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PubMed1984

Coagulation abnormalities in patients with end-stage renal disease treated with hemodialysis.

Plasma levels of various blood coagulation factors, antithrombin III and plasminogen were measured in 18 patients with end-stage renal disease treated by longterm hemodialysis. The results were compared with those obtained in a group of normal volunteers. Factors XII, IX and II activities were significantly reduced; factors VIII, VII and X levels were increased; and factors XI and V activities and high molecular weight kininogen concentration were comparable to the control group. Antithrombin III activity and concentration were significantly reduced. The mean plasma fibrinogen concentration was normal although levels above and below normal limits were noted in a few patients. Similarly the mean platelet count was normal, although mild thrombocytopenia occurred in several patients and thrombocytosis in one. In conclusion, the present study confirms published results about factor VIII and AT-III, and provides new information on changes of other coagulation factors in uremia treated by long-term hemodialysis.

Adult↗
PubMed1980

The "contact system" in health and disease.

In the last 10 years, our understanding of the contact system, particularly its biochemistry, has greatly increased. The components of this system and their interactions have been elucidated from in vitro experiments. Although the activation of the contact system have been implicated in various types of human disease, in only a few instances is its role clearly defined. The physiologic role of the contact system is totally unknown at present. Obviously, more studies are needed to bridge a big gap between in vitro observations and in vivo phenomena.

Blood Coagulation↗
PubMed1979

Hageman-factor-dependent fibrinolysis: generation of fibrinolytic activity by the interaction of human activated factor XI and plasminogen.

Human coagulation factor XI has been purified, and upon activation with Hageman factor fragments, was found to convert the fibrinolytic proenzyme plasminogen to plasmin. This proactivator activity was shown to be functionally and antigenically distinct from prekallikrein. When the gamma-globulin fractions of plasma deficient in Hageman factor, prekallikrein and factor XI were isolated, factor-XI-deficient plasma possessed two-thirds of the plasminogen proactivator activity of the Hageman-factor-deficient plasma, while prekallikrein deficient plasma had only one-third of the plasminogen proactivator activity. Thus, the Hageman-factor-dependent plasminogen proactivator previously reported to be present in the gamma-globulin fraction of normal human plasma is a function of prekallikrein and factor XI, while the activity observed in prekallikrein-deficient plasma is attributable to factor XI. When compared utilizing digestion of iodinated fibrin, prekallikrein and factor XIa had similar potency per active site; they were, however, far less active than urokinase.

Blood Coagulation Disorders↗
PubMed1998

Hemofiltration during cardiopulmonary bypass.

Several factors combine to facilitate the evolution towards heart and multi-organ failure following cardiac surgery. Some of these factors are related to pure cardiac aspects, for example, the existence of a preoperative heart disease, the use of aortic cross clamping or performance of cardiotomy. Cardiopulmonary bypass (CPB) also plays an important role in the occurrence of postoperative organ dysfunctions by two principal means. It induces a profound hemodilution, which impairs oxygen transport through tissues. This phenomenon becomes obvious in the postoperative period by the existence of increased transpulmonary O2 gradients, extravascular lung water volume and subsequent impairments of O2 transport. (2) Cardiopulmonary bypass is deleterious by triggering an important inflammatory reaction. This reaction is largely related to the ratio of the circuit area to the patient's body surface area and is therefore maximal in children. It has been widely demonstrated that the very early paths of this reaction imply several humoral factors including kinins, coagulation factor XII and complement fragments. The activation of these factors is self-amplified and triggers both expression and release of numerous mediators by endothelial cells and leukocytes. Finally, these mediators are responsible for the well described "post-bypass syndrome," which is, from a clinical viewpoint, very close to hyperkinetic septic shock. Several methods have been proposed to reduce the deleterious effects of both cardiac surgery and CPB. The older one is hypothermia that considerably reduces the triggering of the inflammatory mediator network. Heparin-coated circuits may also reduce this reaction to some extent. Hemofiltration has been introduced in the 1990s in CPB management. Because of its very high tolerance in patients with compromised circulatory status this technique was already used in the postoperative period to treat patients with acute renal failure. Initially hemofiltration was intended to correct the accumulation of extravascular water during or immediately following the surgical procedure. Nevertheless, several of its side-effects appeared to be useful, such as the reduction of postoperative blood loss and immediate improvement in hemodynamics. Several studies attempted to point out the mechanism of action of hemofiltration and although removal of inflammatory mediator occurs, there is currently no proof that this removal is the actual mechanism by which this technique acts.

Adult↗
PubMed1998

[Hageman trait].

Explore the source record for details and available documents.

Factor XII↗
PubMed1999

Clinical importance of prothrombotic risk factors in pediatric patients with malignancy--impact of central venous lines.

UNLABELLED: To evaluate the role of inherited thrombophilia in the development of central venous line (CVL)-related thrombosis, the following parameters were determined in 77 pediatric-oncologic patients with CVL: activated protein C (APC)-ratio, factor V (FV) G1691A and prothrombin G20210A mutation, protein C, protein S, antithrombin, coagulation factor XII, lipoprotein (a) and homocysteine. An inherited prothrombotic risk factor was found in 17 patients (23%). Four out of 14 patients with a single detect (hyperlipoproteinemia, heterozygous FV G1691A and prothrombin G20210A mutation, protein C deficiency type I) and all three patients with combined defects (heterozygous FV G1691A mutation combined with heterozygous prothrombin G20210A variant, protein S deficiency or hyperlipoproteinemia) suffered from CVL-related thrombosis. In 11 out of 77 patients (14%) a CVL-related thrombosis was detected. In 2 children thrombosis occurred a few days after asparaginase therapy and in another three thrombosis was associated with CVL-related septicemia caused by Staphylococcus epidermidis. After removal of CVL, thrombosis was detected in 5 children, in 2 without clinical symptoms but in the presence of inherited prothrombotic risk factors. CONCLUSION: The present study demonstrates the clinical importance of CVL in combination with inherited thrombophilia in the development of thrombosis in pediatric-oncologic patients. Before or shortly after insertion of CVL, patients should be tested for the presence of factor V G1691A mutation, prothrombin G20210A variant and increased lipoprotein (a) values.

Adolescent↗
PubMed2000

Kallikrein-kinin system activation in streptococcal toxic shock syndrome.

A retrospective analysis of 7 patients with streptococcal toxic shock revealed isolated prolongation of the activated partial thromboplastin time, which returned to normal during recovery. Levels of factor XII were reduced in 2 patients who had single factor assays performed, consistent with activation of the kallikrein-kinin system. We speculate that bradykinin release following activation of the kallikrein-kinin system in streptococcal toxic shock may underlie the features of pain, capillary leaking, and severe hypotension characteristic of this syndrome.

Bradykinin↗
PubMed1981

Chromogenic substrate spectrophotometric assays for the measurement of clotting function.

Spectrophotometric assays for the measurement of coagulation factor activities in plasma have been developed using a relatively specific chromogenic substrate for thrombin. The tissue-factor-activated assay system involves the activation of factors VII and X and prothrombin. The surface-activated assay system involves the activation of factors XII, PK, XI, IX, VII, X and prothrombin using factors V and VIII as cofactors. The thrombin generated subsequent to activation in these two assay systems is measured via its activity on the chromogenic substrate Sarc-Pro-Arg-pNA. These spectrophotometric assays provide a higher degree of sensitivity as compared with the clotting time assays. The tissue-factor-activated system provides a sensitive method for monitoring coumarin therapy. The surface-activated assay system can detect deficiencies of all the factors measured by the conventional APTT assay system, as well as factor VII. Furthermore, this assay provides a sensitive method for monitoring heparin therapy.

Animals↗
PubMed1994

Resistance to activated protein C: evaluation of three functional assays.

Resistance to Activated Protein C (APC) was evaluated using 3 different methods: two of them were based on the prolongation of the Activated Partial Thromboplastin Time (APTT) using 2 different APTT reagents in the presence of APC, whereas the third method was based on the prolongation of prothrombin time when APC is added. The three methods were significantly correlated. APTT-based assays were sensitive to factor XII deficiency, whereas thromboplastin-based assay was sensitive to factor VII deficiency (< 0.5 UI/ml), which surestimates the response to APC. In contrast, an increase in factor VIII (F. VIII) level is associated with a decreased response to APC, when APTT-based assays are used, whereas thromboplastin-based assay is unmodified. During pregnancy, a decreased response to APC is observed, which is not only due to the increase in F. VIII, since thromboplastin-based assay is also modified. In Protein S (PS) immuno-depleted plasma, the low response to APC is corrected by addition of free PS: the thromboplastin-based assay was the most sensitive one to PS deficiency. However, in patients with congenital PS deficiency, there was no correlation between APC-resistance and free PS level. In patients with lupus anticoagulant, discrepancies were observed between the 3 methods, but with a high frequency of low response to APC. For the 3 assays, there was a good differentiation and correlation between normal and pathological results, the thromboplastin-based assay being perhaps the most discriminating. However, 3 unrelated thrombophilic patients showed normal results using thromboplastin-based assay, although they were APC-resistant using APTT-based assays. For 2 patients, this discrepancy can be explained by high levels of F. VIII. For the last patient, an abnormal F. VIII, resistant to APC can be suspected.

Adult↗
PubMed2005

Impaired bradykinin response to ischaemia and exercise in patients with mild congestive heart failure during angiotensin-converting enzyme treatment. Relationships with endothelial function, coagulation and inflammation.

Inflammation and endothelial dysfunction play important roles in the pathophysiology of congestive heart failure (CHF), and the peptide bradykinin, generated during inflammation, may act as a defence mechanism by inducing vasodilation. Plasma bradykinin levels are increased in experimental heart failure but low in patients with advanced chronic CHF despite treatment with angiotensin-converting enzyme (ACE) inhibitors. It is not currently known how bradykinin behaves in less severe phases of CHF controlled by long-term ACE inhibitor treatment. We studied 10 male patients with clinically stable chronic CHF [New York Heart Association (NYHA) class II] on long-term ACE inhibitor treatment and 10 normal sex- and age-matched control subjects. High performance liquid chromatography/radioimmunoassay methods were used to evaluate plasma levels of bradykinin in relation to an array of parameters of endothelial function, coagulation and inflammation before and after stimuli of forearm arterial occlusion and physical exercise. CHF patients had higher levels of bradykinin (P = 0.008), activated factor XII (P = 0.049), interleukin-6 (P = 0.050) and tumour necrosis factor receptor II (sTNFRII) (P = 0.026) than controls. Arterial occlusion and exercise significantly increased bradykinin and von Willebrand factor levels in controls but not in CHF patients. The increase in brachial artery diameter after arterial occlusion was less in CHF patients (P = 0.036) and inversely related to baseline plasma levels of bradykinin (r = -0.855, P = 0.002) and sTNFRII (r = -0.780, P = 0.008). NYHA class II CHF patients during long-term treatment with ACE inhibitors have increased bradykinin levels and signs of inflammation. They are unable to respond adequately to stimuli of ischaemia and physical exercise which both require vasodilation.

Adult↗
PubMed2001

Assembly of high molecular weight kininogen and activation of prekallikrein on cell matrix.

Investigations determined if extracellular matrix of endothelial cells (EC) is a platform for HK assembly and PK activation. In buffers containing bovine serum albumin, biotin-HK binding to ECV304 cells or their matrix requires > or = 50 microM added Zn2+. Ortho-phenanthroline or a HK domain 5 peptide blocks HK binding. Binding to umbilical vein EC or matrix, but not ECV304 cells or matrix, is mediated by cytokeratin 1. Biotin-HK binds to ECV304 cells or matrix with a Kd of 15.8 or 9.0 nM and a Bmax of 2.6 x 10(7) or 2.4 x 10(7) sites/cell, respectively. PK activation on ECV304 cells or matrix is blocked by antipain or SBTI and corn trypsin inhibitor partially inhibits kallikrein formation. PK activation occurs on ECV304 cells or matrix prepared without serum or in human factor XII deficient serum, indicating that the PK activator is not factor XIIa. EC matrix promotes plasminogen activation after the assembly of HK, PK and pro-urokinase. These studies indicate that matrix of various EC has the ability to assemble HK allowing for PK activation and subsequent activities.

Amino Acid Sequence↗