formation of a blood clot. The majority of patients with pulmonary embolism have some degree of endogenous fibrinolysis with an elevation in D-dimer levels, therefore there is a high negative predictive value in ruling out a pulmonary embolism when D-dimer levels are low. However a wide range of diseases are associated with mild degree of fibrinolysis which elevate D-dimer levels and contribute towards a reduced specificity and a poor positive predictive value of a high D-dimer level. This means that it is more likely that one can rule out a PE with a low D-dimer level, but cannot necessarily confirm the diagnosis of a PE based on a high D-dimer level. Other disease states that can also have a high d-dimer level include pneumonia, congestive heart failure (CHF), myocardial infarction (MI) and malignancy. False-negative values may occur in patients with prolonged symptoms of venous thromboembolism (≥14 days), patients on therapeutic heparin therapy, and patients with suspected deep venous thrombosis on oral anticoagulation, as these patients have will have low D-dimer levels in the presence of a PE.[1][2]
D-dimer prognostic role in thromboembolism recurrence
The recurrence rate within the first few months following a first episode of VTE is not negligeable. In fact, it is estimated to be around 6% at 6 months following the first episode.[3] Because of this, the duration of treatment with oral anticoagulation therapy must be long enough to decrease the risk of recurrence while not too long to cause bleeding complications. The duration of treatment of oral anticoagulation is most problematic in the category of patients suffering from their first episode of unprovoked VTE; therefore, a marker of risk of recurrence of VTE in this population in particular is needed to tailor the duration of their treatment.
An association between changes in D-dimer levels during and following discontinuation of oral anticoagulation was suggested more than a decade ago,[4] and the prognostic role of D-dimer in predicting the rate of recurrence of VTE has been extensively studied.[5] Studies have been consistent in their findings of an association between elevated D-dimer levels and higher rates of recurrence of VTE; as such, they suggest a possible role for D-dimer in predicting recurrence of thromboembolism and tailoring the duration of treatment of oral anticoagulation following VTE.[6] Resuming oral anticoagulation treatment (OAT) in subjects with abnormal D-dimer levels following the discontinuation of the OAT reduced their risk of VTE recurrence.[7]
References
- ↑ Bruinstroop E, van de Ree MA, Huisman MV (2009). "The use of D-dimer in specific clinical conditions: a narrative review". Eur J Intern Med. 20 (5): 441–6. doi:10.1016/j.ejim.2008.12.004. PMID 19712840.
- ↑ Agnelli G, Becattini C (2010). "Acute pulmonary embolism". N Engl J Med. 363 (3): 266–74. doi:10.1056/NEJMra0907731. PMID 20592294.
- ↑ White RH (2003). "The epidemiology of venous thromboembolism". Circulation. 107 (23 Suppl 1): I4–8. doi:10.1161/01.CIR.0000078468.11849.66. PMID 12814979.
- ↑ Kévorkian JP, Halimi C, Segrestaa JM, Drouet L, Soria C (1998). "Monitoring of patients with deep-vein thrombosis during and after anticoagulation with D-dimer". Lancet. 351 (9102): 571–2. doi:10.1016/S0140-6736(05)78559-7. PMID 9492784.
- ↑ Wu C, Bates SM (2009). "Should D-dimer testing be used to predict the risk of recurrence after discontinuation of anticoagulant therapy for a first unprovoked episode of venous thromboembolism?". Pol Arch Med Wewn. 119 (4): 225–30. PMID 19413181.
- ↑ Zhu T, Martinez I, Emmerich J (2009). "Venous thromboembolism: risk factors for recurrence". Arterioscler Thromb Vasc Biol. 29 (3): 298–310. doi:10.1161/ATVBAHA.108.182428. PMID 19228602.
- ↑ Palareti G (2007). "[Current criteria to determine the duration of anticoagulant therapy]". Recenti Prog Med. 98 (12): 603–6. PMID 18369033.