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PubMed1994

[Contemporary views on the problem of sepsis].

Sepsis is due to its lethality, which varies round 25%, one of the major problems of contemporary clinical medicine. Classical therapeutic approaches, i.e. chemotherapy, surgical elimination of foci and intensive therapy focused on maintenance of vital functions have obviously reached the limit of effectiveness beyond which they are unable to advance any further. Therefore great efforts are devoted to research into pathogenetic mechanisms involved in sepsis with the aim to use their effect to improve therapeutic results. In the submitted paper the authors analyze the definition of sepsis, explain the concept of the syndrome of systemic inflammatory response and summarize the contemporary state of knowledge of the pathogenesis. A review of structures and mechanisms involved in the genesis and development of sepsis (complement, factor XII, macrophage, endothelial cell, polymorphonuclear leucocyte, thrombocyte etc.) is supplemented by a list of substances which act as mediators of inflammations. The conclusions for practice summarize contemporary therapeutic possibilities, i.e. classical means as well as more recent approaches (colony stimulating factors, haemodiafiltration, antithrombin III, monoclonal antibody against endotoxin). The authors review briefly therapeutic means which are developed at present and which should make it possible to interfere actively with the pathogenesis of the disease.

Humans↗
PubMed2004

Plasma levels of plasminogen activator inhibitor type 1, factor VIII, prothrombin activation fragment 1+2, anticardiolipin, and antiprothrombin antibodies are risk factors for thrombosis in hemodialysis patients.

Patients with end-stage renal disease are prone to hemorrhagic complications and simultaneously are at risk for a variety of thrombotic complications such as thrombosis of dialysis blood access, the subclavian vein, coronary arteries, cerebral vessel, and retinal veins, as well as priapism. The study was devised for the following purposes: (1) to identify the markers of thrombophilia in hemodialyzed patients, (2) to establish a role for antiphospholipid antibodies in thrombosis of the vascular access, (3) to characterize phospholipid antibodies in hemodialysis patients, and (4) to study the effects of dialysis on coagulation cascade. A group of 20 hemodialysis patients with no thrombotic complications (NTC) and 20 hemodialysis patients with thrombotic complications (TC) were studied along with 400 volunteer blood donors. Patients with systemic lupus erythematosus and those with nephrotic syndrome were excluded. All patients underwent a screening prothrombin time, activated partial thromboplastin time, fibrinogen (Fg), coagulation factors of the intrinsic and extrinsic pathways, antithrombin III (AT-III), protein C (PC), protein S (PS), resistance to activated protein C, prothrombin activation fragment 1+2 (F1+2), plasminogen, tissue type plasminogen activator (t-PA), plasminogen tissue activator inhibitor type-1 (PAI-1), anticardiolipin antibodies type M and G (ACA-IgM and ACA-IgG), lupus anticoagulant antibodies, and antiprothrombin antibodies type M and G (aPT-IgM and aPT-IgG). The study showed that PAI-1, F 1+2, factor VIII, ACA-IgM, and aPT-IgM levels were increased significantly over controls both in TC and NTC, however, they could distinguish patients with thrombotic complications from those without, being increased maximally in the former group. The novelty of the study is represented by the significant aPT increase that was observed in non-systemic lupus erythematosus hemodialysis patients, and particularly in those with thrombotic events. In addition, there was a reduction of factor XII during the treatment. It is possible to assume in the TC group and, to a lesser extent, also in the NTC group that endothelial cells liberate PAI-1 in the vascular lumen, which causes hypofibrinolysis. In addition, an excess of factor VIII is activated by endothelial dysfunction with subsequent activation of the coagulation cascade as shown by increased F1+2 and fibrinogen. ACA-IgM, in turn, is capable of interfering with the system of protein C, a potent anticoagulant factor that inactivates cofactors Va and VIIIa. They also induce the expression of procoagulant factors on the surface of the endothelial cells. In conclusion, the hypercoagulable state caused by alterations of coagulation and fibrinolytic factors is a cause of vascular access dysfunction and thrombosis of other vessels.

Antibodies↗
PubMed1994

Biocompatibility studies of the single-needle technique in plateletpheresis with the Fresenius AS 104 blood cell separator.

To investigate the biocompatibility of the single-needle technique of the Fresenius AS 104 blood cell separator we analyzed coagulation, complement and hemolysis parameters prior to, during and after five thrombocytaphereses. The data were compared with results of the same parameters from identical donors in the dual-needle procedure. The analysis of bilirubin, lactate dehydrogenase, hydroxybutyrate dehydrogenase and haptoglobin showed no relevant hemolysis. However, changes of the concentrations of coagulation factors XII and XI indicated an activation of coagulation. This was confirmed by an increase of the thrombin-antithrombin III complex during apheresis. No significant change in the complement split product content of the samples obtained during apheresis was found. Complement factors, glucose, lactate, leukocytes, morphology score and thrombocytes were measured in platelet concentrates. The comparison of the platelet products showed no significant differences except for leukocyte contamination. Glucose and lactate concentrations were similar in both procedures. Levels of complement activation markers were not statistically different.

Bilirubin↗
PubMed1996

Does resistance to endotoxin in primates correlate with levels of plasma prekallikrein?

Increased release of BK by HK hydrolysis has been correlated with the severity of hypotension in septic patients and animals challenged with gram-negative bacteria or endotoxin (ETX). Since HK hydrolysis in vivo is attributed mainly to the catalytic reaction of kallikrein (KAL) formed by activation of plasma PK, I tested whether the known resistance to ETX-rhesus and baboon > man and chimp-correlated with PK levels. Immunoblots and amidolytic assays showed that PK levels did not correlate. They were in rhesus and man > baboon and chimp. Also, PK did not correlate with levels of other modulators of free KAL levels in plasma-factor XII, HK and KAL inhibitors. Nonetheless, the distribution of PK and its activation products in plasmas activated with kaolin at 37 degrees C is analogous in the 4 primates, suggesting a similar mechanism for KAL inhibition in vitro. The results suggest that factors not yet known must contribute to the differential resistance of primates to ETX. Knowledge of these factors will help in prophylaxis and therapy of septicemia.

Animals↗
PubMed1998

In vitro activation of complement and contact system by lactic acidosis.

The activation of complement and contact systems occurs in reperfusion injuries with initial tissue hypoxia, and lactic acidosis such as mycardial infarction and birth asphyxia. The aim of our experiment was the formal proof of activation by sole lactic acidosis. Lactic acid was added to blood and plasma samples from 10 healthy volunteers. C5a and factor XIIa were measured by EIA after incubation at 37 degrees C for 1 h. Both concentrations increased (P < 0.0001 by Friedman analysis) in blood and plasma samples with increasing amount of added lactic acid. Lactic acidosis can activate C5 from the complement system and factor XII from the contact system directly, even in the absence of cellular components.

Acidosis, Lactic↗
PubMed1989

Coagulation cascade, fibrinolytic system, antithrombin III, protein C and protein S in patients maintained on continuous ambulatory peritoneal dialysis.

We studied the coagulation cascade, fibrinolytic system and naturally occurring anticoagulants in a group of 14 patients with end-stage renal disease maintained on continuous ambulatory peritoneal dialysis (CAPD). The results were compared with those obtained in a group of ten normal volunteers. Plasma procoagulant activities of factors XII, XI, IX, VIII, VII, X and II were significantly greater in the CAPD group as compared to the normal control group. Likewise plasma concentrations of total and free protein S were increased in the CAPD group. Although the mean value for plasma factor V activity in the CAPD group was higher than that found in the control group the difference did not attain statistical significance. In addition plasma fibrinogen concentration and factor VIII-related antigen level were significantly increased in CAPD patients. No significant difference was found between the CAPD patients and the control group with respect to plasma levels of protein C, antithrombin III, plasminogen or alpha 2-antiplasmin. In summary, the results demonstrate a tendency for increased levels of various coagulation factors and protein S in CAPD patients with no significant alterations in the levels of various fibrinolytic and endogenous anticoagulant agents, i.e. antithrombin III and protein C. The clinical significance and the mechanism responsible for the observed changes require further investigation.

Antithrombin III↗
PubMedDate not supplied

[Mechanism of the effect of immobilized noradrenaline on the contact phase of blood coagulation].

A deficiency in the contact phase of blood coagulation, depending on the specific isolation of Fletcher's factor (prekallikreins) from blood plasma, was observed after chromatography of blood plasma on a column with noradrenaline-Sepharose. Activation of kalliklein and dekinination of high-molecular kininogene occurred after the interaction between proenzymes of contact phase of blood coagulation (factor XII, prekallikreins, high-molecular kininogene).

Adolescent↗
PubMed2000

Coagulation and fibrinolysis factors in dialysis patients with and without ischemic heart disease.

Cardiovascular disease is the leading cause of death in patients with end-stage renal disease. In addition, abnormalities of coagulation and fibrinolysis have been reported in patients with uremia. However, whether these hemostatic abnormalities lead to cardiovascular disease in dialysis patients is currently unknown. Therefore, we investigated the association of hemostatic factors with ischemic heart disease (IHD) in patients on peritoneal dialysis and hemodialysis. The study patients comprised 30 continuous ambulatory peritoneal dialysis patients and 18 hemodialysis patients. Twenty healthy subjects served as controls. We evaluated each subject's hemostatic factors, including factor VII, factor XII, thrombin-antithrombin III complex (TAT), fibrinogen, plasmin-antiplasmin complex (PIC), plasminogen activator inhibitor (PAI-1), and D-dimer. In dialysis patients, IHD was diagnosed by documented myocardial infarction or positive result on coronary angiogram or by positive thallium myocardial scintigraphy. Factor VII, fibrinogen, PIC, and D-dimer levels were significantly higher in the two dialysis groups than in controls. All hemostatic variables were similar between the two dialysis groups. Subject age (p = 0.005), PIC (p = 0.005), and D-dimer level (p = 0.003) were significantly higher in patients with IHD than in patients without IHD in the dialysis groups. Multiple logistic regression analysis showed that only patient age and D-dimer levels were independent predictors of IHD. Adjusted odds ratio for IHD was 1.06 for each 10 ng/mL increase of D-dimer (p = 0.06). In CAPD patients, only D-dimer was independently associated with IHD (odds ratio: 1.06, p = 0.03). We conclude that multiple hemostatic abnormalities are present in dialysis patients and that elevated D-dimer levels are independently associated with prevalent IHD.

Antifibrinolytic Agents↗
PubMed1983

Surface-governed molecular regulation of blood coagulation.

Among extracellular biological processes the spatial control of blood clotting is a unique phenomenon. Localization in space has very important consequences in both normal and pathological conditions. Under physiological circumstances a clot is formed only in the vicinity of injury, albeit the prerequisites of coagulation are almost completely given in the whole circulation. The local character of blood clotting is secured by the following major conditions: The regulatory signal initiating coagulation-the damaged vascular wall-is itself a surface on which the majority of clotting reactions take place. The first enzyme, factor XII, of the intrinsic coagulation pathway is activated on the collagen fibers exposed in the damaged vascular wall, although the significance of this reaction in respect of the clotting process is ambiguous. On the membrane of platelets adhered to the damaged blood vessel is activated factor XI, too, which is a well-established participant of the intrinsic clotting process. The further consecutive reactions of coagulation are confined to the surface produced by injury, because the enzymes involved contain gamma-carboxyl-glutamyl side chains which are anchored through calcium bridges to the phospholipids of the platelet membrane. The last enzyme of the sequence is thrombin, which is released from the surface. The reactions taking place on the surface form an enzyme cascade, which amplifies the relatively weak triggering signal by several orders of magnitudes. Amplification is ensured not only by the enzyme-substrate relationship of the consecutive reaction partners, but also by spatial confinement, which endows the process with higher efficacy than could be expected on a statistical basis from reactions in solution. It contributes to the efficiency of enzyme cascade that the non-enzymatic regulatory proteins increase the activity of factors IXa and Xa, and thereby the overall process. While the partner of factor IXa, factor VIII, is captured from plasma, factor V, the partner of factor Xa, is derived from the platelets adhered to the damaged surface and orients the binding of factor Xa. The surface localization ensures the protection of the members of clotting system: In the activator complexes found on the surface, the spatial arrangement of clotting factors prevents the inactivation of factors by physiological inhibitors or by proteolytic enzymes and specific antibodies that appear in the circulation in pathological conditions. Platelet factor 4, derived from platelets, binds heparin and thereby markedly decreases the reactivity of antithrombin III, the physiological inhibitor of clotting factors. The above two circumstances are

Blood Coagulation↗
PubMed1982

[Effect of combined use of dextran sulfate and urokinase in cases of preeclampsia-behavior of blood coagulation-fibrinolysis and inhibitor systems].

UNLABELLED: In the severe cases of toxemia of pregnancy, the coagulation-fibrinolysis pattern and the morphological findings of the kidney suggest participation of chronic DIC. Accordingly, it is considered that management of mother and fetus by administration of drugs with anticoagulant and fibrinolytic activities may be useful. METHOD: For 17 cases of preeclampsia (gestosis index, 9.1 +/- 1.5) daily dose of 3,000-1,500mg DS and 48,000 IU of UK were administered intravenously by one shot or drip (10-30 minutes) twice daily. The following clinical and laboratory examinations were done: Gestosis index (GI), blood pressure (BP), edema, urine volume, urine protein, Ccr (ml/min), platelet counts, PT, PTT, PRT, TT, factors XII, IX, VIII, X, VII, V, II and XIII, Fbg, ELT, eug + SKLA(Std), Plg, SFMC, serum and urine FDP, AT-III, C1-INA, alpha 2-PI, alpha 2-M and alpha 1-AT. RESULT: In the preeclamptic women, increases in intrinsic coagulating factors, marked decreases in the extrinsic coagulating factors, depletion of ELT, rise in SFMC, marked increases in blood and urine FDP, and decreases in AT-III and alpha 2-PI were observed, suggesting the presence of chronic DIC. After administration of DS and UK, improvement of clinical findings such as a fall of BP, disappearance of edema, reduction in urine protein, and increase in Ccr were observed. In addition, normalization of the intrinsic system, recovery of the extrinsic system, ELT and serum FDP to normal levels, increasing tendency of Plg, AT-III, alpha 2-PI, alpha 2-M, alpha 1-AT, and disappearance of urine FDP were demonstrated at the same time. It is therefore concluded that this treatment for severe preeclampsia seems to be effective.

Blood Coagulation↗
PubMed1980

Trypsin activation of human factor XI.

Human factor XI circulates as a zymogen composed of two similar or identical chains of Mr = 80,000. Upon activation either by trypsin or by blood-clotting proteins involving clotting factors XII and high molecular weight kininogen, it undergoes proteolytic cleavage in which the Mr = 80,000 chain reportedly is cleaved to a heavy and light chain of Mr of about 48,000 and 33,000, respectively. In these studies, we have reinvestigated trypsin activation of factor XI and demonstrate that trypsin-activated factor XI contains three chains of apparent Mr = 46,000, 37,000, and 26,000. Kinetic studies lead to the conclusion that the parent chain of Mr = 80,000 is cleaved into chains of Mr = 46,000 and 37,000. This cleavage is followed by a second nondestructive cleavage, most probably of the chain of Mr = 46,000, to yield the third product which migrates as a band of Mr = 26,000.

Enzyme Activation↗
PubMed1995

Posttransfusion anaphylactic reactions in a patient with severe von Willebrand disease: role of complement and alloantibodies to von Willebrand factor.

Previous studies have suggested that activation of the complement system might be a major mechanism for posttransfusion non-immunoglobulin (Ig) E-mediated anaphylactic reactions, but its causative effect has not been clearly demonstrated in human models. Serial plasma samples were collected from a patient with severe von Willebrand disease, IgG alloantibodies against von Willebrand factor (vWF), and a history of posttransfusion anaphylaxis. During an 18-day period the patient was treated with factor VIII-vWF concentrate and with recombinant factor VIII. Complement system activation was assessed from plasma levels of C4a, C3a, cleavage products of complement factor B, soluble terminal complement complex, C1 inhibitor and C4-binding protein, and the contact phase of coagulation was assessed from plasma levels of activated factor XII and cleaved high-molecular-weight kininogen. Plasma levels of antibodies to vWF and complement-fixing IgG-vWF complexes were also evaluated. Symptoms of anaphylaxis and signs of complement activation were present only when IgG antibodies to vWF were measurable during replacement with factor VIII-vWF concentrate (days 1 and 6). IgE, IgA, and IgM antibodies to vWF were not detectable in plasma at any time. Replacement with recombinant factor VIII (days 7 to 18) secured hemostasis and did not elicit anaphylactic reactions, and complement parameters did not significantly change even when antibodies to vWF reached peak plasma levels. This prospective study of a natural clinical model indicates a cause-effect relationship between formation of IgG-vWF complexes and massive complement activation in posttransfusion non-IgE-mediated anaphylactic reactions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1979

Nonplasminogen-dependent protease in human plasma.

Equal volumes of plasma and 0.3 M K2HPO4, pH 7.4, were mixed, diluted 20-fold, and adjusted to pH 5.2. After incubation at 37 degrees C for 30 min, the euglobulin percipitate, redissolved in 0.1 M K2HPO4, pH 7.4, developed caseinolytic activity (0.05 CTA U/ml). Na2HPO4 or NaCl of similar ionic strength could replace K2HPO4. The pH optimum of the protease was 6.5, activity falling off sharply below pH 6.0 and above 7.4. The proteolytic activity was inhibited by diisopropylphosphofluoridate and by pancreatic trypsin inhibitor, but was not inhibited by soybean trypsin inhibitor. The activity was not due to plasmin, contact activation, or coagulation factors, since it was fully generated in plasminogen-depleted, factors XII, XI, VII deficient, and prekallikrein-deficient plasmas. Purified Cl-esterase was not caseinolytic in our system. Redissolved euglobulin precipitate prepared from normal plasma without salt addition could serve as starting material for the generation of caseinolytic activity, as could serum, indicating that the Hageman factor cofactor and thrombin are not required. The protease had no detectable procoagulant or fibrinolytic activity.

Chemical Precipitation↗
PubMedDate not supplied

Extrinsic coagulation factors and tissue factor pathway inhibitor in end-stage chronic renal failure.

The relationship between extrinsic coagulation factors, tissue factor pathway inhibitor (TFPI) and activated factor XII (FXIIa) was examined in 71 patients with end-stage chronic renal failure. They had chronic stable uremia due to regular hemodialysis. The patients were divided into two age- and sex-matched groups with and without diabetes mellitus. As extrinsic coagulation parameters, FVIIa and FVII antigen (FVIIag), tissue factor antigen and TFPI (the activity and antigen) were measured. FXIIa was measured as a marker of contact activation, and thrombin generation was evaluated using the two markers thrombin-antithrombin III complex and prothrombin fragment 1 + 2. In both hemodialysis groups with and without diabetes, significant elevations of FXIIa, FVIIa and tissue factor, with high levels of TFPI, were found. Thus, hyperactivation of the coagulation system was in part compensated by TFPI, and a significant increase in FXIIa could not directly affect FVIIa hyperactivation. No differences of these parameters, except for FVIIag and fragment 1 + 2, were found between the groups with and without diabetes. It is suggested that the long-term hemodialysis might have masked any differences due to the underlying disease in these two subgroups.

Aged↗
PubMed1987

Estimation of apparent quadrupolar coupling constants for complexes of magnesium ions with mono- and dicarboxylic acid ligands. Applications to magnesium ion: protein interactions.

25Mg+2 ion NMR studies of complexes of magnesium ions with acetate and malonate ligands have yielded apparent quadrupolar coupling constants, chi, of approximately 1.5 MHz. The aquo magnesium ion yields a smaller chi value of 0.12 MHz, consistent with its expected higher symmetry. chi values for magnesium ion: acetate and magnesium ion: malonate complexes are utilized to calculate observed linewidths for magnesium ion: bovine prothrombin fragment 1 and magnesium ion: human Factor XII interactions. These calculated values are compared with observed values and implications of the agreement are discussed.

Acetates↗
PubMed1992

Localization of blood coagulation factors in the germinal centers of human Peyer's patches.

The immunohistochemical distribution of 15 blood coagulation factors in the germinal centers (GCs) of human Peyer's patches (PPs) was studied. Although factor VIII, active alpha-thrombin, and fibrinogen were hardly evident in the GCs, the majority of coagulation factors, such as kallikrein, high-molecular-weight kininogen, factors XII, X, IX, VII, V, XIIIa and XIIIb, prothrombin, anti-thrombin III and inactive alpha-thrombin were found, showing a lace-like staining pattern similar to that obtained with a monoclonal antibody, R4/23, specific for follicular dendritic cells (FDCs) in the GCs. By immunoelectron microscopy, positive reactions for factor X and XIIIa were found on the surfaces of FDCs, GC cells, and/or in the intercellular spaces of GCs, being especially marked on the surface of the labyrinth-like structure of FDCs. It is concluded that a majority of coagulation factors are localized in the GCs of human PPs. Furthermore, it is suggested that some of these coagulation factors have a close topographical relationship with FDCs.

Antibodies, Monoclonal↗
PubMed1994

Hemorheological and hemostatic parameters in children with nephrotic syndrome undergoing steroid therapy.

Disturbances in hemostatic and hemorheological parameters have been investigated in a group of 29 children with nephrotic syndrome: 23 children classified as steroid-sensitive and 6 as steroid-resistant. Studies were performed before prednisone treatment and 3 weeks later, after initiation of steroid therapy. Before treatment, the alterations in hemostatic system involved moderate thrombocytosis with spontaneous aggregation in 19 patients. High levels of fibrinogen, factor VIII, Willebrand factor, protein C, protein S and alpha 2-macroglobulin (alpha 2M) were observed. Factor XII and alpha 1-antitrypsin (alpha 1AT) were lower than normal. Antithrombin III (ATIII) level was normal in the majority of patients. A plasma and blood hyperviscosity syndrome was also observed as well as an increase in erythrocyte aggregation. During treatment, an improvement in the hemostatic parameters was observed in the patients who responded to prednisone. The expected increase in factor VIII (frequently described in the literature) was not observed, while there was a significant increase in protein C. In the steroid-resistant patients, the only significant changes observed were decreased fibrinogen and increased protein C. The hemorheological parameters showed a tendency towards normality regardless of whether or not the treatment provided remission of NS. The relationship between hemorheological and hemostatic factors changes are discussed.

Adolescent↗
PubMed1986

[Changes in the plasma coagulation factors in patients subjected to plasmapheresis].

Eleven patients with immune-complex diseases were studied, that had been subjected to a total of 96 plasmaphereses during the day. The quantitative changes were followed up that developed in the active factors of coagulation after plasmapheresis. The results revealed that the plasma exchange, applied to the patients studied, induced the following changes: For factor I (fibrinogen)--mean = 2.39 +/- 1.19 g% (p greater than 0.005); for factor II (prothrombin)--mean = 55.5 +/- 20.9% (p less than 0.001); for factor V (proaccelerin)--mean = 97.6 +/- 13.8% (p greater than 0.01); for factor VII (proconvertin)--mean = 106.8 +/- 8.0% (p greater than 0.01); for factor VIII (AHG A)--mean = 64.5 +/- 22.7% (p less than 0.01); for factor IX (AHG B)--mean = 51.58 +/- 26.0% (p less than 0.001); for factor X--mean = 46.4 +/- 18.5% (p less than 0.001) and for factor XII--mean = 27.0 +/- 23.8% (p less than 0.001). That should be given consideration for the indications of the patients and their pretreatment for plasmapheresis.

Adolescent↗