D-dimer in diagnosis and prevention of venous thrombosis: recent advances and their practical implications

Abstract

D -Dimers and venous thromboembolism 1 extent of fibrinolysis, and clearance of fibrin degradation products.D -Dimer level increases physiologically with age and during pregnancy and puerperium; it may be higher in African -Americans and in smokers. Increased D -dimer level is also observed in several pathologic conditions, in which stabilized fibrin is formed and subsequently degraded, such as in venous and arterial thrombosis, infectious diseases, neoplasms, trauma, surgery, liver disease, renal insufficiency, fibrinolytic therapy, disseminated intravascular coagulation (DIC), acute coronary syndromes, acute cerebrovascular events, subarachnoid hemorrhage, obstetric complications, or autoimmune disorders. 3 D -Dimer measurement D -Dimer level measurement was proposed as a laboratory test for the diagnosis of DIC in the 1970s; since then considerable advances have been made regarding its measurement, and its main clinical role is that in venous thromboembolism (VTE) diagnosis. 2 Introduction During hemostasis, activation of coagulation leads to the production of thrombin, which cleaves fibrinogen into fibrin monomers that finally form fibrin polymer. Thrombin also activates factor XIII, which stabilizes fibrin polymers with cross -linked covalent bonds. Activation of fibrinolysis leads to the production of plasmin, which cleaves cross -linked fibrin into various fragments, including D -dimers 1 (FIguRE 1). Plasmin produces several different degradation products with molecular weight (MW) ranging from 190 to over 10 000 kDa, and MW of D -dimers is about 180 kDa. 1 D -Dimers are mainly cleared by the kidney and reticulo -endothelial system, with a plasma half -life of 6 to 8 hours. 1,2 In physiological conditions, approximately 2%-3% of fibrinogen is converted into fibrin, which is then degraded by the fibrinolytic system. 1,2 As a result, D -dimers can be detected in low amounts in healthy individuals under physiological conditions. Plasma D -dimer concentration depends on the extent of factor XIIIa -stabilized fibrin formation,

Apixaban Versus Vitamin K Antagonists in Patients With Antiphospholipid Syndrome: A Cohort Study

“…D-dimer level is well-established independent risk factor of thromboembolism recurrence and is incorporated in several prediction models; however the presence of antiphospholipid antibodies and elevated D-dimer represent rather independent risk factors. 37,38 Interestingly, the difference was driven by patients on apixaban, since no such association was seen in the VKA group. It might be speculated that D-dimer measurement might help identify patients with APS in whom VKA therapy should be strongly recommended and apixaban is a much less likely effective option, but this practical implication requires further study.…”

Retinal Vessel Analysis and Microvascular Abnormalities in Patients with Philadelphia-Negative Chronic Myeloproliferative Neoplasms

“…In fact, patients with primary myelofibrosis who have the same mutation have a significantly longer overall survival rate compared to subjects positive for other mutations (JAK2, V617F, or MPL). Clinically, patients with essential thrombocythemia who are positive for CALR mutations exhibit a lower incidence of thrombotic events [51,52].…”

A Current Synopsis of the Emerging Role of Extracellular Vesicles and Micro-RNAs in Pancreatic Cancer: A Forward-Looking Plan for Diagnosis and Treatment

“…It has been demonstrated that TF-EVs promote thrombosis in PDAC patients, while baseline TF levels at the start point of chemotherapy constitute a predictive factor of cancer-related thromboembolism, as was demonstrated in Japanese PDAC patient cohorts [ 154 ]. It was also demonstrated in the study of Kobayashi et al (2021) that TF levels above or equal to 100 pg/Ml constitute an independent predictive factor for cancer-associated thromboembolism, while it was also proposed that D-dimers and microvesicle tissue factor (MV-TF) could be utilized as biomarkers for venous thromboembolism in PDAC and may facilitate the identification of patients for whom thromboprophylaxis has to be administrated [ 154 , 155 ].…”