PRIMARY HEMOSTATIC SYSTEM CONDITION IN MUCOVISCIDOSIS IN CHILDREN

2014 ◽  
Vol 11 (1) ◽  
pp. 66
Author(s):  
O. B. Gordeeva ◽  
V. V. Botvinyeva ◽  
O. I. Simonova ◽  
L. S. Namazova-Baranova ◽  
Y. V. Gorinova ◽  
...  
Keyword(s):  
Hemostatic System

Markers of Hemostatic Activation in Affected Coronary Arteries during Angioplasty

1994 ◽  
Vol 72 (05) ◽  
pp. 672-675 ◽  
Author(s):  
Nicolas W Shammas ◽  
Michael J Cunningham ◽  
Richard M Pomearntz ◽  
Charles W Francis
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Venous Blood ◽  
Balloon Inflation ◽  
Blood Samples ◽  
Hemostatic System ◽  
Significant Difference ◽  
Hemostatic Markers ◽  
Artery Disease ◽  
High Doses

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.

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

1997 ◽  
Vol 77 (04) ◽  
pp. 685-689 ◽  
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.

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

1997 ◽  
Vol 78 (05) ◽  
pp. 1327-1331 ◽  
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.

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

2007 ◽  
Vol 148 (36) ◽  
pp. 1691-1697 ◽  
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.

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

2018 ◽  
Vol 17 (1) ◽  
pp. 117-129
Author(s):  
O.E. Ushakova ◽  
◽  
D.Y. Nechipurenko ◽  
A.A. Butylin ◽  
M.A. Panteleev ◽  
...  
Keyword(s):  
Laboratory Diagnostics ◽  
Integral Evaluation ◽  
Hemostatic System ◽  
Flow Systems

INTERRELATION OF ALLELIC VARIANTS OF HEMOSTASIS SYSTEM GENES ON THE DEVELOPMENT AND COURSE OF LUPUS NEPHRITIS

2019 ◽  
Vol 23 (2) ◽  
pp. 77-81
Author(s):  
E. N. Borisov ◽  
L. V. Ivanitsky ◽  
L. M. Samokhodskaya ◽  
T. N. Krasnova ◽  
E. P. Pavlikova ◽  
...  
Keyword(s):  
Lupus Nephritis ◽  
Mutant Allele ◽  
Impaired Renal Function ◽  
Mthfr C677t ◽  
Mthfr Gene ◽  
Renal Survival ◽  
Mutant Genotype ◽  
Hemostatic System ◽  
Allelic Variations ◽  
Pai 1

THE AIM: to evaluate the effect of allelic variations in the hemostatic system genes on the development and course of lupus nephritis. PATIENTS AND METHODS. The study analyzed 100 patients with SLE Caucasians. 80 women and 20 men aged 16 to 73 years (mean age 37, ± 14 years). The duration of observation was for 73 patients over 5 years, for 18 – from 1 year to 5 years and for 9 – less than 1 year A rise in the level of creatinine in the blood above or equal to 2 mg / dl was considered a significant sign of impaired renal function. RESULTS. Among the patients included in the study, kidney damage was detected in 61 people (61%). In 33 of them (54.1%), a variant of renal pathology was observed according to the type of rapidly progressive lupus nephritis (BPVN). In patients with BH, mutations in the MTHFR (C677T) gene were statistically significantly more frequent (p = 0.033). The OR for the mutant genotype is 6.146 with 95% CI from 1.692 to 22.326. In patients with PWHD, mutations in the MTHFR (C677T) gene were statistically significantly more frequent (p = 0.031). The OR for the mutant genotype is 1.625 with 95% CI from 1.034 to 4.771. The five-year renal survival in carriers of the mutant allele of the MTHFR gene (C677T) is statistically significantly lower (72.8%) than in patients without this mutation (81.9%) (p = 0.027). Ten-year renal survival in carriers of the mutant allele of the MTHFR gene (C677T) is statistically significantly less (55.6%) than in patients without this mutation (70.5%) (p = 0.016). In patients with BH, mutations in the PAI-1 gene (4G / 5G 675) were statistically significantly more frequent (p = 0.046). OR for mutant genotype – 1.766 with 95% CI from 1.061 to 4.758. CONCLUSION. The mutant alleles of the MTHFR (C677T) and PAI-1 (4G / 5G 675) genes are likely to be associated with the development of BH. Polymorphism of the MTHFR gene (C677T) is associated with an unfavorable course of HH.

Features of the hemostatic system in patients with endometrioid ovarian cysts

GYNECOLOGY ◽  
2015 ◽  
Vol 17 (3) ◽  
pp. 9-12
Author(s):  
I.A. Lapina ◽  
◽  
L.A Ozolinya ◽  
L.I. Patrushev ◽  
N.I. Nasyrova ◽  
...  
Keyword(s):  
Ovarian Cysts ◽  
Hemostatic System

scholarly journals In Silico Hemostasis Modeling and Prediction

2020 ◽  
Vol 40 (04) ◽  
pp. 524-535
Author(s):  
Dmitry Y. Nechipurenko ◽  
Aleksey M. Shibeko ◽  
Anastasia N. Sveshnikova ◽  
Mikhail A. Panteleev
Keyword(s):  
In Silico ◽  
Physiological Response ◽  
Platelet Adhesion ◽  
State Of The Art ◽  
Thrombus Formation ◽  
The State ◽  
Modeling And Prediction ◽  
Hemostatic System ◽  
Single Enzyme

AbstractComputational physiology, i.e., reproduction of physiological (and, by extension, pathophysiological) processes in silico, could be considered one of the major goals in computational biology. One might use computers to simulate molecular interactions, enzyme kinetics, gene expression, or whole networks of biochemical reactions, but it is (patho)physiological meaning that is usually the meaningful goal of the research even when a single enzyme is its subject. Although exponential rise in the use of computational and mathematical models in the field of hemostasis and thrombosis began in the 1980s (first for blood coagulation, then for platelet adhesion, and finally for platelet signal transduction), the majority of their successful applications are still focused on simulating the elements of the hemostatic system rather than the total (patho)physiological response in situ. Here we discuss the state of the art, the state of the progress toward the efficient “virtual thrombus formation,” and what one can already get from the existing models.

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