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PubMed1991

[Thrombin.antithrombin III complex].

Increase of TAT is reflected by the generation of thrombin in hypercoagulable state. TAT might increase in DIC characterized by the formation of disseminated micro-thrombosis. DIC was classified into three groups according to the results of screening tests (FDP, platelet count, fibrinogen, prothrombin time). TAT values significantly increased in the stage of pre-DIC compared with the control group consisting of DIC prone underlying disease. Pre-DIC was easily detected by an increase of TAT during the clinical course. Management of high TAT began with the use of an anticoagulant such as heparin under the condition of sufficient ATIII level. The lowering effect of TAT was easily obtained by the anticoagulant. In ATIII-deficient DIC, the high TAT reduced with the substitution of ATIII concentrate, though a transient increase of TAT was found during the administration of ATIII. To reduce the high TAT under the deficient state of ATIII, MD805, a synthetic thrombin inhibitor, was introduced to avoid further consumption of ATIII. The TAT was decreased by the use of MD805 without administration of ATIII. MD805 could be used as an effective anticoagulant in high TAT due to DIC under an ATIII-deficient state. Although the TAT improved with an adequate anticoagulation in DIC, spontaneous bleeding sometimes appeared as a complication associated with the high level of alpha 2 plasmin inhibitor plasmin complex. In this case, the combined use of tranexamic acid relieved the bleeding.

Antithrombin III↗
PubMed1990

[Thrombotic and hemostatic problems in pregnancy and labor and their significance for the fetus and newborn infant].

The following problems are considered: Thrombosis: Safe diagnosis with phlebographic verification is recommended. Heparin has been an established treatment with the great advantage that it does not enter the fetal blood stream. In selected cases surgery or thrombolytic therapy has to be considered. Owing to the high risk of recurrence, prophylactic treatment with Heparin is required throughout pregnancy. Coumarol derivatives traverse the placental membrane to the foetus and have to be avoided because of a risk for teratogenetic injury and intracranial hemorrhage in the foetus. During the puerperium, warfarin might be given because its concentration in breastmilk is low. However, administration of vitamin K1 is recommended to prematures. Attention should be given to the side-effects of Heparin i.e. thrombocytopenia and osteoporosis. The possibility of antithrombin III deficiency should not be overlooked. In such cases it is also risk of thrombosis in the newborn. Premature separation of placenta: In most cases of abruptio placenta immediate delivery by caesarean section is necessary. In cases with partial separation of placenta and immature foetus, treatment with the fibrinolytic inhibitor tranexamic acid (Cyklokapron) has proved useful to prolong pregnancy with maturation of the foetus. Thrombocytopenia: Severe hemorrhage seldom occurs above a level of 50 x 10(9)/l. Treatment with Prednisolon has proved to be of great value. The risk of the child having thrombocytopenia is about 50%. Intraventricular bleedings: Such bleedings mainly occur in prematures. Preliminary results have shown decreased concentrations of specific plasminogen activator inhibitors.

Abnormalities, Drug-Induced↗
PubMed1990

Early deaths and anti-hemorrhagic treatments in acute promyelocytic leukemia. A GIMEMA retrospective study in 268 consecutive patients.

The records of 268 consecutive patients with acute hypergranular promyelocytic leukemia, treated at 29 Italian centers between January 1984 and December 1987, have been reviewed to assess the incidence of early hemorrhagic deaths and the effectiveness of various antihemorrhagic treatments. Three separate groups were considered: 94 patients were treated with heparin, 67 with anti-fibrinolytics (tranexamic acid, epsilon-aminocaproic acid, or aprotinin), and 107 with supportive therapy alone. The overall incidence of early hemorrhagic death (within the first 10 days of treatment) was 9.4%, with no significant differences between the various groups. Similarly, there were no differences in complete remission rates or duration of survival. The consumption of packed red blood cells and platelet concentrates was similar for two of the groups, and there was a significantly greater use of platelet concentrates for heparin-treated patients. High blast cell counts on the day of admission were significantly associated with hemorrhagic death within the first 10 days. These counts, plus high blast cell counts and low platelet counts, were associated with death within 24 hours.

Adolescent↗
PubMed1986

Dental extraction in congenital hemorrhagic patients.

125 dental extractions were performed in patients with hemophilia A, B, von Willebrand disease and rare coagulopathies. The missing factor was brought to a level of 15-40% according to the degree of surgical trauma. In the majority of cases a single pre-extraction administration of concentrate was sufficient. Antifibrinolytics were administered to the patients (tranexamic acid, 60 mg/kg/day) for 8-10 days. After tooth extraction, a fibrin sponge was positioned using anti-traumatic cross suture. In 90% of cases there was no bleeding, in the others modest easily controllable hemorrhagic episodes. Our results show that it is sufficient in hemophilia A and B to use low doses of antihemophilic concentrate (10-20 U/kg) and frequently a single pre-extraction administration. In rare coagulopathies the hemostatic procedure and dental management have also to be similar to those used in hemophilia A and B.

Adult↗
PubMed1989

Use of fibrin glue as a substrate for in vitro endothelialization of PTFE vascular grafts.

The shear stress resistance of cultured human endothelium was investigated on 6 mm polytetrafluoroethylene vascular grafts. Endothelial cell attachment was promoted by precoating the grafts with fibrin glue, which contained human fibronectin and inhibitors of fibrinolysis (aprotinin and tranexam acid). To evaluate the possible effect of fibrinolysis on cell detachment, seven grafts were lined with adult human saphenous vein endothelial cells (AHSVEC) and 11 with fibrinolytically almost inactive human umbilical vein endothelial cells (HUVEC). Endothelial cell seeding was performed in a microprocessor-controlled rotation device, allowing a low inoculum of 12 X 10(4) endothelial cells/cm2. Grafts were then cultivated for 9 days to enable the maturation of the cytoskeleton, before they were exposed to pulsatile shear stress for 48 hours. A mock circulation simulated the flow patterns and the wall shear forces of the femoral artery. After a 3-hour seeding process, 45% of AHSVEC and 43% of HUVEC were attached to the fibrin matrix, forming a confluent monolayer. After 24 hours of perfusion, a cell loss of 23% in AHSVEC- and of 42% in HUVEC-lined grafts was encountered. In spite of a further cell loss during the following 24 hours of perfusion, the majority of the graft surface was still covered by endothelial cells. Therefore we conclude that fibrin glue is a suitable substrate for the formation of a shear stress-resistant endothelial cell monolayer on polytetrafluoroethylene vascular grafts.

Aprotinin↗
PubMed1989

[Current clinical aspects in hemophilia treatment].

The introduction of factor VIII and IX concentrates in the early 1960s brought a significant change in the hemophiliac's life. In consequence hemophilia treatment has been improving rapidly since, and today most life-threatening hemorrhages are controlled by replacement therapy. Hemophilic arthropathy through recurrent joint and muscle bleedings occurs later in life and is often limited to one joint only. Major surgery in hemophiliacs involves little more risk than in non-hemophilic patients, provided of course there is close teamwork between surgeon and hematologist. The most frequent causes of death are no longer hemorrhages but blood-product-associated AIDS and hepatic failure. Fortunately these side effects have been overcome by the use of virus-inactivated concentrates which in Switzerland have been generally administered since 1986. Factor VIII and IX concentrates must contain a precisely declared quantity of factor VIII and IX activity respectively, with a high specific activity. High-purity concentrates should be preferred because of the hazardous effect of foreign proteins administered intravenously in large quantities over a long period. Activation of fibrinolysis with consequent failure of hemostasis or even worsening of hemorrhage may be a clinically relevant side-effect of DDAVP therapy. When DDAVP is used for prophylactic treatment before surgery, an interval of one hour between the intravenous administration of DDAVP and surgery ensures the latter is performed at the time of highest factor VIII and von Willebrand factor level but with already decreased t-PA and fibrinolytic activity. If DDAVP is used in case of hemorrhage or postoperatively, however, the whole fibrinolytic potential must be taken into account. In these cases subcutaneous administration is advantageous due to more protracted t-PA release and the subsequent lower fibrinolytic activity, which can more easily be neutralized by tranexamic acid. To prevent hemophilic arthropathy, correct replacement therapy in hemarthroses is essential: it should be performed as early as possible, preferably in a home therapy program; adequate levels of factor VIII or IX should be achieved and maintained over a sufficient length of time. Hemophiliacs who did not receive replacement therapy during childhood often need major surgery because of severely destructed joints. Joint replacement by total knee and hip prostheses has proved very successful if certain special conditions are fulfilled. Surgical indications should, however, be carefully considered and the possibilities and limits of replacement therapy should be well known. Blood-product-associated hepatitis will be of prognostic relevance in many hemophiliacs treated formerly with non-virus-inactivated concentrates.(ABSTRACT TRUNCATED AT 400 WORDS)

Acquired Immunodeficiency Syndrome↗
PubMed1989

Down-regulation of plasmin receptors on human sarcoma cells by glucocorticoids.

After incubation of confluent monolayer cultures of human HT-1080 fibrosarcoma cells with purified native human plasminogen in plasminogen-depleted serum-containing medium, bound plasmin activity could be specifically eluted from the cells with tranexamic acid, an analogue of lysine. Dexamethasone reduced the amount of recoverable bound plasmin activity in a dose-dependent manner. Dexamethasone was also found to induce a time- and dose-dependent decrease in the ability of the cells to bind added plasmin. Untreated HT-1080 cells bound added plasmin with a high capacity (600,000 molecules bound per cell), and this decreased to an undetectable level after treatment with 100 nM dexamethasone. The kinetics of the loss of plasmin binding by the dexamethasone-treated sarcoma cells, a clear decrease after 4 h, correlated with those for the loss of cell-bound urokinase (u-PA) activity. Plasmin was not, however, bound to the active site of u-PA: an anti-catalytic monoclonal antibody to u-PA had no effect on plasmin binding. Other glucocorticoids, such as hydrocortisone and corticosterone, had a similar effect to dexamethasone on plasmin binding to HT-1080 cells. The effect of glucocorticoids on the plasmin receptor seemed to occur at least partly via a decrease in the affinity for plasmin, since the Kd for plasmin with untreated cells was 5.4 x 10(-9) M, and with cells treated with 5 nM dexamethasone, the Kd value for plasmin was 1.2 x 10(-7) M. These results show that glucocorticoids induce down-regulation of plasmin receptors on the surface of HT-1080 cells: a novel mechanism, in addition to the known effects of glucocorticoids on u-PA and PA inhibitors, by which human tumor cells may be disarmed of their pericellular proteolytic activity.

Cell Line↗
PubMed1989

[Medical hemostasis. II. Systemic hemostatics, a critical evaluation].

The control of spontaneous and traumatic haemorrhage is a matter of constant concern to veterinary practitioners. In some instances, the control of bleeding may be relatively simple using some topical therapeutic procedure, but when haemostatic defects are present, treatment with topical agents alone might not be sufficient, and more radical and life-saving procedures are indicated: replacement therapy with blood or blood products. As this is not easy to perform in most veterinary clinical situations, any therapeutic agent, which facilitates control of haemorrhage is a welcome addition to the therapeutic armament. Besides vitamin K, blood products and agents for topical use, there are only a few agents having a well-defined action on the mechanism of haemostasis. On the other hand several drugs are propagated in the Netherlands as systemic haemostatics in the treatment of bleeding disorders and prevention of haemorrhage during operation. None of these is of proven clinical value in veterinary practice. The only agent, which possibly showed some clinical effect: ethamsylate, has recently been withdrawn from the Dutch market by the manufacturers. Double-blind prospective trials with quantitation of loss of blood showed that antifibrinolytic agents such as tranexamic acid are clinically effective in certain conditions in humans. Because of their mode of action, it might reasonably be expected that these drugs might have positive results in veterinary medicine. Therefore, clinical trials with antifibrinolytic agents are urgently indicated to evaluate the effectiveness and side-effects of these drugs in animals showing severe bleeding or in the prevention of peroperative haemorrhage.

Animals↗
PubMed1989

[Prevention of hemorrhagic cerebral injury in newborn and premature infants subjected to mechanical ventilation].

The newborn brain, and even more so the brain of the premature child, can be considered as an authentic target organ for numerous pathological conditions, some of which exist outside the central nervous system (changes involving primarily both respiratory function and cardiocirculatory function with serious repercussions at encephalic level). In the premature, this greater "vulnerability" is related to the reduced or absent capacity for self-regulation of the cerebral blood low (mechanism influenced negatively by hypoxia, hypercapnia and metabolic acidosis conditions) and the important role played by numerous factors in protecting newborns from haemorrhagic damage. Of these the most important are the state of prematurity, the presence of vascular, intravascular and extravascular changes, the effects exerted on cerebral haemodynamics by mechanical ventilation and by certain drugs employed in treatment. In mechanically ventilated newborns and premature, prevention of haemorrhagic damage (periendoventricular) is currently based on the application of clear-cut protocols of intensive and rehabilitative treatment. The following form part of these protocols: low damage ventilation techniques (high frequencies, low PJP, low MAP), curarisation (to avoid fluctuations in cerebral blood flow), neuroprotection (phenobarbital), the use of substances and drugs which, by exploiting different mechanisms, go to reduce the extent of the haemorrhage (vitamin E, indomethacin, ethamosylate, tranexamic acid).(ABSTRACT TRUNCATED AT 250 WORDS)

Brain↗
PubMed1989

Muscle fibre necrosis induced by intramuscular injection of drugs.

A number of amphiphilic and lipid-soluble drugs of heterogeneous pharmacological properties, when injected into rat anterior tibial muscles, induced acute muscle fibre necrosis. The myotoxic agents were: penicillin, cloxacillin, phenobarbital, haloperidol, diazepam, hydantoin, metoclopramide, pentazocine and chlorpromazine. The regenerative process, studied using the latter three medications, showed rapid regeneration, complete within 3 weeks. Injection of the water-soluble drugs aminophylline, tranexamic acid and vitamins B6 and B12 produced no tissue damage. The pathogenesis of muscle fibre necrosis is suggested to involve direct damage to cell membranes by lipid soluble drugs.

Animals↗
PubMed1989

[Consumption coagulopathy found in mitral stenosis associated with atrial thrombus].

Two cases of consumption coagulopathy found in the patients having mitral stenosis with atrial thrombus were reported. In case 1, although anticoagulant (Warfarin) administration did not correct the hemostatic abnormality, combination of tranexamic acid with anticoagulant was effective. In case 2, atrial thrombus found in the echocardiography prior to the onset of thromboembolism in the lower limbs has been disappeared after embolism. Anticoagulant was effective for the improvement of hemostatic abnormality. We considered mitral stenosis with atrial thrombus as one of causes of the consumption coagulopathy.

Aged↗
PubMed1987

A lysine-binding protein in SLE sera inhibits the binding of immune complexes to normal erythrocyte CR1 (complement receptor type 1).

The binding of 125I-labelled immune complexes (IC) to normal human erythrocyte CR1 (complement receptor type 1) by sera from patients with SLE was found to be significantly decreased compared to normal sera. In 13/29 patients, there was an inhibitor which decreased the binding of opsonized IC in normal sera to normal erythrocytes. It was found in each of the nine patients who had clinically active disease. The inhibitor was shown to be a globulin that was labile at 56 degrees C and bound to lysine; low concentrations of tranexamic acid and of lysine abolished the effects of the inhibitor which suggests that it possesses lysine-binding sites: these may block the CR1-binding site on IC opsonized with complement. This inhibitor may decrease the efficiency of IC carriage by erythrocyte CR1.

Antigen-Antibody Complex↗
PubMed1988

Tissue-type plasminogen activator in patients with intracranial meningiomas.

Three of 13 patients with intracranial meningiomas showed the pre- and postoperative elevation of tissue-type plasminogen activator (t-PA) related fibrinolytic activity in euglobulin fractions (EFA). During operation, two of these three patients showed a significant elevation of the level of fibrin(ogen) degradation products and oozing in the operating field. However, oozing was not observed in the third patient who had been given tranexamic acid preoperatively. Fibrin autography revealed that a broad lytic band of mol wt 50-60 kDa, probably free t-PA, appeared in the plasma obtained from two of the three patients after operation when EFA elevated significantly. In all patients studied, the t-PA antigen levels were normal preoperatively but increased both during and after operation, and correlated mainly with the intensities of a lytic band of mol wt 110 kDa, probably t-PA complexed with its major inhibitor (PAI-1). These results suggest that the excessive fibrinolysis can induce the local hemorrhagic diathesis during operation and may be related to t-PA function in plasma.

Adult↗
PubMed1988

Influence of thrombin-induced disseminated intravascular coagulation on the arteriolar mechanics in the rat mesentery.

Microcirculatory disturbances in experimental disseminated intravascular coagulation (DIC) were analyzed. Fibrinolysis was inhibited by the intravenous injection of tranexamic acid (100 mg/kg) 15 minutes before thrombin infusion, and thrombin (200 IU/body) was infused for the following 60 minutes. After stopping the thrombin infusion, laparotomy was performed for the observation of the microcirculation in the mesentery. The internal diameter of arterioles (20-30 microns) was measured by the image-splitting method incorporated with a television monitor. The microcirculatory disturbances such as sludge and petechia appeared in the early period, and the arteriolar diameter increased gradually. The vasoconstrictive response to catecholamines was enhanced dose dependently. Experimental data suggest that dangerous disorders in the microcirculation might occur as a result of excessive treatment of DIC using catecholamines.

Animals↗
PubMed1988

[Hydrocephalus after aneurysmal subarachnoid hemorrhage].

Diagnosis of hydrocephalus after aneurysmal subarachnoid hemorrhage has been facilitated by CT, but the true incidence and pathogenesis of the condition remain to be clarified. Extent of ventricular dilatation does not necessarily correlate with clinical symptoms and the indication of shunting operation is by no means definite. Consecutive 117 patients with ruptured aneurysm were retrospectively studied for possible factor(s) for development of hydrocephalus in the chronic stage. The incidence of chronic hydrocephalus was found to be high in those patients with aneurysm of the anterior communicating artery, those harboring acute hydrocephalus, those admitted with higher clinical grades, those showing thick clots and gyral enhancement on initial CT, and those who received tranexamic acid in excess of 30 g.

Adult↗
PubMed1985

C1-inhibitor--biochemical properties and clinical applications.

C1-inhibitor (C1-INH) is an alpha-2-neuraminoglycoprotein with a molecular weight of 105,000 daltons. It has a broad spectrum control of the many blood cascades including the complement system. Inherited deficiency of this molecule has been associated with the development of hereditary angioneurotic edema (HANE), a dominant genetic disorder. The liver and monocytes are the primary sites of C1-INH synthesis. The genetic basis of dysfunctional C1-INH is a defect at the structural locus for one C1-INH gene; both the dysfunctional C1-INH gene and the normal C1-INH gene products are present in the plasma of the affected person. The absence of C1-INH permits spontaneous activation of the first component of the complement system (C1); this, in turn, activates C4 and C2. A kinin derived from C2 may be elaborated, which then increases vascular permeability. However, recent investigations have indicated that kinin activity generated from C1-INH-depleted plasma is not derived from C2 but implicates kallikrein, an enzyme which is also controlled by C1-INH, in the formation of a kinin which is most probably bradykinin. A number of therapeutic approaches have been used to treat HANE patients, including antifribrinolytic drugs such as tranexamic acid, plasma infusion, and steroids. The anabolic steroids such as danazol and stanazolol have been used widely to treat HANE patients. We discuss in this review the potential mechanisms by which danazol promotes selective synthesis of C1-INH and several other proteins in the liver.

Angioedema↗
PubMed1985

Intractable periocular hemangioma of infancy.

A case of intractable giant periocular hemangioma in an infant is described. This histologically benign but locally invasive tumour is reviewed from the point of view of complications and available treatment modalities. The indications for therapy with a relatively new antifibrinolytic agent, tranexamic acid, are cited.

Blepharoptosis↗
PubMed1982

A familial hemorrhagic diathesis in a Dutch family: an inherited deficiency of alpha 2-antiplasmin.

This study concerns a case of congenital homozygous deficiency in alpha 2-antiplasmin associated with a severe hemorrhagic diathesis. Heterozygous family members also show a mild bleeding tendency. The propositus is a 17-yr-old male born of white parents and showing a severe hemorrhagic diathesis characterized by spontaneous bleeding in the joints since his early childhood. He was originally suspected of having factor XIII deficiency but was found to have normal functions of the coagulation system and the platelets. Except for alpha 2-antiplasmin, all protease inhibitors showed normal plasma values. With the immediate plasmin inhibition test (synthetic substrate), only 2% of normal functional inhibition was detected, while no reaction with monospecific antisera for alpha 2-antiplasmin was observed. Inhibition of activator-induced fibrinolysis in vitro was reduced. No enhanced spontaneous in vitro fibrinolysis was detected nor were there signs of increased in vivo fibrinolysis during an asymptomatic period. During recovery from a hemorrhagic episode, signs of previous consumption of antithrombin III, alpha 2-macroglobulin, factor XIII, and inter-alpha-trypsin inhibitor were noted. After the diagnosis was made, treatment with tranexamic acid (4 daily doses of 1 g) was effective for about 2 yr. Among the 37 family members studied, a separate group of 16 individuals (including the father and mother of the propositus) with approximately one-half normal plasma levels of alpha 2-antiplasmin both functionally (59% +/- 6%) and immunologically 48% +/- 8%) was discovered. The defect appeared to be inherited as an autosomal recessive gene; no ancestral consanguinity could be shown. The group of apparent heterozygotes as a whole showed increased levels of alpha 1-antitrypsin (142% +/- 39%; p less than 0.01), indicating systemic consequences of the deficiency and reduced binding (+/- 50%) of alpha 2-antiplasmin to fibrin. Six exhibited a mild hemorrhagic diathesis for which no explanation was provided by routine screening of coagulation and platelet functions; also, within the group of heterozygotes, the occurrence of the bleeding tendency did not correlate with differences in residual alpha 2-antiplasmin levels and functions. It is concluded that not only the absence of alpha 2-antiplasmin but also a reduction in its plasma level to +/- 60% of normal may predispose to a hemorrhagic diathesis.

Adolescent↗