D-Dimer Testing within the Routine Clinical Chemistry Profile

Vukovich, Th.; Hamwi, A.; Bieglmayer, Christian

doi:10.1093/clinchem/44.7.1557

Cited by 12 publications

(6 citation statements)

References 8 publications

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“…D-dimer concen-trations were higher in segmental PE than in subsegmental PE (Tinaquant: 3012 ± 481 vs. 1599 ± 292; VIDAS: 2510 ± 409 vs. 1365 ± 246 ng/ml; P <0.0001 for both) and in subsegmental PE not significantly different from the patients without PE (Tinaquant: P = 0.10; VIDAS, P = 0.23). With regard to the fact that the above latex D-dimer levels are consistently higher than the ELISA levels, 10-20%, it is noted here that the same trend was observed in blood samples from the emergency ambulance submitted for routine clinical chemistry and coagulation examinations (10).…”

supporting

confidence: 70%

Comparison of a Quantitative Latex and a Quantitative ELISA Plasma D-Dimer Assay in the Exclusion of Segmental and Subsegmental Pulmonary Embolism

Sijens¹,

Oudkerk²,

Berghout³

et al. 2001

Thromb Haemost

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supporting

confidence: 70%

Comparison of a Quantitative Latex and a Quantitative ELISA Plasma D-Dimer Assay in the Exclusion of Segmental and Subsegmental Pulmonary Embolism

Sijens¹,

Oudkerk²,

Berghout³

et al. 2001

Thromb Haemost

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“…The longer PT and aPTT times suggest consumption of coagulation factors, and have been associated with death in SNV infections [ 55 ]. As our study samples were originally collected in EDTA tubes (instead of citrate) [ 95 ] it was not possible for us to examine the subsequent samples for serial changes in coagulation factors including d-dimers. For this patient, active PAI-1 was 50 fold above control samples on day of admission and dropped on subsequent days before the patient died.…”

Section: Resultsmentioning

confidence: 99%

Elevated Cytokines, Thrombin and PAI-1 in Severe HCPS Patients Due to Sin Nombre Virus

Bondu

Schrader

Gawinowicz

et al. 2015

Viruses

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Sin Nombre Hantavirus (SNV, Bunyaviridae Hantavirus) is a Category A pathogen that causes Hantavirus Cardiopulmonary Syndrome (HCPS) with case fatality ratios generally ranging from 30% to 50%. HCPS is characterized by vascular leakage due to dysregulation of the endothelial barrier function. The loss of vascular integrity results in non-cardiogenic pulmonary edema, shock, multi-organ failure and death. Using Electric Cell-substrate Impedance Sensing (ECIS) measurements, we found that plasma samples drawn from University of New Mexico Hospital patients with serologically-confirmed HCPS, induce loss of cell-cell adhesion in confluent epithelial and endothelial cell monolayers grown in ECIS cultureware. We show that the loss of cell-cell adhesion is sensitive to both thrombin and plasmin inhibitors in mild cases, and to thrombin only inhibition in severe cases, suggesting an increasing prothrombotic state with disease severity. A proteomic profile (2D gel electrophoresis and mass spectrometry) of HCPS plasma samples in our cohort revealed robust antifibrinolytic activity among terminal case patients. The prothrombotic activity is highlighted by acute ≥30 to >100 fold increases in active plasminogen activator inhibitor (PAI-1) which, preceded death of the subjects within 48 h. Taken together, this suggests that PAI-1 might be a response to the severe pathology as it is expected to reduce plasmin activity and possibly thrombin activity in the terminal patients.

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“…The higher D-dimer concentration in heparin plasma is probably attributable to the introduction of a dilution factor in citrate-containing blood tubes. Although Vukovich et al reported that heparinized and citrated samples yielded identical D-dimer values (Ddimer Gold V R , Agen Biochemical) samples, they recommended using a correction factor of 0.84 to take into account the dilution of the citrate anticoagulant, a process that may be confusing in routine practice [40]. Local evaluation of other matrices should be validated before they are used in clinical practice, especially when the manufacturer recommends using only citrated samples.…”

Section: Anticoagulant Sample (Or Tube Additive)mentioning

confidence: 99%

D-dimer: Preanalytical, analytical, postanalytical variables, and clinical applications

Favresse

Lippi

Roy

et al. 2018

Critical Reviews in Clinical Laboratory Sciences

149

103

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D-dimer is a soluble fibrin degradation product deriving from the plasmin-mediated degradation of cross-linked fibrin. D-dimer can hence be considered a biomarker of activation of coagulation and fibrinolysis, and it is routinely used for ruling out venous thromboembolism (VTE). D-dimer is increasingly used to assess the risk of VTE recurrence and to help define the optimal duration of anticoagulation treatment in patients with VTE, for diagnosing disseminated intravascular coagulation, and for screening medical patients at increased risk of VTE. This review is aimed at (1) revising the definition of D-dimer; (2) discussing preanalytical variables affecting the measurement of D-dimer; (3) reviewing and comparing assay performance and some postanalytical variables (e.g. different units and age-adjusted cutoffs); and (4) discussing the use of D-dimer measurement across different clinical settings.

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D-Dimer Testing within the Routine Clinical Chemistry Profile

Cited by 12 publications

References 8 publications

Comparison of a Quantitative Latex and a Quantitative ELISA Plasma D-Dimer Assay in the Exclusion of Segmental and Subsegmental Pulmonary Embolism

Comparison of a Quantitative Latex and a Quantitative ELISA Plasma D-Dimer Assay in the Exclusion of Segmental and Subsegmental Pulmonary Embolism

Elevated Cytokines, Thrombin and PAI-1 in Severe HCPS Patients Due to Sin Nombre Virus

D-dimer: Preanalytical, analytical, postanalytical variables, and clinical applications

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