Role of the Fibrinogen Degradation Products and D-Dimer in the Differential Diagnosis of Pulmonary Tuberculosis and Community-Acquired Pneumonia

2018 ◽  
Vol 64 (01+02/2018) ◽  
Author(s):  
Wang Min ◽  
Jiang Zi-Feng ◽  
Xu Jian-Lin ◽  
Fang Hao-Hui
Keyword(s):  
Differential Diagnosis ◽  
Pulmonary Tuberculosis ◽  
Degradation Products ◽  
Community Acquired Pneumonia ◽  
Fibrinogen Degradation Products ◽  
D Dimer

Role of D Dimer in Patients with Elevated Fibrinogen Degradation Products in Serum: Further Study in Chronic Myelogenous Leukemia

1990 ◽  
Vol 84 (3) ◽  
pp. 149-155 ◽  
Author(s):  
Masanori Saito ◽  
Hidesaku Asakura ◽  
Hiroshi Jokaji ◽  
Chika Uotanzi ◽  
Ichiro Kumabashiri ◽  
...  
Keyword(s):  
Chronic Myelogenous Leukemia ◽  
Degradation Products ◽  
Myelogenous Leukemia ◽  
Fibrinogen Degradation Products ◽  
D Dimer

scholarly journals The Role of Serum Coagulation Factors in the Differential Diagnosis of Patients with Pneumonia and Parapneumonic Effusion

PRILOZI ◽  
2016 ◽  
Vol 37 (2-3) ◽  
pp. 81-88
Author(s):  
Sanja Petrusevska Marinkovic ◽  
Irena Kondova Topuzovska ◽  
Zvonko Milenkovic ◽  
Biserka Kaeva
Keyword(s):  
Differential Diagnosis ◽  
Cellular Proliferation ◽  
Coagulation Factors ◽  
Community Acquired Pneumonia ◽  
Coagulation Cascade ◽  
Parapneumonic Effusion ◽  
Laboratory Profile ◽  
And Migration ◽  
D Dimer

Abstract The aim of this study was to identify the participations of the serum coagulations and fibrinolysis factors that contribute to the differential diagnosis of the patients with community-acquired pneumonia (CAP) without effusion, uncomplicated parapneumonic effusion (UCPPE) and complicated parapneumonic effusion (CPPE). The coagulations system is fundamental for the maintenance of homeostasis, and contributes to the inflammatory process responsible for CAP and the parapneumonic effusion. The factors of coagulations and fibrinolysis participate in the cellular proliferation and migration as in the synthesis of the inflammatory mediators. We evaluated the laboratory profile of coagulations and fibrinolysis in the serum of 148 patients with CAP without effusion, 50 with UCPPE and 44 with CPPE. We determined the test of the coagulation cascade which measures the time elapsed from the activation of the coagulation cascade at different points to the fibrin generation. As a consequence, there is an activation of the fibrinolytic system with the increased D-dimer levels measured in the plasma in the three groups. The patients were with mean age ± SD (53,82 ± 17,5) min – max 18–93 years. A significantly higher number of thrombocytes was in the group with CPPE with median 412 × 109/L (rank 323–513 × 109/L). The extended activation of the prothrombin time (aPTT) was significantly higher in the same group of patients with median of 32 sec. (rank 30–35 sec). The mean D-dimer plasma level was 3266,5 ± 1292,3 ng/ml in patients with CPPE, in CAP without effusion 1646,6 ± 1204 ng/ml and in UCPPE 1422,9 ± 970 ng/ml. The coagulations system and the fibrinolysis play important role in the development and pathophysiology of CAP and the parapneumonic effusions.

The Leukocyte Digestion of Fibrinogen Degradation Products (FDP)

1971 ◽  
Vol 26 (03) ◽  
pp. 523-525
Author(s):  
K Gibiński ◽  
B Lipiński ◽  
M Trusz-Gluza
Keyword(s):  
Degradation Products ◽  
Fibrinogen Degradation Products

SummaryWhile the native fibrinogen is not digested by the leucocyte proteases both the early and late FDP are digestible without any denaturating reagent. Thus, this reaction may occur in vivo indicating an unknown role of granulocytes in paracoagulation.

Role of C-reactive protein, D-dimer, and fibrinogen levels in the differential diagnosis of central and peripheral vertigo

2007 ◽  
Vol 24 (5) ◽  
pp. 1068-1077 ◽  
Author(s):  
Emine Akinci ◽  
Gulbin Aygencel ◽  
Ayfer Keles ◽  
Ahmet Demircan ◽  
Fikret Bildik
Keyword(s):  
Differential Diagnosis ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Peripheral Vertigo ◽  
D Dimer

THE ROLE OF VARIOUS HAEMOSTASIS PARAMETERS IN MONITORING FIBRINOLYSIS WITH PRO-UROKINASE/STREPTOKINASE IN TREATMENT OF MYOCARDIAL INFARCTION

1987 ◽  
Author(s):  
F Keller ◽  
P Schanzenbächer ◽  
F Dati ◽  
J Huber ◽  
K kochsiek
Keyword(s):  
Myocardial Infarction ◽  
Degradation Products ◽  
Therapy Monitoring ◽  
Latex Agglutination ◽  
Systemic Activity ◽  
Thromboplastic Activity ◽  
Specific Degradation ◽  
D Dimer

The new drug pro-urokinase, a proenzyme of urokinase (scu-PA), seems to have advantages in comparison with other fibrinolytic agents. Properties like higher fibrin specifity, non-systemic activity and lower antigenity may lead to a lower rate of complications. In a pilot study 10 patients with acute myocardial infarction have been treated under angiographical control with pro-urokinase (3-9 millions IU) by i.v. application. In case of no perfusion a further administration of streptokinase was carried on. The blood samples were obtained at therapy begin and after 5, 10, 30, 60 and 120 minutes. The therapy monitoring was performed by determination of established haemostasis parameters, like fibrinogen, fibrin(ogen)-split products (FSP), a2-antiplasmin. Plasminogen and batroxobin-time. Furthermore, the diagnostic relevance of new laboratory tests for fibrinolysis, D-Dimer and thrombin-anti thrombin Ill-complex (TAT) has been investigated considering some typical follow-ups. D-Dimer were determined by latex agglutination test and TAT by enzyme immunoassay.Generally the application of pro-urokinase in contrast to streptokinase results in minimal changes of the classic fibrinolysis parameters like fibrinogen, FSP, batroxobin-time etc. demonstrating no systemic lysis. The appearance of plasmic degradation products of cross-linked fibrin (D-Dimer) is a specific indi-cater of the release of thrombotic material. Other non-specific degradation products (fibrinogenolysis) were detected by the measurement of FSP. In some cases in which perfusion ocurred an increase of TAT followed by a rapid decrease was observed. This indicates a higher thromboplastic activity which may originate from the infarcted area producing TAT complex formation.

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