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PubMed1988

Determinants of kallikrein proteolysis of apolipoprotein B-100 in human blood plasma.

The formation of apolipoprotein B-74, a fragment of apolipoprotein B-100, in blood plasma in vitro is shown to occur only at temperatures below 15 degrees C, and is promoted by exposure to glass and other surfaces known to activate factor XII. Removal of C-I esterase inhibitor from plasma permits formation of apolipoprotein B-74 at room temperature. These observations are consistent with conversion of prekallikrein to kallikrein by factor XII, and with evidence that kallikrein proteolysis in vitro is activated in the cold by alteration of its binding to C-I esterase inhibitor. Since the two proteolytic fragments of apolipoprotein B-100 produced by kallikrein digestion are identical to apolipoproteins B-74 and B-26, it is concluded that apolipoproteins B-74 and B-26 are in-vitro products produced in low density lipoproteins of normal plasma in the cold by kallikrein.

Anticoagulants↗
PubMed1998

Hemostatic effects of oral contraceptives in women who developed deep-vein thrombosis while using oral contraceptives.

OBJECTIVE: Comparison of the effect of oral contraceptives on hemostatic variables in venous thrombosis patients (thrombosis while using oral contraceptives) with the effect in healthy control subjects. Our aim was to assess whether some of these effects were more pronounced in women who had suffered thrombosis, i.e., whether these were "hemostatic hyperresponders". STUDY DESIGN: A population-based case-control study, the Leiden Thrombophilia Study. MATERIALS AND METHODS: We investigated 99 pre-menopausal women, age 15-49 years, who had used oral contraceptives at the time of a first, objectively confirmed episode of deep-vein thrombosis. They were not pregnant, nor in puerperium, nor had had a recent miscarriage, and were not using injectable progestogens, nor suffering from inherited coagulation defects. The median time between occurrence of deep-vein thrombosis and venepuncture was 18 months, and 30 of the 99 women were still using oral contraceptives, while 69 had discontinued oral contraceptive use. In addition, a group of 153 control women (54 of them were oral contraceptive users and 99 were non-users) were studied. The following hemostatic variables were measured: APTT, factor VII, factor VIII, factor XII, fibrinogen, prothrombin, total antithrombin, normalised activated protein C sensitivity ratio (n-APC-sr), protein C, protein S and free protein S. RESULTS: We found marked and significant effects of oral contraceptive use on the levels of several clotting factors, with an increase in factor VII, factor XII, protein C and a decrease in antithrombin, n-APC-sr and protein S. Less marked effects that were non-significant or only significant in either patients or controls, were an increase in factor VIII, fibrinogen and prothrombin and a decrease in the APTT and free protein S. In the former thrombosis patients several of these effects of oral contraceptives were more pronounced than in healthy women: specifically on factor VII, antithrombin, n-APC-sr and protein C. CONCLUSIONS: Our results of the effects of oral contraceptives generally confirm previous reports in healthy volunteers. Our data also show that in former deep-vein thrombosis patients these effects are more pronounced. Apparently some women become "high hemostatic responders" when exposed to oral contraceptives, and they may be the women most vulnerable to its thrombogenic effects.

Abortion, Spontaneous↗
PubMed1988

Enzymes of the contact phase of blood coagulation: kinetics with various chromogenic substrates and a two-substrate assay for the joint estimation of plasma prekallikrein and factor XI.

Kinetic constants (Km and kcat) of kallikrein and factor XIa for the chromogenic substrates H-D-L-prolyl-L-phenylanyl-L-arginine-p-nitroanilide (S-2302) and L-pyroglutamyl-L-propyl-L-arginine-p-nitroanilide (S-2366) were determined. The determined constants allow the use of S-2302 and S-2366 in an assay that leads to the joint estimation of factor XI and prekallikrein in activated plasma. The assay reports approximately 3.1 micrograms/ml factor XIa and 34.5 micrograms/ml kallikrein in kaolin-activated plasma (kaolin content 2 mg/ml). The dual-substrate amidolytic assay shows good correlation with the coagulant assay of both factors (0.92 with the prekallikrein assay and 0.98 with the factor XI assay). It is capable, through the joint estimation of factor XI and prekallikrein levels, of differentiating among plasma samples deficient in components of the contact phase of blood coagulation. Kinetic constants of factor beta-XIIa (factor XII fragment) for these substrates and for N-benzol-L-isoleusyl-L-glutamyl-glycyl-L-arginine-P-nitro ani lide (S-2222) were determined, and they allowed the assessment of the contribution of this factor to this assay and its estimation in the activated phase.

Blood Coagulation↗
PubMed1988

Modulation of the human monocyte binding site for monomeric immunoglobulin G by activated Hageman factor.

Macrophage Fc gamma receptors play a significant role in inflammation and host defense. One monocyte/macrophage Fc gamma receptor, Fc gamma RI, the binding site for monomeric IgG, appears to be especially responsive to modulatory signals by hormones and mediators. Since Factor XIIa is generated during inflammation, we studied the effect of XIIa on Fc gamma RI. Factor XIIa, in a concentration-dependent manner (0.01-0.19 microM), reduced the number of monocyte binding sites for monomeric IgG up to 80% without altering the affinity of binding. Its precursor, Factor XII, and the low molecular weight fragment of XIIa, lacking most of the heavy chain region, did not reduce the expression of Fc gamma RI. Neither corn trypsin inhibitor (36 microM) nor diisopropylfluorophosphate (3.6 mM) diminished the effect of Factor XIIa on Fc gamma RI, although each completely inhibited the coagulant and amidolytic activity contained on the light chain of Factor XIIa. Protein synthesis was not a requirement for this effect of Factor XIIa, nor was internalization of Fc gamma RI necessary. In contrast to similar concentrations of IgG, Factor XIIa failed to displace significantly monomeric IgG from the monocyte surface, suggesting that Factor XIIa does not directly compete for Fc gamma RI. The data suggest that the heavy chain of XIIa, which contains domains that may have cell hormone activity, also contains a domain that regulates Fc gamma RI on monocytes. In addition to other hormones and mediators, Factor XIIa may serve a regulatory function in modulating Fc gamma receptor expression during inflammation.

Binding Sites↗
PubMedDate not supplied

Prekallikrein activator (Hageman factor fragment) in human plasma fractions.

The recent finding that hypotensive reactions to blood products can be attributed to the presence of a prekallikrein activator in the products, prompted us to measure the distribution of this substance among plasma fractions produced by the cold ethanol method. While the levels observed varied among different production lots, prekallikrein activator was found to be present in four lots of fibrinogen, four lots of immune serum globulin, one lot of immune serum globulin for intravenous use, and nine lots of antihemophilic factor. Nineteen lots of 25% albumin were tested and found to be free of detectable amounts of prekallikrein activator. In addition to 25% albumin and the fraction V rework fractions leading to it, only supernatant III from the fraction II + III reworks was found to be free of the prekallikrein activator. All other fractions contained significant amounts of activity. Chloroform treatment, used to move kallikrein inhibitors was found to destroy the prekallikrein activator in fractions with low protein levels. The prekallikrein activator in antihemophilic factor preparations was formed during contact with glass, and its behavior led to the conclusion that these concentrates contained Hageman factor (Factor XII).

Esterases↗
PubMed2000

Activation of coagulation during treatment with haemodialysis.

Generation of factor XII, thrombin antithrombin complexes, prothrombin fragment 1+2 and thrombus precursor protein has been monitored in 16 subjects during haemodialysis. Immediately after starting treatment, contact of blood with the negatively charged surfaces of the polyacrylnitril membrane AN-69 resulted in a 9-45% decrease in factor XII activity. Peak concentrations for thrombin antithrombin complexes (50 to 120 microg/L) were observed 30 min after the start of haemodialysis. Establishment of thrombus precursor protein concentrations yielded steadily increasing results without any tendency to decrease during treatment. Determination of thrombin antithrombin complexes is considered to establish the most sensitive short-term reacting parameter indicating activation of coagulation. A steady generation of fibrin and fibrinogen-fibrin complexes during treatment with haemodialysis is indicated by increasing results for thrombus precursor protein. In order to prevent clotting during haemodialysis, an additional supplementation of anticoagulant is needed.

Adult↗
PubMed1988

Coagulation factors of contact phase of haemostasis are normal in well-controlled type-I diabetic patients despite presence of diabetic retinopathy.

Alterations of plasma coagulation factors have been reported in diabetic patients with severe microangiopathy and metabolic derangement. No information is available, however, for well-controlled type-I diabetic patients. Thus, we studied coagulation factors of the contact phase and inhibitors in 80 fairly well-controlled diabetics (42 female, 38 male, age 28 +/- 11 SD years). Mean HbA1c in these patients was 6.6 +/- 1.0 SD, duration of diabetes ranged from 6 months to 30 years, and 36% had retinopathy shown by fluorescein angiography. The well-controlled diabetic patients did not differ from controls in terms of the activity of prekallikrein, factor XII, high molecular weight kininogen, kallikrein inhibitor, C-1-esterase inhibitor and antithrombin III. Only alpha-2-macroglobulin, an inhibitor of the contact phase of blood coagulation, was elevated significantly in these patients (p less than 0.05). Diabetics with retinopathy had similar activities of prekallikrein, factor XII, high molecular weight kininogen, kallikrein inhibitor, c-1-esterase inhibitor and antithrombin III when compared with patients without retinopathy and controls respectively. alpha-2-macroglobulin did not differ in patients with and without diabetic retinopathy but were significantly elevated in both groups compared with controls. Correlation analysis showed significant positive correlation between HbA1c and the activity of high molecular weight kininogen, kallikrein inhibitor and alpha-2-macroglobulin. In patients with poor metabolic control (n = 11; 6 female, 5 male; age 25 +/- 5 SD years; HbA1C 10.7 +/- 0.9) prekallikrein (p less than 0.05), kallikrein inhibitor (p less than 0.005) and alpha-2-macroglobulin (p less than 0.005) were significantly elevated compared to the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

A model for thromboembolization on biomaterials.

A model was developed to describe the kinetics of protein and platelet deposition and embolization on biomaterials. The model assumes that proteins can be adequately represented by fibrinogen, albumin, and Factor XII, that protein adsorption is Langmuir-type, that surfaces are homogeneous, and that all adsorption and deposition steps are first order. Eleven model parameters were determined from literature experimental data from ex vivo experiments utilizing canine and baboon blood on Silastic, one parameter came from adsorption of Factor XII on glass, and three parameters were obtained by minimizing differences between experimental and predicted fibrinogen adsorption, and platelet deposition and embolization behavior. The model well predicted observed behavior for fibrinogen adsorption, platelet deposition, and platelet embolization on Silastic, and platelet embolization from both polyacrylamide and HEMA-MAAC.

Animals↗
PubMed2001

Analysis of the activated partial thromboplastin time test using mathematical modeling.

Activated partial thromboplastin time (APTT) is a laboratory test for the diagnosis of blood coagulation disorders. The test consists of two stages: The first one is the preincubation of a plasma sample with negatively charged materials (kaolin, ellagic acid etc.) to activate factors XII and XI; the second stage begins after the addition of calcium ions that triggers a chain of calcium-dependent enzymatic reactions resulting in fibrinogen clotting. Mathematical modeling was used for the analysis of the APTT test. The process of coagulation was described by a set of coupled differential equations that were solved by the numerical method. It was found that as little as 2.3 x 10(-9) microM of factor XIIa (1/10000 of its plasma concentration) is enough to cause the complete activation of factor XII and prekallikrein (PK) during the first 20 s of the preincubation phase. By the end of this phase, kallikrein (K) is completely inhibited, residual activity of factor XIIa is 54%, and factor XI is activated by 26%. Once a clot is formed, factor II is activated by 4%, factor X by 5%, factor IX by 90%, and factor XI by 39%. Calculated clotting time using protein concentrations found in the blood of healthy people was 40.5 s. The most pronounced prolongation of APTT is caused by a decrease in factor X concentration.

Blood Coagulation Disorders↗
PubMed1986

Prekallikrein deficiency in a family of miniature horses.

Two sibling miniature horses, a male and a female, had a normal 1-stage prothrombin time and a prolonged activated-partial thromboplastin time (APTT). The addition of as little as 5% of a normal equine plasma pool to the plasma samples of both horses shortened their prolonged APTT to within normal limits. Coagulation factor analysis revealed deficiencies in factor XII (12 and 13 U/dl, control population 77 to 128 U/dl), when determined with a feline factor XII-deficient plasma substrate, but normal concentrations (119 and 96 U/dl) when a human factor XII-deficient plasma substrate was used. Deficiencies of another factor, prekallikrein, were detected with a human prekallikrein-deficient plasma substrate (16 and 6 U/dl, control population 70 to 173 U/dl). Other intrinsic coagulation factors were present in normal concentrations. The APTT was measured with plasma from the 2 horses after various incubation periods (1 to 15 minutes) with a contact activator before the addition of Ca ions. With incubation times of greater than or equal to 10 minutes, the APTT of both horses were essentially the same as that of the normal equine plasma pool. Several family members of the 2 prekallikrein-deficient miniature horses appeared to be heterozygous carriers of the prekallikrein deficiency.

Animals↗
PubMed1994

Blood compatibility of sputter-deposited alumina films.

The surface modification of metals by the application of blood compatible ceramics is one approach to developing durable and blood-compatible materials. The blood compatibility of sputter-deposited alumina films was investigated in vitro. The alumina films were prepared by reactive sputtering and conventional sputtering. Diffractometer studies of the alumina films indicate that the sputter-deposited alumina films have amorphous structures. Electron spectroscopy chemical analysis studies of the alumina films indicate that the sputter-deposited alumina films are nonstoichiometric (O/A1 ratio of 1.15-1.66). We examined the platelet reaction to the alumina films and the intrinsic coagulation factor XII activation by the alumina films. Medical grade segmented polyurethane was also tested. The alumina films experienced an adhesion of about 50% fewer platelets than the segmented polyurethane. Also, fewer platelet morphologic changes were observed on the alumina films than on the segmented polyurethane. Factor XII activation was less on the alumina films than on the segmented polyurethane. Surface modification by the sputter-deposited alumina films is promising for developing blood-compatible and durable materials.

Aluminum Oxide↗
PubMed2001

Phosphatidylethanolamine participates in the stimulation of the contact system of coagulation by very-low-density lipoproteins.

We have analyzed the influence of plasma lipoproteins on the activation of the contact pathway of blood coagulation in platelet-rich plasma (PRP). The formation of thrombin in PRP incubated in vitro was abolished by the factor XIIa antagonist corn trypsin inhibitor and by severe factor XII deficiency, indicating mediation by the contact system. Addition of VLDL to the PRP shortened the lag period and increased the generation of thrombin. There was no effect of HDL and LDL. In whole blood, VLDL accelerated the rate of fibrin formation, the procoagulant effect being prevented by factor XII deficiency and by corn trypsin inhibitor. The thrombin formation in the PRP was strongly increased by microemulsions of the VLDL lipids while it was reduced by the aqueous phase of the particles. Separation of the VLDL lipids indicated the phospholipid component as the major activating principle. Vesicles supplemented with all VLDL phospholipids but lacking specifically the fraction containing phosphatidylethanolamine (PE) prolonged the lag time. The PE containing fraction alone as well as vesicles enriched with egg PE shortened the lag period. In summary, VLDL stimulates the contact pathway of blood coagulation, ethanolamine phospholipids being the most active components of the particles.

Adult↗
PubMedDate not supplied

Prothrombotic states associated with retinal venous occlusion in young adults.

BACKGROUND: The etiology of retinal venous occlusion in young patients is not well understood although thrombosis does occur histologically. A search for the risk factors that may lead to thrombosis is highly desirable may contribute to our understanding of the pathogenesis of this complication and may improve our therapeutic strategies. METHODS: We studied 17 patients with retinal venous occlusion. All patients were under 45 years of age (mean 37.8 +/- 7.1). Antiphospholipid antibodies (APAs) and certain hemostatic factors were determined. The results obtained in these patients were compared to those of normal controls. RESULTS: We found APAs in 8 out of 17 patients compared to 5 out of 60 controls (p = 0.0002). In patients with major trunk occlusion, there was a trend for the presence of APAs in those with poor visual acuity at presentation. Deficiencies of the coagulation inhibitor proteins C and S and antithrombin III activities were detected in 6 patients, and reduced levels of Factor XII were found in 4 patients. Levels of hematocrit, erythrocyte sedimentation rate. Fibrinogen, alpha 1-globulin, and alpha 2-globulin were significantly higher in patients compared to the controls (p = 0.019; 0.014; 0.0001; 0.011; 0.047), indicating increased blood viscosity in patients with retinal venous occlusion. CONCLUSION: Prothrombotic changes in the form of APAs and/or deficiencies of coagulation inhibitors and Factor XII may contribute to the etiology of retinal venous occlusion in young adults. Young patients with retinal venous occlusion should be evaluated for these prothrombotic states.

Adult↗
PubMed2003

Parental history of hypertension is associated with coagulation-fibrinolytic balance disorders.

It has been previously shown that essential hypertension (EH) is associated with coagulation-fibrinolytic balance disorders. Our study was conducted in order to investigate disturbances in coagulation-fibrinolysis in offsprings of hypertensive parents. Two groups were studied: 44 healthy normotensive individuals (17 male, 27 female, age range 12-22 years) with a documented family history of hypertension and 33 individuals (14 male, 19 female, age range 11-21 years) without a family history of essential hypertension. The following parameters were determined in both groups: plasminogen activator inhibitor-1 antigen, tissue plasminogen activator antigen, fibrinogen, fibrin degradation products, thrombomodulin, protein S antigen, protein C activity, von Willebrand factor Ag, factor VII and factor XII activity. Additionally, systolic and diastolic blood pressure, insulin levels, blood lipids and heart rate were determined. The two groups were not found to have differences with respect to age, gender, body mass index, blood lipids and insulin levels. Hypertensive offsprings had significantly higher plasma levels of plasminogen activator inhibitor-1 antigen, fibrinogen, fibrin degradation products, protein S antigen and factor XII activity, while no differences were observed to the other haemostatic variables studied. Hence, offsprings of hypertensives had significantly higher diastolic blood pressure and heart rate. In conclusion, alterations regarding blood pressure, heart rate and fibrinolytic function exist in offsprings of hypertensive parents compared to individuals without family history of hypertension.

Adolescent↗
PubMed2006

Effect of varying the ratio of n-6 to n-3 fatty acids by increasing the dietary intake of alpha-linolenic acid, eicosapentaenoic and docosahexaenoic acid, or both on fibrinogen and clotting factors VII and XII in persons aged 45-70 y: the OPTILIP study.

BACKGROUND: Elevated fibrinogen, activated factor XII (FXIIa), and factor VII coagulant activity (FVIIc) are associated with higher risk of fatal ischemic heart disease. This study tested the hypothesis that lowering the dietary ratio of n-6 to n-3 polyunsaturated fatty acids (n-6:n-3) would modify these risk factors in older men and women. OBJECTIVE: The objective of the study was to measure fasting hemostatic risk factors and postprandial changes in activated FVII (FVIIa) concentrations after a 6-mo alteration in dietary n-6:n-3. DESIGN: In a randomized, parallel design in 258 subjects aged 45-70 y, we compared 4 diets providing 6% of energy as polyunsaturated fatty acids at an n-6:n-3 between 5:1 and 3:1 with a control diet that had an n-6:n-3 of 10:1. The diets were enriched in alpha-linolenic acid, eicosapentaenoic (EPA) and docosahexaenoic (DHA) acid, or both. RESULTS: Fasting and 3-h plasma triacylglycerol concentrations were 11.1% and 7.2% lower with the diet that had an n-6:n-3 of approximately 3:1 and that was enriched with EPA and DHA than with the other diets. Fasting fibrinogen, FXIIa, FVIIc, FVIIa, and FVII antigen and postprandial FVIIa were not influenced by the diets. Avoiding foods high in fat the day before measurement decreased FVIIc and FVIIa by 8% and 19.2%, respectively. A test meal containing 50 g fat resulted in a mean 47% (95% CI: 42%, 52%) increase in FVIIa 6 h later, but the response did not differ by n-6:n-3. CONCLUSION: Decreasing the n-6:n-3 to approximately 3:1 by increasing the intake of EPA and DHA lowers fasting and postprandial plasma triacylglycerol concentrations in older persons but does not influence hemostatic risk factors.

Aged↗
PubMed1987

Posttraumatic acute cholecystitis. Relationship to the initial trauma.

Posttraumatic acute cholecystitis is an often unrecognized and potentially fatal complication seen among patients hospitalized for trauma, and differs in etiology from cholecystitis which develops de novo. The cause, although not yet clearly defined, is believed to be related to bile stasis, ischemia, bacterial infection, sepsis, the activation of factor XII, and the Shwarzman reaction. A case is described in which a 53-year-old man with pelvic fractures developed acute acalculous cholecystitis and died of multiple organ failure 3 weeks following cholecystectomy. The histopathological findings are also reported; these are most likely attributed to the Shwarzman reaction or the activation of the factor XII pathways. There has been a tendency to regard posttraumatic acute acalculous cholecystitis as induced by trauma, and calculous as mere coincidence. We believe, however, that it is not calculous but histopathological findings that determine whether acute cholecystitis following trauma was more than coincidence or just mere coincidence. Although progress in clinical care has improved the chances of survival of severely traumatized patients, posttraumatic acute cholecystitis has been increasing in frequency. We cannot be careful enough in judging the relationship of this fatal complication to the initial trauma.

Acute Disease↗
PubMed1984

Blood coagulation and fibrinolytic factors and their inhibitors in critically ill patients.

In a search for new variables, for the diagnosis of disseminated intravascular coagulation (DIC) and for guidelines of therapy in such conditions, 22 severely ill patients were studied. The diagnosis of DIC was based on determinations of platelet counts, prothrombin complex (Normotest), antithrombin (AT), fibrinogen degradation products and fibrinogen. Nine patients were diagnosed as having DIC, eight patients were referred to a suspected DIC group and five to a group of no DIC. The laboratory findings were found to agree with the clinical status. In addition several new parameters were investigated: factor XII, prekallikrein, Simplastin A--another prothrombin complex factor method, factor X, plasminogen (PLG), antiplasmin (AP) and kallikrein inhibitors (KI). Platelet counts, prothrombin complex and antithrombin were mostly pathological in DIC-patients. Of the alternative tests prothrombin complex, fibrinopeptide A and the kallikrein inhibitor as well as the two tests for fibrinolysis (PLG and AP) were significantly altered in DIC-patients. The inhibitor capacity (AT, APV and KI) was lower in patients who died than in survivors and decreased still further in those of the non-survivors who had DIC. Thus the inhibitors can be used as predictors of outcome and hopefully for guiding therapy. To establish the diagnosis of DIC we suggest measurement of platelet count, prothrombin complex, plasminogen as well as of the inhibitors.

Adolescent↗
PubMed1985

Activation and inhibition of Hageman factor-dependent pathways and the complement system in uncomplicated bacteremia or bacterial shock.

Levels of components of the contact activation, coagulation, and complement systems and their main inhibitors were measured in 45 critically ill patients during 61 episodes of uncomplicated bacteremia or bacterial shock. Levels of Hageman factor (factor XII), prekallikrein, high-molecular-weight kininogen, factor XI, factor VII, total hemolytic complement, alternative pathway activity, and C3 were within the normal range during uncomplicated bacteremia (n = 29), but during fatal bacterial shock (n = 13) a significant decrease by 40%-50% was observed in all measurements. During nonfatal bacterial shock (n = 19) a moderate decrease was observed in most of these measurements. The capacity of plasma to inactivate kallikrein was significantly higher during bacteremia than during bacterial shock because of a significant increase in the level of C1 esterase inhibitor. Levels of antithrombin III and alpha 2-macroglobulin were below normal in all groups. Thus increased inhibition of the contact activation and complement systems is beneficial during bacteremia.

Angiotensin III↗