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PubMed1994

Recombinant activated factor VII (rFVIIa) therapy for intracranial hemorrhage in hemophilia A patients with inhibitors.

We report the use of recombinant VIIa (rFVIIa) in the treatment of five ICHs in two factor VIII-deficient patients with inhibitors. In four of five ICHs, rFVIIa was the only factor replacement used at doses of 60-135 micrograms/kg every 2-4 hr for 12-14 days. Hemostasis at the primary site of bleeding was achieved in all cases, and all patients survived with no permanent neurologic deficits. However, the patient who received the highest dose of rFVIIa during the first 4 days of therapy developed clinical symptoms consistent with a cerebral vascular accident of the brainstem characterized by acute onset of truncal ataxia and upward-gaze nystagmus on day 8 of rFVIIa therapy. While receiving rFVIIa therapy for treatment of these five ICHs, four treatment courses were complicated by bleeding at sites other than the primary site, including two episodes of localized oozing at central line insertion sites, two episodes of hemarthrosis, and two episodes of epistaxis. Antifibrinolytic therapy with tranexamic acid was effective in two of these episodes. Laboratory evaluation revealed shortening of the PT, variable shortening without normalization of the APTT, peak factor VII activity levels 7-30-fold higher than normal baseline values, and normal antithrombin III (ATIII) and alpha 2-antiplasmin levels. In four of five ICHs, there was a 20-40% decrease in fibrinogen levels from baseline. The decrease in fibrinogen was accompanied by an increase in fibrin degradation products in 3/5 episodes and a 15-35% decrease in plasminogen activity levels in 2/5 episodes. Tissue factor pathway inhibitor (TFPI) levels remained stable and in the normal range. Although rFVIIa is an effective new therapy for the treatment of ICH in hemophilia patients with inhibitors, its optimal use with respect to safety and efficacy requires further clinical study.

Cerebral Hemorrhage↗
PubMed1993

Epileptic seizures after subarachnoid hemorrhage.

We studied predictive factors for the occurrence of epilepsy in 381 consecutive patients admitted within 72 hours after they had a subarachnoid hemorrhage from a ruptured intracranial aneurysm. Fits occurring in the presence of hyponatremia or within 12 hours after the initial bleed, rebleeding, or aneurysm surgery were classified as associated with these acute events and we did not regard these fits subsequent epileptic seizures. Thirty-five patients (9%) had one or more epileptic seizures, 12 hours to 1,761 days after the initial bleed (median value, 18 days). The following variables were included in the analysis: sex, age, history of hypertension, history of cardiovascular disease, loss of consciousness at ictus, sum score on the Glasgow Coma Scale on admission, sum score for the amount of cisternal blood and presence of intraventricular blood based on the initial computed tomography (CT) scan, occurrence of ictal seizures (seizures occurring within 12 hours after the onset), acute hydrocephalus, rebleeding, delayed cerebral ischemia, fluid intake, treatment with tranexamic acid, ventricular drainage, and aneurysm surgery. After multivariate analysis by means of Cox proportional hazards model with stepwise forward selection of the variables, a high cisternal blood score and rebleeding proved to be significantly related to epilepsy (hazard ratio = 2.06, p = 0.040; and hazard ratio = 3.02, p = 0.016), even after the exclusion of 28 patients who received perioperative prophylactic anticonvulsant therapy (hazard ratio = 2.31, p = 0.022; and hazard ratio = 3.65, p = 0.006, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

A new model of osteoarthritis in rabbits. III. Evaluation of anti-osteoarthritic effects of selected drugs administered intraarticularly.

A battery of steroidal and nonsteroidal antirheumatic drugs and protease inhibitors were tested by intraarticular injection for effects on osteoarthritis of the knees of rabbits subjected to partial lateral meniscectomy and section of the sesamoid and collateral fibular ligaments. Among the standard drugs, only the glucocorticoid, triamcinolone hexacetonide, and the protease inhibitor, tranexamic acid, exhibited significant anti-osteoarthritic activity. An experimental drug, GPA 2163, also offered some protection against joint degeneration. The nonsteroidal antiinflammatory drugs had no effect on the development of osteoarthritis in the model.

Animal Diseases↗
PubMed1989

Surgery in patients with von Willebrand's disease.

The risk of bleeding complications in the surgical treatment of patients with von Willebrand's disease has been evaluated. Sixty-four major surgical procedures were performed in 51 patients with various forms of von Willebrand's disease. In 18 cases, the bleeding disorder was unknown at the time of surgery, resulting in bleeding complications in 12 cases (67 per cent). Forty-five operations were carried out in patients in whom the diagnosis of von Willebrand's disease was known at the time of surgery. In these patients, the following haemostatic preparations were given: factor concentrate, fresh plasma, tranexamic acid and desmopressin. Haemostatic complications occurred in three of these operations (6.7 per cent); all were managed easily. No mortality was observed. It is concluded that patients with von Willebrand's disease do not carry an increased operative risk if appropriate precautions are taken.

Adolescent↗
PubMed2002

Effect of fibrin sealant composition on human neutrophil chemotaxis.

The use of fibrin sealants offers one of the most physiologically compatible approaches to preventing postoperative adhesions. Although a number of fibrin sealant formulations have been developed, little is known about how the various components of these preparations affect the wound-healing process. Because one of the key steps in wound healing is the migration of phagocytic leukocytes, such as neutrophils, into the site of injury, we performed studies to characterize systematically the effects of various fibrin sealant components on neutrophil chemotaxis. Using a transwell chemotaxis assay, we found that increasing fibrin concentration resulted in an inhibition of the ability of the cells to migrate through the clots in a dose-dependent manner, and at fibrin clot concentrations >2.0 mg/mL chemotaxis was completely blocked. Factor XIII crosslinking of the clots also had a significant impact on neutrophil chemotaxis, and sealant preparations deficient in Factor XIII allowed neutrophil migration at much higher fibrin concentrations. The presence of various other fibrin sealant components such as plasminogen and fibrinolysis inhibitors (aprotinin and tranexamic acid) did not have any significant effects on the ability of neutrophils to migrate through fibrin clots as compared to control clots without these components. Overall, these studies show that the composition of fibrin sealant preparations can significantly affect neutrophil migration into the site of injury, which could possibly influence the wound healing process.

Chemotaxis, Leukocyte↗
PubMed1994

Relationship of the plasminogen activator/plasmin cascade to osteoclast invasion and mineral resorption in explanted fetal metatarsal bones.

An attempt was made to establish whether the activation of plasminogen into plasmin is necessary either for the preparatory phases to bone resorption, involving the recruitment of osteoclast precursors, their migration toward mineralized surfaces, and their final differentiation, or for the subsequent osteoclastic resorption phase. 45Ca-labeled fetal (17 day) mouse metatarsals were cultured under conditions in which they pursue their modeling for a few days. In this model, the resorption phase, monitored by the release of 45Ca into the medium, is entirely dependent on the preparatory phases affecting osteoclast precursors. It was, as expected, stimulated by parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D3 and inhibited by calcitonin. PTH also enhanced the activity of tissue-type plasminogen activator (PA) in extracts of metatarsals but not that of urokinase (which is, however, the main PA present in the mouse fetal metatarsal culture model). The resorption processes were not dependent on the presence of plasminogen in the media, even when the rudiments were precultured with tranexamic acid to remove their endogenous plasminogen. Moreover, they were not influenced by inhibitors of plasmin, either the plasma inhibitors alpha 2-antiplasmin, alpha 2-macroglobulin, and alpha 1-antitrypsin, or aprotinin, which was tested under a variety of conditions. Aprotinin also did not influence the resorption (loss of calcium and hydroxyproline) of 19 day fetal mouse calvariae cultured with PTH in a medium devoid of plasminogen. It is concluded that the various steps implicated in the bone resorption processes that occur in the metatarsals and in the calvariae culture models are not dependent on the activity of plasmin. The function of PAs in bone, however, could be exerted through direct proteolysis of extracellular proteins other than plasminogen or be mediated by a molecular structural domain distinct from their catalytic domain.

Animals↗
PubMed1992

Plasmin generation induces neutrophil aggregation: dependence on the catalytic and lysine binding sites.

We established that plasmin (10(-10) M to 10(-6) M) caused neutrophils (PMN) to aggregate using an in vitro assay. Plasminogen had no PMN aggregatory activity even at a concentration of 2 microM. However, plasminogen caused PMN to aggregate when incubated with plasminogen activators [tissue plasminogen activator (25-200 U/ml) or urokinase (5-500 U/ml)]. Tissue plasminogen activator and urokinase alone had no PMN aggregatory activity. Analysis of these incubation mixtures indicated that plasmin was generated in the process and that the time course of plasmin generation correlated with the aggregation response. Active-site-inhibited plasmin did not induce PMN aggregation, indicating that a functional catalytic site was required for the response. Pretreatment of PMN with either active-site-inhibited plasmin or tranexamic acid prevented PMN aggregation by plasmin, indicating that both binding of plasmin to the cell surface via the lysine binding sites and catalysis were required for the response. The generation of plasmin during activation of fibrinolysis may play a pro-inflammatory role by mediating aggregation of PMN.

Binding Sites↗
PubMed1993

Biochemical aspects of autologous fibrin glue derived from ammonium sulfate precipitation.

The autologous fibrin glue (AFG) was produced from 30 human donors using the ammonium sulfate precipitation method, and a study of its biochemical composition was performed. The fibrinogen concentration ranged 13 to 57 mg/mL, the yield averaged 54.6%, and there was a direct relationship between the level of fibrinogen in plasma and AFG which had been made from the same donor's plasma. Our results suggest that the quality of this category of AFG depends partially on the fibrinogen level of donor's plasma. Quality control of the AFG is discussed. Additionally, the effectiveness of three fibrinolysis inhibitors were compared to find an optimum one which inhibits autofibrinolysis of this glue. Tranexamic acid and epsilon aminocaproic acid (EACA) were acceptable alternatives to aprotinin.

Ammonium Sulfate↗
PubMed1994

The receptor for urokinase-type plasminogen activator of a human keratinocyte line (HaCaT).

It is assumed that plasmin participates in pericellular proteolysis in the epidermis. Plasmin is generated by keratinocyte-associated plasminogen activators from the proenzyme plasminogen; plasminogen activation can proceed at the keratinocyte surface. The resultant plasmin interferes with cell to matrix adhesion and does possibly contribute to keratinocyte migration during reepithelialization. Here we describe the receptor for urokinase-type plasminogen activator (uPA-R) in the human keratinocyte cell line HaCaT, which serves to direct plasminogen activation to the cell surface; we relate the receptor to the uPA-R previously described in human myelo-/monocytes. Binding of uPA to the receptor accelerated plasminogen activation by a factor of approximately 10, compared to uPA in solution. Receptor-bound uPA was susceptible to inhibition by the plasminogen activator inhibitors 1 and 2. uPA and uPA-R antigen, as well as uPA activity, were localized to the leading front of expanding sheets of HaCaT cells. Exposure of HaCaT cells to plasminogen was followed by detachment of the cells. Detachment was prevented by an anticatalytic anti-uPA antibody, by the plasmin-specific inhibitor aprotinin, and by the lysine analogue tranexamic acid, the latter of which prevents plasmin(ogen) binding to the cell surface. Our findings support the hypothesis that uPA-mediated plasminogen activation is characteristic of mobile rather than sessile keratinocytes. Moreover, the uPA-R seems to focalize plasminogen activation to the surface of cells at the site of keratinocyte migration.

Base Sequence↗
PubMed1983

Minimization of inflammation in the treatment of bladder tumors by intravesical instillation of adriamycin.

The purpose of this trial was to minimize local inflammation caused by intravesical instillation of antitumor agents, especially Adriamycin, in the treatment of bladder tumor. Tranexamic acid was chosen as the solvent vehicle for Adriamycin and IV bolus injection of an antiallergic drug, Stronger neo-minophagen C, was given at the time of each instillation. Of 81 cases scheduled for Adriamycin instillation therapy, nine cases (11.1%) dropped out due to severe bladder inflammation, while 17 other cases (21%) experienced local side-effects which were tolerated. Of 62 evaluable cases in whom more than eight instillations were performed, complete regression was observed in six cases (9.7%) and partial regression in 20 cases (32.3%).

Animals↗
PubMed1988

Rebleeding, ischaemia and hydrocephalus following anti-fibrinolytic treatment for ruptured cerebral aneurysms: a retrospective clinical study.

350 patients with subarachnoid haemorrhage from aneurysmal rupture--admitted in the years 1966-1983--were selected for a retrospective controlled study on the efficacy of antifibrinolytic therapy (AFT). Patients treated with antifibrinolytics were divided into two groups, according to the day of hospital admission and onset of therapy, respectively between 0 and 3 days (SG 1) and between 4 and 7 days from SAH (SG 2); treated patients (260 cases) received i.v. tranexamic acid (6 gr/day) for at least two weeks. Patients admitted before 1974, not receiving antifibrinolytics (90 cases), were selected as controls and divided into two groups (CG 1 and CG 2), according to the day of admission. In the first study group (admission 0-3 days) the rebleeding rate within 2 weeks was 9% versus 23% in controls (p less than 0.01). The incidence of rebleeding within 3 and 4 weeks was also significantly lower (p less than 0.05) than in controls. No significant difference was observed in the rebleeding rate in treated and untreated patients with late admission (4-7 days). Mortality from rebleeding was 16% in the first study group versus 17% in controls; in the second study group the figure was 6% versus 8% in controls. Seventy-five cases of ischaemic disorders (29%) were registered in treated patients versus 13 cases in controls (14%; p less than 0.01). Thirty-seven patients receiving AFT (14%) developed significant ventricular dilatation requiring shunt insertion, versus one patient in the control groups (1%; p less than 0.001). Final outcome was similar in the 4 groups. In conclusion--according to our data--AFT modifies the behaviour of rebleeding and the patients' course, although it does not modify the outcome after SAH. Clinical use of antifibrinolytic therapy appears still justified in those patients who cannot be operated on in the acute stage after SAH, provided that an associated anti-ischaemic therapy is undertaken.

Adolescent↗
PubMed1994

Thrombolysis in thromboembolic diseases.

Thrombolysis in many manifestations of thromboembolic disease offers a valuable alternative to surgery. However, as thrombolysis is always associated with a bleeding hazard (though low) one should always weigh the risks against the expected benefits when the decision for or against this therapeutic option is made. Furthermore, in selecting the appropriate thrombolytic agent, one should be led by the urgency of reperfusion to maintain organ function. If one decides on an aggressive, high-dose, brief-duration regimen, reperfusion may be achieved more rapidly but may be incomplete in the majority of cases. On the other hand, by selecting an intermediate- or long-duration, low-dose regimen, reperfusion may happen too late to improve the patient's prognosis. Above all, one should keep in mind that the hazard of serious bleeding constantly increases with duration of thrombolysis. No matter which strategy is regarded as the best to resolve a clot in a particular patient with a particular type of thromboembolic disease, thrombolysis should be accompanied by high doses of i.v. heparin. Finally, if bleeding occurs in spite of all precautions taken, the new generation of fibrin-specific thrombolytic agents offers the advantage of short half-lives. In addition--in contrast to streptokinase--the hemostatic defect that they cause may be rapidly reversed by the infusion of antagonist drugs such as aprotinin, tranexamic acid, or epsilon-aminocaproic acid. This adds to the clinical safety profile of these thrombolytic agents.

Contraindications↗
PubMed2003

Successful aortic valve replacement in severe pancytopenia related to myelodysplastic syndrome.

We report a 60-year-old man with myelodysplastic syndrome (MDS) whose aortic valve was replaced successfully. He suffered from dyspnea on exertion and was confirmed by echocardiography and cardiac catheterization to have severe aortic stenosis. A peripheral blood examination showed pancytopenia and a bone marrow examination showed MDS with a subtype of refractory anemia with excess blasts. His preoperative neutrophil count was 468/mm3, hemoglobin 9.8 g/dl, and platelet count 27,000/mm3. We conducted aortic valve replacement (AVR) using a bioprosthesis in July 2001. Pre- and postoperatively, we injected granulocyte colony-stimulating factor to keep the neutrophil count at 2,000/mm3 or more. We also transfused platelet concentrate and infused tranexamic acid. Despite potential risks of infection and bleeding, the AVR involved no significant complications. Careful preoperative planning thus plays an important role in managing such cases.

Aortic Valve↗
PubMed1978

A case of Menetrier's disease associated with protein-losing gastropathy and abnormal serum complement profile.

A 44-year-old man with Menetrier's disease associated with protein-losing gastropathy and with abnormal serum complement profile is reported. He was treated by an antifibrinolytic compound tranexamic acid (trans-AMCHA) since he was found to have elevated fibrinolytic activity in the biopsied gastric mucosa. The therapy brought his serum protein from 3.8 g/dl to 5.6g/dl, however could not reduce his mucosal disorder. Substitution of a placebo for trans-AMCHA resulted in marked depression of his serum protein to 3.7 g/dl. It was concluded that trans-AMCHA was effective in raising his serum protein to a certain extent but failed to block the vicious circle of "mucosal disorder", "increased tissue fibrinolysis" and "hypoproteinemia" (Kondo, M. et al. Gastroenterology 70, 1045, 1976). Abnormal serum complement profile seen in this patient was found to be due to cold activation of the classical complement pathway (Kondo, M. et al. J. Immunol. 117, 486, 1976). Although no correlation between the phenomenon and Menetrier's disease has been clarified yet, the appearance of wheezing as in asthma when exposed to cold suggested that cold activation of complement occurred in vivo and resulted in increasing of the vascular permeability in the lungs.

Adult↗
PubMed1996

[The use of a C1-inhibior concentrate for short-term preoperative prophylaxis in two patients with hereditary angioedema].

A commercially available C1 inhibitor (C1-INH) concentrate was used for short-term prophylaxis before surgery in two patients with hereditary angioneurotic oedema. The patients suffered from recurrent subcutaneous and submucosal oedema of the face, extremities, and gastrointestinal tract as the result of a hereditary C1-INH deficiency. Both patients were receiving tranexamic acid or danazol therapy as oral long-term prophylaxis. Over the years the patients underwent several operations in regional and general anaesthesia, with mask ventilation or intubation. The C1-INH plasma concentrations measured preoperatively were always very low (0.02-0.06 g/l, normal range 0.15-0.35 g/l), despite the oral long-term prophylaxis. Substitution treatment with 500-1000 U C1-INH was performed 1 h before surgery. No side effects were seen following the concentrate infusions. With this substitution treatment no specific symptoms of hereditary angioneurotic oedema were recognized in either case. The measurement of C1-INH plasma concentration 2 h or 4 h after C1-INH substitution showed a marked rise in both patients, though normal values were not reached in either. We suggest that infusion of C1 concentrate is an appropriate form of preoperative substitution treatment in patients with hereditary angioneurotic oedema, in view of the lower risk of infection than with infusion of fresh-frozen plasma and the observed effectiveness.

Adult↗
PubMed2006

[Thrombocytopathy and blood complications in uremia].

Bleeding diathesis and thrombotic tendencies are characteristic findings in patients with end-stage renal disease. The pathogenesis of uremic bleeding tendency is related to multiple dysfunctions of the platelets. The platelet numbers may be reduced slightly, while platelet turnover is increased. The reduced adhesion of platelets to the vascular subendothelial wall is due to reduction of GPIb and altered conformational changes of GPIIb/IIIa receptors. Alterations of platelet adhesion and aggregation are caused by uremic toxins, increased platelet production of NO, PGI(2), calcium and cAMP as well as renal anemia. Correction of uremic bleeding is caused by treatment of renal anemia with recombinant human erythropoietin or darbepoetin alpha, adequate dialysis, desmopressin, cryoprecipitate, tranexamic acid, or conjugated estrogens. Thrombotic complications in uremia are caused by increased platelet aggregation and hypercoagulability. Erythrocyte-platelet-aggregates, leukocyte-platelet-aggregates and platelet microparticles are found in higher percentage in uremic patients as compared to healthy individuals. The increased expression of platelet phosphatidylserine initiates phagocytosis and coagulation. Therapy with antiplatelet drugs does not reduce vascular access thrombosis but increases bleeding complications in endstage renal disease patients. Heparin-induced thrombocytopenia (HIT type II) may develop in 0-12 % of hemodialysis patients. HIT antibody positive uremic patients mostly develop only mild thrombocytopenia and only very few thrombotic complications. Substitution of heparin by hirudin, danaparoid or regional citrate anticoagulation should be decided based on each single case.

Hemorrhage↗
PubMed1987

Newer agents available for treatment of stress-related upper gastrointestinal tract mucosal damage.

Results of animal studies and human clinical trials assessing the efficacy of newer agents in the treatment of stress-related mucosal damage have been reviewed. Currently available data suggest that prostaglandin treatment is as effective in preventing and treating stress-induced mucosal injury as more established therapeutic modalities, but that the proposed efficacy of somatostatin infusion and tranexamic acid administration is highly suspect. Promising agents yet to be evaluated include omeprazole, allopurinol, and epidermal growth factor.

Animals↗
PubMed1993

Autoimmune C1 inhibitor deficiency: report of eight patients.

PURPOSE: In this study, we investigated the clinical and biochemical features and the responses to treatment of eight patients with auto-antibody-mediated C1 inhibitor (C1-INH) deficiency and symptoms of angioedema. PATIENTS AND METHODS: In addition to the 8 patients with acquired angioedema (AAE), we also studied 36 subjects with hereditary angioedema (HAE), 15 of them treated with C1-INH plasma concentrate, and 26 patients with different autoantibodies in their plasma (10 with systemic lupus erythematosus, 6 with lupus-like anticoagulant, and 10 with chronic liver disease). Functional C1-INH was measured with the reagent kit of Immuno (Vienna, Austria); C1-INH, C4, and C1q antigen were determined by radial immunodiffusion; and autoantibodies to C1-INH were detected by an enzyme-linked immunosorbent assay method. RESULTS: Four patients with AAE had no other diseases, one had breast cancer, one liver hydatidosis, one Waldenström's disease, and one a benign M component. Functional C1-INH levels were below 30% of normal, and C1q plasma levels were low in seven patients but normal in one. Autoantibodies to C1-INH were detectable in all eight AAE patients but in none of the others. Prophylactic treatment with attenuated androgens was successful in one of four patients, and with antifibrinolytic agents (tranexamic acid) in six of seven patients. Laryngeal attacks in five patients were treated with C1-INH plasma concentrate; two patients had marked clinical and biochemical responses. In three, the symptoms resolved only with high doses, and the biochemical parameters did not significantly increase. CONCLUSIONS: Our results suggest that patients with autoimmune AAE are clinically and biochemically heterogeneous. They have different responses to treatment that seem to be related to variable C1-INH consumption.

Aged↗