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PubMed1983

[Treatment of obstetrical disseminated intravascular coagulation--sequential changes of coagulation and fibrinolytic system in DIC rabbits].

A model was experimentally made with 2 hours serial infusion of thromboplastin (Tp) into rabbits to examine the drug's effect on a hemorrhagic tendency and to elucidate the coagulation and fibrinolytic system in acute DIC encountered in obstetrics, and the system was periodically observed. Groups given the drug, given it during pregnancy, those which bled massively, and those with accelerated fibrinolysis were prepared. The results are as follows. 1) Fibrinogen, PT, APTT, TEG, ELT, AT-III, antiplasmin activity, and platelet count varied markedly from the initiation of Tp injection, and returned to normal following termination. 2) Blood from the heparin dose group showed non-coagulation but decreases in the platelet count and fibrinogen were inhibited. 3) In the aprotinin dose group, serial 2 hour administration induced inhibition of fibrinolysis despite the relatively delayed appearance of anti-fibrinolytic activity. 4) No fibrinolytic effects were seen in anti-plasmin activity or ELT in the tranexamic acid dose group. 5) Lowering of parameters examined was marked in the Tp dose group during pregnancy. 6) The mortality rate up to 6 hours after Tp infusion was 54.5% with solely given, and 10% with group given drug. 7) Death within one hour of Tp infusion in the mass bleeding group, being rated for 50%, was improved to 16.7% by the pre-administration of urokinase.

Animals↗
PubMed1983

Cryptic and active plasminogen activators secreted by line 10 tumor cells in culture.

Line 10 guinea pig carcinoma cells cultured in serum-free medium for 4 hr elaborate plasminogen activator (PA) activity that remained in the supernatant after ultracentrifugation (100,000 X g, 90 min). PA activity in line 10 conditioned medium occurred in both active and cryptic forms. The vast majority of active PA adsorbed to lysine-Sepharose and could be eluted at low pH as several activities that electrophoresed in the Mr 50,000 to 80,000 range on nonreduced sodium dodecyl sulfate-polyacrylamide gel electrophoresis. A small amount of active PA, running in the Mr 50,000 to 60,000 region, and cryptic PA did not adhere to lysine-Sepharose. Treatment of lysine-Sepharose-nonadherent fractions with catalytic amounts of plasmin or trypsin induced substantial new PA activity that adsorbed to lysine-Sepharose, bound [3H]diisopropylfluorophosphate, and that electrophoresed as several bands of activity with molecular weights from 50,000 to greater than 100,000 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Of additional interest, the amount of active PA measured in conditioned medium was substantially increased when certain protease inhibitors, tranexamic acid, epsilon-aminocaproic acid, or Trasylol, were included during culture.

Animals↗
PubMed1993

Hemophilia with factor VIII and factor IX inhibitors, incidence, bleeding problems and management.

Among 117 cases of hemophilia, there were 7 hemophilia A and 2 hemophilia B with factor VIII and factor IX inhibitors diagnosed at the Department of Pediatrics, Siriraj Hospital, Bangkok, Thailand. The overall incidence of hemophilia with inhibitors was 7.7%. Eight cases (6 hemophilia A. 2 hemophilia B) were severe hemophilia and 1 moderate hemophilia A. The average age of the inhibitor detection was about 5 years. Of the 9 cases, 7 had high inhibitor titers and 2 had low inhibitor titers. The frequency of bleeding problems before and after inhibitor detection were not different. The bleedings included hemarthrosis, mucosal bleed, hematoma, oozing from wound, hematuria and intracranial hemorrhage. The treatment of hemarthrosis in hemophilia A with low inhibitor titers was the combination of short course of prednisolone and single large dose factor VIII. In high inhibitor titer patients with acute hemarthrosis (both hemophilia A and hemophilia B), the treatment consisted of prednisolone short course and single high dose of PCC. For bleeding control in both high and low inhibitor titer with mucosal bleeds, oozing from wounds, central nervous system bleeding and hematuria, the combination was used of high dose factor VIII or factor IX for 2 days, and tranexamic acid, prednisolone, cyclophosphamide were required. In life-threatening hemorrhage and surgical operation, plasmapheresis and large dosage factor VIII or factor IX were the treatment of choice. All supportive measures were also important in every case of mucosal bleeds, wounds and surgical operations. The result of treatment revealed one death from massive intracranial hemorrhage and 8 survivals, with joint contracture in 2 cases. All still have inhibitor detected, but in low titer.

Child↗
PubMed1993

Clinical problems in the C1-inhibitor deficient patient.

The clinical course of C1-INH deficiency is presently well established. There is an inherited form (Hereditary Angioedema) characterized by recurrence of cutaneous and mucous swellings appearing early in life and usually accompanied by substantial family history, and an acquired form (Acquired Angioedema) where identical symptoms start after the fourth decade of life without family history. The acquired form can be associated with other diseases, mainly B cell disorders, and/or with autoantibodies to C1-INH. The biochemical characteristic is the functional deficiency of C1-INH and of C4 and C2. Moreover a marked deficiency of C1 is present in most acquired forms, but never in the inherited ones. C1-INH deficiency can be corrected by attenuated androgens that increase C1-INH levels in a few days and are effective in the prophylaxis of attacks, or by substitutive therapy with C1-INH plasma concentrate that is the life-saving drug in laryngeal edema. Patients with the inherited form have a uniformly good response to both these treatments which are otherwise effective only in a minority of patients with the acquired deficiency. In these subjects C1-INH concentrate needs to be given in higher doses and prevention of attacks is obtained with antifibrinolytic agents (Tranexamic acid).

Adolescent↗
PubMed1993

[Preoperative monitoring of blood coagulation in urologic operations: diagnosis of familial factor XI deficiency within the scope of preoperative blood coagulation studies].

Presurgical coagulation diagnosis should--apart from coagulation monitoring in the laboratory based on a stepwise diagnosis for detection of coagulations disorders, starting with global tests (NT/APTT) followed by appropriate specific investigation in case of pathological findings--consist of an adequate hemostaseological anamnesis and physical checkup of the patient. This would allow detection of important signs of hemostaseological impairment during the pre-analytical phase already and permit subsequent initiation of more specific coagulation tests. The casuistics of a patient with factor XI-deficiency ("Minor Form"), a condition which is extremely infrequent in our country, demonstrates the coagulation diagnostic procedure which led to detection of his inherited factor XI-deficiency. In addition the pre-, peri- and postsurgical therapeutical management of this particular patient using an antifibrinolytic drug (tranexamic acid) is presented.

Blood Coagulation Tests↗
PubMed1977

Hereditary angioneurotic oedema in Finland. Clinical, immunological and genealogical studies.

A total of 7 families with hereditary angioneurotic oedema (HANE) have been found in Finland. Six HANE patients have died from laryngeal oedema, 27 patients with diagnosed HANE are alive and 21 members have a haematological abnormality typical of HANE, i.e. a deficiency of the inhibitor of the activated first component of complement (C1-INH), but no manifest symptoms. The largest family has 363 living members, 303 of whom were investigated for C1-INH, C4 and C3. Fourteen patients had HANE, 18 relatives were symptomless but had C1-INH deficiency, and 3 members of the family had died from laryngeal oedema. In two families only one case of HANE was diagnosed, the parents in both cases being symptomless with normal C1-INH levels. All patients who had died from laryngeal oedema and 10 of the 27 HANE patients still alive had a typical triad of paroxysmal abdominal pain, peripheral oedema and laryngeal oedema. Six patients have had abdominal attacks alone, three peripheral oedema alone and two only laryngeal oedema. The age at onset of symptoms was 1-51 years. Three patients, who have received continuous methyltestosterone therapy, had hardly any symptoms during the treatment. Thirteen patients have received tranexamic acid, either during an attack or continuously, with positive effects in all except two. Cinnarizine treatment was beneficial in three out of four cases, both when given continuously or during an attack.

Abdomen↗
PubMed1996

[The role of urokinase type plasminogen activator in invasion of bile duct carcinoma].

OBJECTIVE: To study the role of urokinase type plasminogen activator (u-PA) in the invasive process of bile duct carcinoma. METHODS: The secretion of u-PA and the invasive potential of tumor cell in vitro in a newly established cell line of bile duct carcinoma, QBC939, were observed by using an amnion invasion culture system. RESULTS: QBC939 cells secreted u-PA with high invasive potential. The inhibitors of u-PA and plasmin, tranexamic acid and 6-aminocaproic acid, obviously inhibited the u-PA activity and the invasive potential of QBC939 cells. CONCLUSION: u-PA is one of the important enzymes in tumor invasion. Inhibiting u-PA or plasmin may be a prospective therapy for tumor treatment.

Bile Duct Neoplasms↗
PubMed1997

[Hemorrhagic syndrome and isolated alpha 2-antiplasmin deficiency. Apropos of a case].

An isolated alpha 2 plasmin inhibitor deficiency is reported in a 33 years old male, presenting repeated intramuscular hematomas since 5 years, spontaneously or after minor traumas. None of other family members were suffering from abnormal bleeding. Screening hemostatic examinations were normal except for a moderately shorted euglobulin lysis time (2 hours). Evaluation of fibrinolysis parameters (plasminogen, plasminogen activator inhibitor type 1, tissue plasminogen activator, fibrin and fibrinogen degradation products, alpha 2 plasmin inhibitor) showed normal values except for alpha 2 plasmin inhibitor which is markedly decreased (activity: 14%, antigen: < 5%). Familial hemostasis investigations have not been performed. This isolated alpha 2 plasmin inhibitor deficiency has been confirmed by two repeated control prelevments. Bleedings episodes were treated with antifibrinolytics agents (tranexamic acid). This case report shows the importance of the diagnostic approach in the laboratory to detect such rare hemostatic abnormalities associated with bleeding tendency.

Adult↗
PubMed1997

Ethanol increases surface-localized fibrinolytic activity in cultured endothelial cells.

Epidemiological studies demonstrated a positive association between moderate alcohol consumption and reduced cardiovascular mortality that may be mediated, in part, through increased fibrinolysis. These studies were conducted to determine whether low concentrations of alcohol (0.025 to 0.1%, v/v) directly affected the surface-localized versus secreted/solution phase fibrinolytic activity in live cultured endothelial cell (EC) types. Confluent live cultured ECs [human umbilical vein ECs (HUVECs), human saphenous vein ECs (HSVECs), and porcine aortic ECs (PAECs)] were preincubated (0 to 20 min, 4 degrees C) in the absence or presence of varying concentrations of alcohol (0 to 0.1%, v/v), in the presence of saturating levels of 125I-labeled Glu-plasminogem (2 microM) and 125I-Plasmin M(r) 20-kDA light-chain formation quantitated by phosphorimaging autoradiography analysis. Endogenous plasminogen activator (PA)-mediated fibrinolytic activity was time- and dose-dependent; reached a maximum approximately 5- to 10-fold increase at 0.05% alcohol in HUVECs, HSVECs, and PAECs; was completely inhibited by anti-t-PA IgG in HUVECs; and partially inhibited by both anti-t-PA (approximately 40%) and anti-u-PA IgG (approximately 60%) in HSVECs. Complete inhibition of alcohol-induced (0.05%) fibrinolytic activity in cultured HUVECs by 2 mM tranexamic acid (an antagonist of plasminogen binding) indicated that the increased fibrinolytic activity was receptor-bound and localized to the EC surface, rather than present in or secreted into the medium (solution phase). Finally, the alcohol-induced increased fibrinolytic activity in cultured HUVECs returned to essentially normal control levels in approximately 1 hr. These studies have demonstrated a direct effect of low alcohol on EC fibrinolytic activity that may contribute, in part, to the decreased risk for thrombosis, coronary artery disease, and myocardial infarction associated with moderate alcohol consumption.

Culture Techniques↗
PubMed1998

Dysfunctional uterine bleeding.

BACKGROUND: Dysfunctional uterine bleeding (DUB) affects about 5% of menstruating women. yet the majority of medical practitioners who manage the problem do not adequately understand the underlying pathophysiology nor the principles involved in appropriate management. OBJECTIVE: This article is an attempt to provide a brief overview of the problem and to review the current information regarding the diagnosis, incidence, cause and management of DUB. DISCUSSION: The majority of cases of DUB occur in the 5-10 years before the menopause or after the menarche, when the ovaries are in an unstable responsive state. Hormonal dysfunction is responsible for most cases of DUB and the condition will usually respond to appropriate hormonal therapy. In those instances where hormones are not a viable option or have not controlled the problem, then prostaglandin inhibitors or the use of tranexamic acid may allow short term relief from excessive bleeding. Surgery by endometrial ablation of hysterectomy should only be considered when all other options have failed.

Adult↗
PubMed1998

Experiences with continuous infusion of recombinant activated factor VII.

A questionnaire was sent to 28 haemophilia treatment centres known to have used recombinant activated factor VII (rFVIIa; NovoSeven, Novo Nordisk, Bagsvaerd, Denmark), to collect data on continuous infusion of this product. This mode of administration was recently introduced for rFVIIa but there are several questions which remain to be answered in order to optimize this technique. Of the 26 responding centres, 14 had used rFVIIa in continuous infusion for 40 treatment episodes over a total of 283 days. In most of the cases the treatment was targeted at a factor VII level of 10 IU/ml, monitored by the one-stage clotting assay. This seemed to be adequate for most of the haemorrhagic and surgical procedures. Pretreatment pharmacokinetic evaluation was performed in only a minority of the cases but is probably of great importance given the wide variation observed in the clearance values. A strategy was necessary to prevent local thrombophlebitis, at least for infusions in peripheral veins; parallel infusion of heparin, saline or dextrose-saline proved effective. The question of optimal monitoring needs further attention. Haemorrhagic complications were significantly less frequent when treatment was combined with the antifibrinolytic tranexamic acid.

Drug Monitoring↗
PubMed1998

Mechanisms of restenosis after angioplasty and approach to therapy (Review).

Angioplasty is a principal treatment for occlusive vascular disease but 30-50% of patients show a restenosis of the vessel. There is no clinical effective therapy for this disease. It has been demonstrated, in animal models, that various drugs such as NO-donor, plasminogen inhibitor tranexamic acid and MMP (matrix metalloproteinases) reduce the rate of restenosis. Other therapeutic approaches are cytotoxic therapy, and strategies to inhibit cell cycle progression. Systemic administration of conventional pharmacologic agents inhibit cell cycle kinases and vascular lesion formation in animal models. As cell cycle progression is accompanied by fluctuations in the concentration of adenosine 3',5-monophospate (cAMP) and in the activity of the cAMP dependent protein kinase (PKA), local administration of cAMP and phospodiesterase-inhibitor drugs (aminophylline or amrinone) markedly inhibit neointima formation. The successful use of local radiation therapy to inhibit neointima formation after vascular injury may reflect a similar combination of cell-cycle arrest and vascular cell apoptosis. The most effective therapy for occlusive vascular disease will likely combine intravascular stenting with an antiproliferative therapy.

Journal Article↗
PubMed2005

Biochemical characterization of autologous fibrin sealants produced by CryoSeal and Vivostat in comparison to the homologous fibrin sealant product Tissucol/Tisseel.

Different principles for production of "autologous fibrin sealant" have been established, and commercial devices employing these methods are nowadays available and used in clinical routine. Users might anticipate for these autologous fibrin sealants features comparable to commercial homologous fibrin sealants, used in surgical routine for many years. However, only little is known about biochemical properties, formation, cross-linking and stability of fibrin sealant clots produced for autologous use with the aid of commercially available devices. We have investigated protein composition, formation and stability of clots obtained from autologuous fibrin sealants produced with commercially available devices (CryoSeal and Vivostat) and compared these parameters to those of the industrially produced homologous fibrin sealant Tissucol/Tisseel. The CryoSeal product is a mixture of many plasma proteins; the Vivostat product and Tissucol/Tisseel appear as comparatively pure plasma derivatives. The products differ in their protein composition and concentrations, including their concentration in fibrin. Significant fibrin alpha and gamma-chain cross-linking by FXIIIa occurs only in Tissucol/Tisseel clots. In test tubes CryoSeal and Vivostat (tranexamic acid-free formulation) fibrin clots liquefy within 1-2 days, but Vivostat (tranexamic acid containing formulation) clots were stable for 4 days and showed partial liquefaction after 5 days. Tissucol/Tisseel clots, containing the protease inhibitor aprotinin, appeared unchanged over the observation period of 5 days. In an in vitro model mimicking in vivo conditions (diffusion of protease inhibitors and proteolytic digestion) clot liquefaction occurs at day 1 for all autologous fibrin sealants clots, with an observable delay for the tranexamic acid containing Vivostat, and day 5 for Tissucol/Tisseel clots. Characterization of the CryoSeal and Vivostat fibrin sealants and Tissucol/Tisseel and their performance show a clear difference in biochemical properties.

Blood Coagulation↗
PubMed1989

[The synthesis of 4'-(2-carboxyethyl)phenyl trans-4-aminomethyl cyclohexane carboxylate hydrochloride (cetraxate hydrochloride) by means of enzymatic debenzylation].

Cetraxate hydrochloride (1) (antiulcer agent) has been industrially produced by the chemical protective method of p-hydroxy propionic acid derivatives. Screening of enzymes which quantitatively hydrolyzed cetraxate benzyl ester hydrochloride (2) into 1 was undertaken to establish a novel enzymatic method of production of 1. It was found that the enzyme activity for debenzylation of 2 is contained in cellulase enzymes originated from Aspergillus sp. Lower alkyl groups or phenyl groups of p-hydroxy propionic acid derivatives are likewise selectively hydrolyzed by the cellulase enzyme. This enzymatic synthetic method is very useful for the industrial preparation of 1.

Anti-Ulcer Agents↗
PubMed1989

Partial purification, and some properties and reactivities of cetraxate benzyl ester hydrochloride-hydrolyzing enzyme.

Debenzylating enzyme from Aspergillus niger enzyme (commercial crude cellulase) catalyzes the hydrolysis of cetraxate benzyl ester hydrochloride (2), a precursor of the antiulcer agent (1). The enzyme was highly purified by three kinds of chromatographies (hydrophobic, ion exchange, gel filtration) with a recovery of 36%. The content of the debenzylating enzyme was about 0.1% in the crude cellulase, but the enzyme showed no cellulase activity. The purified enzyme was inactivated by Hg2+, and diisopropyl phosphorofluoridate (DFP). It was a monomer with a molecular weight of about 35,000, and its isoelectric point was estimated to be 5.3. It showed a debenzylating activity for the phenylpropionic acid benzyl ester moiety of various benzyl ester derivatives, and the benzyl ester of phenylalanine or that of tyrosine was also well hydrolyzed.

Aspergillus niger↗