Application of flow systems in laboratory diagnostics for the integral evaluation of the hemostatic system

SummaryTo characterize the extent of early activation of the hemostatic system following angioplasty, we obtained blood samples from the involved coronary artery of 11 stable angina patients during the procedure and measured sensitive markers of thrombin formation (fibrino-peptide A, prothrombin fragment 1.2, and soluble fibrin) and of platelet activation ((3-thromboglobulin). Levels of hemostatic markers in venous blood obtained from 14 young individuals with low pretest probability for coronary artery disease were not significantly different from levels in venous blood or intracoronary samples obtained prior to angioplasty. Also, there was no translesional (proximal and distal to the lesion) gradient in any of the hemostatic markers before or after angioplasty in samples obtained between 18 and 21 min from the onset of the first balloon inflation. Furthermore, no significant difference was noted between angioplasty and postangioplasty intracoronary concentrations. We conclude that intracoronary hemostatic activation does not occur in the majority of patients during and immediately following coronary angioplasty when high doses of heparin and aspirin are administered.

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Inhibition rather than Enhancement of Hemostatic System Activation during Initiation of Oral Anticoagulant Treatment

Thrombosis and Haemostasis ◽

10.1055/s-0038-1656034 ◽

1997 ◽

Vol 77 (04) ◽

pp. 685-689 ◽

Cited By ~ 11

Author(s):

Paul A Kyrle ◽

Johannes Brockmeier ◽

Ansgar Weltermann ◽

Sabine Eichinger ◽

Wolfgang Speiser ◽

...

Keyword(s):

High Intensity ◽

Oral Anticoagulant ◽

Protein C ◽

Venous Blood ◽

Rapid Decline ◽

Oral Anticoagulant Treatment ◽

Shed Blood ◽

Low Intensity ◽

Hemostatic System ◽

System Activation

SummaryCoumarin-induced skin necrosis is believed to be due to a transient hypercoagulable state resulting from a more rapid decline of the protein C activity relative to that of coagulation factors (F) II, IX and X during initiation of oral anticoagulant therapy. We studied hemostatic system activation during early oral anticoagulant treatment with a technique that investigates coagulation activation in the microcirculation.We determined in 10 healthy volunteers the concentrations of prothrombin fragment F1+2 (f1.2) and thrombin-antithrombin complex (TAT) in blood emerging from an injury of the microvasculature (bleeding time incision) before and after initiation of both high-inten- sity and low-intensity coumarin therapy. In addition, f1.2, TAT, activated F VII (F Vila) and the activities of FII, F VII, F X and protein C were measured in venous blood.A rapid decline of F VII and protein C was observed in venous blood with activities at 24 h of 7 ± 1% and 43 ± 2%, respectively, during the high-intensity regimen. A 20 to 30% reduction of f1.2 and TAT was seen in venous blood at 72 h with no major difference between the high- and the low-intensity regimen. F Vila levels were substantially affected by anticoagulation with a >90% reduction at 48 h during the high-intensity regimen. Following high-intensity coumarin, a >50% decrease in the fl.2 and TAT levels was found in shed blood at 48 h suggesting substantial inhibition of thrombin generation during early oral anticoagulation. An increase in the f1.2 and TAT levels was seen neither in shed blood nor in venous blood.Our data do not support the concept of a transient imbalance between generation and inhibition of thrombin as the underlying pathomechanism of coumarin-induced skin nekrosis.

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Levels of Prothrombin Fragment F1+2 in Patients with Hyperhomocysteinemia and a History of Venous Thromboembolism

Thrombosis and Haemostasis ◽

10.1055/s-0038-1665405 ◽

1997 ◽

Vol 78 (05) ◽

pp. 1327-1331 ◽

Cited By ~ 21

Author(s):

Paul A Kyrle ◽

Andreas Stümpflen ◽

Mirko Hirschl ◽

Christine Bialonczyk ◽

Kurt Herkner ◽

...

Keyword(s):

Venous Thromboembolism ◽

Thrombin Generation ◽

Oral Anticoagulant Therapy ◽

Oral Anticoagulants ◽

Control Group ◽

Prothrombin Fragment ◽

Hemostatic System ◽

Significant Difference ◽

System Activation ◽

One Year

SummaryIncreased thrombin generation occurs in many individuals with inherited defects in the antithrombin or protein C anticoagulant pathways and is also seen in patients with thrombosis without a defined clotting abnormality. Hyperhomocysteinemia (H-HC) is an important risk factor of venous thromboembolism (VTE). We prospectively followed 48 patients with H-HC (median age 62 years, range 26-83; 18 males) and 183 patients (median age 50 years, range 18-85; 83 males) without H-HC for a period of up to one year. Prothrombin fragment Fl+2 (Fl+2) was determined in the patient’s plasma as a measure of thrombin generation during and at several time points after discontinuation of secondary thromboprophylaxis with oral anticoagulants. While on anticoagulants, patients with H-HC had significantly higher Fl+2 levels than patients without H-HC (mean 0.52 ± 0.49 nmol/1, median 0.4, range 0.2-2.8, versus 0.36 ± 0.2 nmol/1, median 0.3, range 0.1-2.1; p = 0.02). Three weeks and 3,6,9 and 12 months after discontinuation of oral anticoagulants, up to 20% of the patients with H-HC and 5 to 6% without H-HC had higher Fl+2 levels than a corresponding age- and sex-matched control group. 16% of the patients with H-HC and 4% of the patients without H-HC had either Fl+2 levels above the upper limit of normal controls at least at 2 occasions or (an) elevated Fl+2 level(s) followed by recurrent VTE. No statistical significant difference in the Fl+2 levels was seen between patients with and without H-HC. We conclude that a permanent hemostatic system activation is detectable in a proportion of patients with H-HC after discontinuation of oral anticoagulant therapy following VTE. Furthermore, secondary thromboprophylaxis with conventional doses of oral anticoagulants may not be sufficient to suppress hemostatic system activation in patients with H-HC.

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QUESTIONNAIRE SURVEY OF THE STUDENTS OF THE CHAIR OF CLINICAL LABORATORY DIAGNOSTICS AS A METHOD OF STUDYING EXPECTATIONS AND POSSIBILITIES OF FORMING A STEADY LEVEL OF KNOWLEDGE

Философия образования ◽

10.15372/phe20170206 ◽

2017 ◽

Keyword(s):

Questionnaire Survey ◽

Clinical Laboratory ◽

Laboratory Diagnostics ◽

Steady Level ◽

Level Of Knowledge

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Disorders of hemostatic system in patients with malignant disease, especially in view of venous thromboembolism

Orvosi Hetilap ◽

10.1556/oh.2007.28130 ◽

2007 ◽

Vol 148 (36) ◽

pp. 1691-1697 ◽

Cited By ~ 3

Author(s):

Géza Bozóky ◽

Éva Ruby ◽

Ilona Góhér ◽

Andrea Mohos ◽

Csilla Bálint ◽

...

Keyword(s):

Venous Thromboembolism ◽

Malignant Disease ◽

Hemostatic System

A szolid malignus kórképekben laboratóriumi módszerekkel igazolható fokozott trombózishajlam a daganatsejtek haemostasisrendszerre gyakorolt aktiváló hatása következtében alakul ki. Az aktiváló hatás a daganatsejtek és a koagulációs rendszer különböző alkotóelemei (véralvadási faktorok, thrombocyták, endothel, fibrinolitikus rendszer) közötti interakció révén alakul ki, s ez vezet a protrombotikus állapottól a haemostasisrendszer klinikailag megnyilvánuló zavaraihoz. Célkitűzés: Retrospektív analízis során a szerzők arra kerestek választ, hogy nagy esetszámú szolid malignus daganatos betegben milyen jellegű és gyakoriságú haemostaticus rendellenességek fordulnak elő. Módszer: Az 1996 és 2004 közötti időszakban 1381 betegben hisztológiai és/vagy citológiai vizsgálat révén kórisméztek szolid malignus megbetegedést. A betegek többsége primer bronchopulmonalis kiindulású karcinómában szenvedett ( n = 1140). A többi esetben emlő-, colorectalis, vese-, húgyhólyag-, pajzsmirigy- és pancreaslokalizációjú volt a malignus folyamat, mesotheliomát hat betegben kórisméztek. A stádiummegállapító vizsgálatok alapján a betegek nagyobb hányada előrehaladott klinikai stádiumú volt. A daganatos betegekben azt vizsgálták, hogy milyen jellegű és gyakoriságú haemostaticus rendellenesség fordul elő, különös tekintettel a vénás thromboemboliák előfordulására. Külön is figyelmet fordítottak a meglevő nem malignus társbetegség szerepére a haemostaticus rendellenességek kialakulása szempontjából. Eredmények: Az 1381 rosszindulatú daganatos betegben 397 esetben (28,7%) észleltek klinikailag megnyilvánuló haemostaticus rendellenességet. Leggyakoribbnak a mélyvénás trombózis és akut pulmonalis embólia bizonyult ( n = 305, 22%). Egyéb jellegű haemostasiszavar (migráló felületes thrombophlebitis, szeptikus trombózis, akut diffúz intravascularis coagulatio, microangiopathiás haemoliticus anaemia) 71 betegben fordult elő, amely 6,7%-nak felel meg. A haemostaticus eltéréssel járó malignus kóresetek 40%-ában nem malignus társbetegséget észleltek, különböző cardialis megbetegedések, valamint a krónikus obstruktív tüdőbetegség dominanciájával. A fokozott trombóziskészséget kiváltó szisztémás okok mellett közel 10%-os gyakoriságban a jelentős nagyságú lokoregionális tumorvolumen is hozzájárult a vénás keringési zavar kialakulásához. Következtetések: Szolid malignus betegekben a daganatsejtek és a koagulációs szisztéma egyes alkotóelemei közötti interakció fokozott trombózishajlam kialakulásához vezet, melynek következtében különböző klinikai megjelenésű haemostasis-rendellenességek jelentkezhetnek. Ezen haemostasiszavarok közül a klinikai gyakorlatban leggyakrabban a vénás thromboemboliák fordulnak elő. Idiopátiás vénás trombózisok eseteiben célzott vizsgálatok elvégzése indokolt az aszimptomatikus (okkult) malignus betegség igazolása, illetőleg kizárása céljából.

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