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PubMed1991

Localization of blood coagulation factors and fibrinolysis factors within lymphoid germinal centers in human lymph nodes.

The presence of nineteen blood coagulation factors and fibrinolysis factors was immunohistochemically evaluated in human lymph node germinal centers (GCs). Twelve of these factors were detected within lymphoid GCs. The predominant pattern was dendritic with occasional crescent-shaped, ring-shaped or 'moth-eaten' appearance. Immunostains of factor VIII-related antigen, factor I, protein C, tetranectin, antithrombin III, type 2-plasminogen activator inhibitor, and alpha 2-plasmin inhibitor were almost entirely absent from GCs, although they reacted in vascular wall and lumen, respectively. The immunostaining to high molecular weight kininogen, kallikrein, factors XII, X, V, II, XIIIa, XIIIs, plasminogen, tissue-plasminogen activator, and type 1-plasminogen activator inhibitor more frequently revealed a positive dendritic pattern. Immuno-electron microscopy demonstrated factor X and factor XIIIa attached to the cell surfaces of lymphocytes, macrophages, and follicular dendritic cells (FDCs); and in the intercellular space within GCs, especially attached to the labyrinthine-like structure of FDCs. No reaction products were observed in the perinuclear cisternae and rough endoplasmic reticulum in either lymphocytes or FDCs. Our data demonstrate that human lymphoid GCs really contain some of the proteins related to the blood coagulation and fibrinolysis cascades.

Dendritic Cells↗
PubMed2000

Genetic determinants of hemostasis phenotypes in Spanish families.

BACKGROUND: Recent studies have described genetic mutations that affect the risk of thrombosis as a result of abnormal levels of such hemostatic parameters as protein C, protein S, and the activated protein C resistance ratio. Although these mutations suggest that genes play a part in determining variability in some hemostasis-related phenotypes, the relative importance of genetic influences on these traits has not been evaluated. METHODS AND RESULTS: The relative contributions of genetic and environmental influences to a panel of hemostasis-related phenotypes were assessed in a sample of 397 individuals in 21 extended pedigrees. The effects of measured covariates (sex, age, smoking, and exogenous sex hormones), genes, and environmental variables shared by members of a household were quantified for 27 hemostasis-related measures. All of these phenotypes showed significant genetic contributions, with the majority of heritabilities ranging between 22% and 55% of the residual phenotypic variance after correction for covariate effects. Activated protein C resistance ratio, activated partial thromboplastin time, and Factor XII showed the strongest heritabilities, with 71.3%, 83.0%, and 67.3%, respectively, of the residual phenotypic variation attributable to genetic effects. CONCLUSIONS: These results clearly demonstrate the importance of genetic factors in determining variation in hemostasis-related phenotypes that are components of the coagulation and fibrinolysis pathways and that have been implicated in risk for thrombosis. The presence of such strong genetic effects suggests that it will be possible to localize previously unknown genes that influence quantitative variation in these hemostasis-related phenotypes that may contribute to risk for thrombosis.

Adolescent↗
PubMedDate not supplied

An analysis of the contact phase of blood coagulation: effects of shear rate and surface are intertwined.

This work analyzes, for the first time, the combined role of blood flow, protein transport and the reaction network of the contact phase up to the "common pathway" of the blood coagulation cascade. The model is comprised of a set of 20 dominant reactions with 11 components. Systems of ODEs reducible to 4 coupled equations describe rigorously the dynamic behavior, while systems of algebraic equations, reducible to a single polynomial equation, model the steady state concentrations of the coagulants. The analysis showed that there is never more than one stable steady state. This is in contrast to the analysis of common pathway that gives rise to multiple concentration states. It also revealed a general robustness of the system to changes in procoagulant concentrations, inhibition rates and most activation rate constants. The system is largely impervious to the level of activated Factor XII, given that a trace (non-zero) level is present. In contrast, the system displays a dual response to flow and surface activity: A change in either of these factors alone can promote, have no effect on, or (in the case of flow) impede the progress of coagulation, depending on the value of the other factor. Their effects must therefore be examined in unison. These results may help resolve contradictory findings attributed to one or the other factor alone.

Blood Coagulation↗
PubMed1988

[Disorders in the contact phase system of blood coagulation as a cause of increased partial thromboplastin time].

Deficiency conditions in the contact phase system of the blood coagulation belong to the rare hereditary defects. Clinically, there is as a rule no inclination to haemorrhage but an increased risk of thrombosis. Therefore, the diagnosis is frequently made on the basis of incidental findings within the framework of routine examinations. Indicating sign is a greatly prolonged partial thromboplastin time (PTT) without clinical signs of haemorrhage. 3 patients with factor XII deficiency are presented and the diagnostic method in prolonged PTT is explained.

Blood Coagulation Tests↗
PubMed1991

[Increased activated partial thrombin time: analysis of 250 cases discovered at laboratory].

This study evaluates and discusses the potential utility (clinical value) of complementary coagulation tests performed in cases with a prolonged aPTT of no obvious etiology from a total of 85,500 routine coagulation tests carried out in our general hospital. aPTT was measured using Actin F.S.L. (Dade, plant-derived and rabbit phospholipids complex with ellagic acid as activator) and Diagen (Biotrol, rabbit phospholipids with kaolin). Tests for acquired anticoagulants and endogenous pathway factors (XII, XI, IX, VIII) were assayed if the aPTT was prolonged by 7 sec or more. 250 abnormal aPTT of previously unknown etiology were found over a 14 months period. 46% of them were without any obvious cause, and were considered "spontaneous" increases: 2/3 of these spontaneous increases were 7-9 (group A), and 1/3 were 10-19 (group B). The diagnoses found in group A were mostly deficits in the contact system, while group B contained mostly cases with acquired anticoagulants and deficits in the contact system. In group C (increases over 20"), an etiology could be established in all cases, with a predominance of acquired anticoagulants and some deficits in factors VIII and XII.

Blood Coagulation Disorders↗
PubMed1997

Proposal for objective evaluation of the performance of various functional APC-resistance tests in genotyped patients.

The aim of the present study was to evaluate the relative performance of five screening methods for APC resistance caused by the factor V:Q506 mutation: the original method Coatest APC Resistance Chromogenix, a modified method using the same reagents but a predilution 1+4 of the plasma in a factor V deficient plasma from Stago (Stago deficient V) or from Chromogenix (V-DEF Plasma), the Coatest APC Resistance V (Chromogenix), and Accélérimat from bioMérieux. Normalization was done against a pool of normal plasmas for the methods from Chromogenix. The study included 350 subjects, 219 were genotyped (174 FV:R506R, 42 FV:Q506R, 3 FV:Q506Q) and most of them were assessed by more than one method. Uncertainty in predicting the FV genotype was evaluated by statistical analysis, which provided a way to quantitate the performance of the different diagnostic approaches. Performance of each test was evaluated by its sensitivity, specificity, R.O.C. curves, positive and negative likelihood ratios (LR), and the overall performance was determined by two parameters derived from the LR curves : the maximum LR value obtained at the crossover of the two curves, and the distance between the two curves for LR = 10. Coatest APC Resistance V and Accélérimat were proven to be the methods most able to discriminate for factor V:Q506, while normalization was not shown to improve the screening performance. The original method from Chromogenix was confirmed to undergo many influences (factor XII, PAI-1, thrombin-antithrombin complexes, antithrombin III, hematocrit). Although a very good improvement was provided by the newest methods, they were shown to be influenced by protein S and/or factor V levels in the sample plasma.

Blood Coagulation Tests↗
PubMed1977

The binding and cleavage characteristics of human Hageman factor during contact activation. A comparison of normal plasma with plasmas deficient in factor XI, prekallikrein, or high molecular weight kininogen.

The ability of human Hageman factor (coagulation factor XII) to bind to a glass surface and its susceptibility to limited proteolytic cleavage during the contact activation of plasma have been studied using normal human plasma and plasmas genetically deficient in factor XI, prekallikrein, or high molecular weight kininogen (HMWK). When diluted normal plasma containing (125)I-Hageman factor was exposed to a glass surface for varying times, the Hageman factor was found to bind to the surface, and within 5 min became maximally cleaved from its native 80,000 mol wt to yield fragments of 52,000 and 28,000 mol wt. Hageman factor in factor XI-deficient plasma behaved similarly. In prekallikrein-deficient plasma, the binding of Hageman factor to the glass surface occurred at the same rate as in normal plasma but the cleavage was significantly slower, and did not reach maximum until 60 min of incubation. Cleavage of Hageman factor in HMWK-deficient plasma occurred at an even slower rate, with greater than 110 min of incubation required for maximal cleavage, although the rate of binding to the glass was again the same as in normal plasma. Normal rates of cleavage of Hageman factor were observed for the deficient plasmas after reconstitution with purified human prekallikrein or HMWK, respectively. These observations suggest that normal contact activation in plasma is associated with proteolytic activation of surfacebound Hageman factor. The cleavage of the surface-bound Hageman factor molecule responsible for the formation of the 52,000-and 28,000-mol wt fragments occurred at two closely situated sites, one of which was within a disulfide loop. Cleavage at the site external to the disulfide bond resulted in the release from the surface of the 28,000-mol wt fragment. Cleavage at the site within the disulfide loop resulted in the formation of a 28,000-mol wt fragment which remained surface bound, presumably by virtue of the disulfide linkage to the larger fragment.

Blood Coagulation Disorders↗
PubMed2007

Activation of the tissue factor pathway of blood coagulation in patients with chronic urticaria.

BACKGROUND: In patients with chronic urticaria (CU), plasma shows signs of thrombin generation and autologous plasma skin tests score positive in as many as 95% of cases. OBJECTIVE: To evaluate the initiators of blood coagulation that lead to thrombin generation and fibrinolysis in CU. METHODS: Activated factor VII, activated factor XII, fragment F(1+2), and D-dimer plasma levels were measured in 37 patients with CU and 37 controls. Skin specimens from 10 patients with CU and 10 controls were tested for tissue factor immunohistochemically. RESULTS: Mean F(1+2) levels were higher in patients than controls (2.54 [SD 2.57] nmol/L vs 0.87 [0.26] nmol/L; P < .001); disease activity was moderate or severe in 9 of 11 (82%) and 9 of 26 (35%) patients showing high or normal F(1+2) levels, respectively (P < .025). Mean D-dimer plasma levels were higher in patients than controls (329 [188] ng/mL vs 236 [81] ng/mL; P < .01); disease activity was moderate or severe in 6 of 8 (75%) and 11 of 29 (38%) showing elevated or normal plasma D-dimer levels (P = NS). Factor VIIa levels were higher in patients than controls (2.86 ng/mL [0.66] vs 1.97 ng/mL [0.65]; P < .001). Activated factor VII and F(1+2) levels were correlated (r = 0.529; P = .008). Tissue factor reactivity was observed only in CU skin specimens. CONCLUSION: The extrinsic pathway of clotting cascade is activated in CU. Disease severity is associated with the activation of the coagulation cascade. CLINICAL IMPLICATIONS: The involvement of the coagulation pathway in CU opens new perspectives for a better understanding of the pathogenesis and, possibly, for the treatment of this disease.

Adolescent↗
PubMed1985

On the role of sulfolipids in mammalian metabolism.

Sulfolipids of mammalian origin include sulfosphingolipids, sulfoglycerolipids and steroid sulfates. Sulfosphingolipids (sulfogalactosylceramide) may be involved in sodium transport, interaction of opiates with their receptors, activation of oxygen radical generating system, and blood coagulation Factor XII. Sulfoglycerolipids and steroid sulfates may be involved in spermatogenesis and sperm capacitation.

Animals↗
PubMed1986

[Effect of urinastatin on disseminated intravascular coagulation].

Effect of urinary enzyme inhibitor urinastatin (MTI) on disseminated intravascular coagulation (DIC) was investigated. The prolongation of PTT and increase in FDP in endotoxin-induced DIC in rats were restored by the intravenous infusion of MTI. The reduction in platelet counts, decrease in fibrinogen level and prolongation of PT were partially suppressed by the drug. Furthermore, in vitro addition of MTI prevented the decrease in r and k values and increase in ma and m epsilon values in the thromboelastogram of whole blood in endotoxin-induced DIC in rabbits. It is suggested that MTI might prevent DIC in vivo and in vitro through the inhibition of Factor XII activity and through the prevention of thromboplastin release caused by endotoxin.

Animals↗
PubMed1985

Clotting activities and antigen concentrations of contact factors in kidney disease.

Factor XII, prekallikrein (PK) and high molecular weight kininogen (HMWK) clotting activities and antigen concentrations in kidney disease patients were studied. Chronic hemodialysis led to a reduction of F XII, PK and HMWK clotting activities. F XII and PK antigen levels were also low. In contrast, the HMWK antigen was normal with respect to concentration as well as electrophoretic migration behaviour on 2 D-immunelectrophoresis. In kidney transplant recipients more than three month after the transplantation, we found an increased of F XII and PK clotting activities, which appeared to depend on the time elapsed since the operation. However, the antigen levels remained normal. The group of chronic kidney disease patients not requiring hemodialysis exhibited normal mean values of all three clotting activities as well as normal F XII and HMWK antigen levels. The PK antigen was reduced. However, a separate evaluation of F XII clotting activities (F XII:C) in patients with glomerular nephritis showed elevated F XII:C which correlated with the BUN values. During acute processes of the kidney disease we observed very high PK clotting activities, which normalized with stabilization of the patients. Our results show that the contact phase coagulation factors behave abnormally in certain kidney disease patients.

Blood Coagulation↗
PubMed1984

Effect of exercise and oral contraceptive agents on fibrinolytic potential in trained females.

It has been shown that physical exercise increases blood fibrinolytic potential, primarily by inducing a release of extrinsic plasminogen activator from the vessel wall. Synthetic estrogens have also been reported to influence fibrinolytic activity. The effect of exercise and the possible additional effect of oral contraceptive agents (OCA) on the fibronolytic system were studied in 20 competitive female rowers. Ten females used OCA (users), and 10 others did not (nonusers). All participants were subjected to standardized exhaustive exercise. Preexercise data revealed higher factor XII, total plasminogen, and free plasminogen levels together with a significantly lower C1-inactivator level in the group of users. No differences were observed in prekallikrein, high-molecular-weight kininogen, alpha 2-antiplasmin, alpha 2-macroglobulin, antithrombin III, and histidine-rich glycoprotein plasma levels. The factor XII-dependent fibrinolytic activator activity and the extrinsic (tissue-type) plasminogen activator were significantly higher; however, the urokinase-like fibrinolytic activator activity was significantly lower. These observations suggest a greater susceptibility to activation of the fibrinolytic pathways during OCA medication. Exercise resulted in a decrease of all factors under study but an increase in all fibrinolytic activities. No differences were observed between the two groups in the percentages of change that occurred with exercise.

Adult↗
PubMed1978

Determination of prekallikrein in human plasma: optimal conditions for activating prekallikrein.

A method for the assay of human plasma prekallikrein in which a chromogenic synthetic tripeptide, PPAN, is used as a substrate for kallikrein is described. The conversion of prekallikrein to kallikrein is achieved by cold activation (0 degrees C) with water-soluble dextran sulfate. Conditions for obtaining optimal amounts of free kallikrein with respect to concentration of dextran sulfate, activation time, inhibitors (C-1-inactivator), and requirement of factor XII have been determined. The activation procedure is compared to other known procedures. The assay system was worked out for pooled normal plasma and is applicable to any plasma sample not liable to unwanted preactivation or incomplete inactivation, as revealed by control experiments. A survey in 15 apparently health individuals showed a mean activity of 476 +/- 58 (S.D.) mU/ml with a range of 385 to 586 mU/ml.

Acetone↗
PubMedDate not supplied

[Study of the mechanism of adsorption and activation of enzymes of the contact phase of blood coagulation].

Desorption of enzymes, participating in contact phase of blood coagulation, from silica surface was studied under effect of increased ion strength, in presence of urea, EDTA and surface-active substances. All these agents varied in their capacity to decrease the enzymes activity and to cause the desorption of contact factors. Ionic and hydrogen bonds were shown to carry out the leading role in adsorption of factor XII and in the initiation of the contact phase of blood coagulation.

Adsorption↗
PubMed1994

Varicella and thrombotic complications associated with transient protein C and protein S deficiencies in children.

We report six cases of protein S deficiency secondary to varicella. Five cases were complicated by thrombotic and vascular events, namely purpura fulminans and necrotic vasculitis, deep vein thrombosis and stroke. Two cases were associated with protein C deficiency and one case revealed a heterozygous factor XII deficiency. The underlying mechanism of this acquired protein S deficiency is unclear but could be related to a direct effect of zoster virus.

Chickenpox↗
PubMed2004

The implementation of factor analysis for the evaluation of selected blood parameter changes induced by hyperbaric exposure.

This paper discusses the application of factor analysis when used to compare selected blood parameter (a three-parameter smear, hematocrit, C3c, C4, IgG, IgA, IgM, CRP, fibrinogen and the level of factor XII) properties, just before, and after exposure to pressure changes, and 24-hours after the completion of decompression. To-date the most popular method of statistical analysis was based only on investigation of the significance of the separated individual parameters. This factor analysis that has not been applied previously in the analysis of such problems, enabled the neutral hierarchic evaluation of the significant parameter changes within their chosen range, and mutual relationships. It seems that the application of this method is purposeful and it can be an objective tool for evaluating the significance of changes in blood constituency induced by pressure.

Adult↗
PubMed1985

Reduction of contact factors in sickle cell disease.

Surface-mediated reactions of clotting were compared in 21 black children with homozygous sickle cell disease, 12 age-matched controls, and 15 adults. Both the coagulant and antigen titers of Hageman factor (factor XII) were decreased in asymptomatic patients compared with those in the control groups. These findings were associated with slight but significant reductions in the plasma titers of prekallikrein and high molecular weight kininogen. A further decrease from the initially low titers of these contact factors was observed during vaso-occlusive crises. Additionally, we observed a disparate relationship between Hageman factor coagulant activity and its antigen titers. These data provide evidence for reduction of the contact factors in patients with homozygous sickle cell disease.

Adolescent↗
PubMed1996

Blood protein interactions with titanium surfaces.

Protein adsorption and complement activation were studied on thin evaporated films of titanium (Ti). The surfaces were cleaned in either a radio frequency (RF) plasma unit, or washed sequentially in trichloroethylene, acetone, ethanol, and water. Both methods resulted in hydrophilic surface with low carbon contamination on the outermost oxide (approximately 11-13 at%). In situ ellipsometry suggested that Ti is an intrinsic coagulation activator in vitro, since significant amounts of factor XII (F XII) and high molecular weight kininogen (HMWK) were found on the surfaces after 1 min incubation in heparin plasma. Ellipsometry, performed after serum incubations ranging from 15 s to 30 min showed that the total amount of serum proteins and the deposition of antibodies to complement factor 3c (C3c) increased with serum incubation time. ELISA methods showed increased levels of free iC3b in serum after 10 min incubation of the surfaces, but no detectable amounts of C3 convertase fractions C4d or Bb. Ellipsometric results indicated, however, an increased deposition of antibodies to CIq and IgG on Ti after short serum incubation times. The combined results indicate that Ti-surfaces initially activate complement through the classical pathway. The activation then continues via a positive amplification loop where increased amounts of C3 are deposited on the surfaces via the alternative pathway.

Acetone↗