SEARCH · PubMed Health

Results for “Tranexamic Acid”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 757 records · Page 42Linked to original sources

PubMed1982

[Changes in the course after spontaneous subarachnoid hemorrhage from the neurological point of view].

In order to recognize changes in the course after spontaneous subarachnoid hemorrhage (sSAH) cases hospitalized between 1974 and 1981 were divided in two groups: group 1 contained 53 patients from 1974 to 1976, group 2 84 patients from 1977 to 1981. With respect to age and clinical condition at admission to the hospital (grading according to Hunt and Hess, 20) the two groups were not different and were comparable to the patient population of epidemiologic studies. Due to the high percentage of cases of older age and with poor prognosis mortality in our patients was high when compared to the selected material of neurosurgical and randomized studies, but letality decreased markedly from 47,2% between 1974 and 1976 to 35,7% between 1977 and 1981. Good clinical outcome increased from 41,5% in group 1 to 54,7% in group 2; favourable outcome after surgical treatment (69,5%) had a high impact on this result. This change in the clinical course after sSAH was attributed to more intensive conservative treatment and to improved surgical technique with better defined selection of operable cases and with a tendency to operate early after the bleed. By reducing the number and postponing the occurrence of rebleeding antifibrinolytic therapy with tranexamic acid was of supportive value.

Adult↗

PubMed2001

Plasminogen binding is increased with adipocyte differentiation.

The purpose of this study was to examine the role of the plasminogen system in the development of adipose tissue. Plasminogen binding capacity was determined in differentiated and undifferentiated cells from adipose tissue of plasminogen deficient mice and 3T3 cells, a well-characterized tissue culture model. In 3T3 cells, plasminogen binding was fivefold higher in differentiated cells compared to the undifferentiated cells. Inhibition of binding by carboxyl-terminal lysine analogs was similar for the differentiated and undifferentiated cells with tranexamic acid > EACA > lysine. The binding of plasminogen was concentration-dependent and approaches saturation in the both cell types. The number of plasminogen binding sites was tenfold higher in the differentiated compared to the undifferentiated cells. In isolated mature fat cells and stromal cell cultures from mouse adipose tissue, plasminogen binding was also higher in the differentiated mature fat cells and differentiated stromal cells compared to undifferentiated stromal cells. Plasminogen binding was elevated in the differentiated cells from the Plg-/- mice compared to cells from the WT mice. These results suggest that the plasminogen system plays an important role in adipose tissue development.

3T3 Cells↗

PubMed1990

Benefits and risks of antifibrinolytic therapy in the management of ruptured intracranial aneurysms. A double-blind placebo-controlled study.

One hundred patients with a verified subarachnoid haemorrhage were studied in a double blind, placebo-controlled trial at a single centre to determine the value and relative risks of tranexamic acid (TXA) in the management of ruptured intracranial aneurysms. The incidence of recurrent haemorrhage between active and placebo groups was identical (12%) and the mortality from recurrent haemorrhage was 7% and 5%, respectively. The overall incidence of cerebral infarction before surgery, at discharge and at 6 months follow-up was greater in the TXA group (27%) than in the control group (11%). Post-operative cerebral ischaemia was significantly more frequent in the active, 18 of 29 as compared to 6 of 32 patients, in the placebo group. In a fifth of the patients in whom cerebral blood flow was estimated there was a significant reduction of cerebral blood flow (CBF) on the side of the ruptured aneurysm in the TXA treated group. It is suggested that this may be the cause of the increased incidence of cerebral ischaemia in this group. There was no significant difference in the incidence of cerebral vasospasm, hydrocephalus, visual disturbances and gastrointestinal disturbances. More fatalities were encountered from ischaemia and recurrent haemorrhage in the TXA group but these differences did not reach statistical significance at the 5% level. Given that disability was due to either vasospasm or recurrent haemorrhage than a patient under TXA treatment was significantly more likely to have disability due to vasospasm (p less than 0.04); the reverse was true for the placebo patient (p less than 0.05).

Adult↗

PubMed1980

Traumatic hyphaema treated ambulatory and without antifibrinolytic drugs.

Forty-four patients referred consecutively over a period of one year for treatment of traumatic hyphaema have been treated ambulatory and with no drugs. Four patients developed secondary haemorrhage; three regained normal visual acuity. The frequency of secondary haemorrhage is not statistically different from that in two previously published patient groups treated with bed rest and with tranexamic acid, respectively.

Adolescent↗

PubMed2004

Gastric antral vascular ectasia (GAVE) syndrome.

Gastric antral vascular ectasia (GAVE) syndrome is an uncommon cause of chronic gastrointestinal bleeding and iron deficiency anaemia. We describe two cases of GAVE, one pernicious anaemia related and the other portal hypertension related. In both the cases, progressive mucosal changes, which lead to development of GAVE, were documented. Those changes were progression of multiple antral erythematous spots into linear configuration and lastly to watermelon stomach. One of the cases was treated with tranexamic acid with good response.

Aged↗

PubMed2005

Are antifibrinolytic drugs equivalent in reducing blood loss and transfusion in cardiac surgery? A meta-analysis of randomized head-to-head trials.

BACKGROUND: Aprotinin has been shown to be effective in reducing peri-operative blood loss and the need for re-operation due to continued bleeding in cardiac surgery. The lysine analogues tranexamic acid (TXA) and epsilon aminocaproic acid (EACA) are cheaper, but it is not known if they are as effective as aprotinin. METHODS: Studies were identified by searching electronic databases and bibliographies of published articles. Data from head-to-head trials were pooled using a conventional (Cochrane) meta-analytic approach and a Bayesian approach which estimated the posterior probability of TXA and EACA being equivalent to aprotinin; we used as a non-inferiority boundary a 20% increase in the rates of transfusion or re-operation because of bleeding. RESULTS: Peri-operative blood loss was significantly greater with TXA and EACA than with aprotinin: weighted mean differences were 106 mls (95% CI 37 to 227 mls) and 185 mls (95% CI 134 to 235 mls) respectively. The pooled relative risks (RR) of receiving an allogeneic red blood cell (RBC) transfusion with TXA and EACA, compared with aprotinin, were 1.08 (95% CI 0.88 to 1.32) and 1.14 (95% CI 0.84 to 1.55) respectively. The equivalent Bayesian posterior mean relative risks were 1.15 (95% Bayesian Credible Interval [BCI] 0.90 to 1.68) and 1.21 (95% BCI 0.79 to 1.82) respectively. For transfusion, using a 20% non-inferiority boundary, the posterior probabilities of TXA and EACA being non-inferior to aprotinin were 0.82 and 0.76 respectively. For re-operation the Cochrane RR for TXA vs. aprotinin was 0.98 (95% CI 0.51 to 1.88), compared with a posterior mean Bayesian RR of 0.63 (95% BCI 0.16 to 1.46). The posterior probability of TXA being non-inferior to aprotinin was 0.92, but this was sensitive to the inclusion of one small trial. CONCLUSION: The available data are conflicting regarding the equivalence of lysine analogues and aprotinin in reducing peri-operative bleeding, transfusion and the need for re-operation. Decisions are sensitive to the choice of clinical outcome and non-inferiority boundary. The data are an uncertain basis for replacing aprotinin with the cheaper lysine analogues in clinical practice. Progress has been hampered by small trials and failure to study clinically relevant outcomes.

Aminocaproic Acid↗

PubMed2004

Postmenopausal bleeding due to chronic DIC.

'Bleeding disorders' are listed as a cause of postmenopausal bleeding even though there appear to be no reported cases. We present a case of postmenopausal bleeding, because of chronic DIC, which resulted from aortic aneurysm and was managed with replacement blood products and tranexamic acid.

Aged↗

PubMed1981

Clinical presentation and diagnosis of hereditary angio-oedema in five families.

The clinical features of 16 patients with deficiency of C1 esterase inhibitor are described. Severity ranged from no symptoms in 2 young subjects to repeated and severe abdominal pain and angio-oedema. Diagnostic techniques are described and the ease with which the diagnosis can be established is emphasized. A functional assay is required in addition to immunological determination of the protein in order to detect a minority of patients who have ineffective inhibitor. Experience of treatment with tranexamic acid is reviewed and its place in management in relation to androgens is discussed.

Adult↗

PubMed1988

Binding site of alpha 2-plasmin inhibitor to plasminogen.

Peptide T-11, a carboxyl terminal tryptic fragment of alpha 2-plasmin inhibitor, inhibits the reversible first step of the reaction between plasmin and alpha 2-plasmin inhibitor. To elucidate which amino-acid residues played a important role in the inhibitory activity of peptide T-11, we prepared the various synthetic derivatives of peptide T-11 and determined the peptide concentration that inhibited the apparent rate constant of the reaction between plasmin and alpha 2-plasmin inhibitor by 50% (IC50). Peptide III, which lacked the residues Gly-1 to Pro-7 of peptide I (peptide T-11), had a strong inhibitory activity, like peptide I (IC50: peptide I, 7 microM; peptide III, 13 microM). The peptides that lacked the Leu-9 and Lys-10 or Lys-26 of peptide III showed much weaker activity, and the loss or amidation of the C-terminal lysine of peptide III also markedly reduced the inhibitory activity. Peptide III competitively inhibited the binding of [14C]tranexamic acid to kringle 1 + 2 + 3 (K1-3) and kringle 4 (K4) in a binding assay performed by the gel-diffusion method. The respective dissociation constants (Kd) of peptide III for K1-3 and K4 were 0.85 microM and 35.2 microM. These data suggest that the amino residue of Lys-10 and the carboxylic acid of Lys-26 in peptide T-11 play crucial roles in the ionic binding of alpha 2-plasmin inhibitor to the tranexamic acid-binding site (lysine-binding site) of plasminogen. Peptide T-11: H-G-D-K-L-F-G-P-D-L-K-L-V-P-P-M-E-E-D-Y-P-Q-F-G-S-P-K-OH.

Amino Acid Sequence↗

PubMed1982

Congenital deficiency of alpha 2-plasmin inhibitor in three sisters.

3 young Japanese sisters with congenital alpha 2-plasmin inhibitor (alpha 2-PI) deficiency are reported. They have mild umbilical bleeding and/or repeated prolonged bleeding after minor trauma, but rarely spontaneous bleedings. The most characteristic hemostatic findings were shortened whole blood clot lysis time and euglobulin lysis time. Activities of all hemostatic factors except alpha 2-PI were within normal range. Both functional and immunological absence of alpha 2-PI were found in the plasma, and this failure to detect alpha 2-PI was not corrected by the addition of the patient's plasma of the first described case of alpha 2-PI deficiency. Clinical and laboratory data revealed that these patients were probably homozygous for alpha 2-PI deficiency and born of heterozygous parents, but not of consanguineous ones. Bleeding episodes due to deficiency of alpha 2-PI in these patients were well controlled by an antifibrinolytic agent, tranexamic acid.

Blood Coagulation Tests↗

PubMed2003

[Anesthetic management of a patient with congenital plasminogen activator inhibitor-1 deficiency].

Congenital plasminogen activator inhibitor-1 (PAI-1) deficiency is an extremely rare disorder characterized by a bleeding diathesis due to hyperfibrinolysis as a result of decreased PAI-1 activity. A 21-year-old male with congenital PAI-1 deficiency underwent wisdom teeth extraction of the mandible under general anesthesia using propofol, nitrous oxide, sevoflurane, fentanyl, and vecuronium. No complications including prolonged bleeding and rebleeding after the operation were observed because hemostatic management was successful by using intravenous tranexamic acid.

Adult↗

PubMed2003

Görög Thrombosis Test: a global in-vitro test of platelet function and thrombolysis.

This is the first laboratory evaluation of a new instrument, designed to test both platelet function and thrombolytic activity from a native blood sample, in vitro. The inventor assumed that the reduction and arrest of blood flow was due to activation, aggregation and stabilized thrombus formation by shear-activated platelets, and that re-establishment of flow was due to thrombolysis. Morphologic and functional studies presented here confirm these mechanisms. In vitro tests provided incontestable evidence for the principal role of platelets in the obstruction of flow (occlusion time) and for thrombolysis as the principal mechanism underlying the restoration of blood flow (lysis time). In addition to aggregation, it is the explosive generation of thrombin by shear-activated platelets that results in the formation of an occlusive haemostatic thrombus. Anticoagulation of blood completely prevented occlusion. Platelet-rich thrombus formation (occlusion time) was dose-dependently inhibited by monoclonal antibody against platelet glycoprotein (GP) Ib (6B4 and 12E4), aurin tricarboxylic acid, monoclonal antibody against platelet GPIIb/IIIa (MA-16N7C2 and abciximab), a synthetic GPIIb/IIIa antagonist (TAK-029), thrombin inhibitor (argatroban), and anti-von Willebrand factor, but not by anti-fibrinogen. Plasminogen activator streptokinase (Varidase) and tissue-type plasminogen activator (Monteplase) dose-dependently enhanced thrombolysis (lysis time) without affecting platelet function (occlusion time). The test is specific for thrombolysis. The plasmin inhibitor tranexamic acid prevented plasminogen activator-induced thrombolysis, while inhibition of clot retraction by cytochalasin B did not affect the lysis time. This rapid and sensitive global test of platelet function and thrombolytic activity could be of great value both in research and in clinical practice.

Adult↗

PubMed1986

Acquired C1 esterase inhibitor deficiency.

A case of acquired C1 esterase inhibitor deficiency and its anaesthetic implications is presented. Prophylaxis against angioneurotic oedema using danazol and tranexamic acid is described and the resultant complication of mesenteric venous thrombosis reported.

Angioedema↗

PubMed2006

Efficacy of FDA-approved hemostatic drugs to improve survival and reduce bleeding in rat models of uncontrolled hemorrhage.

Several FDA-approved intravenous drugs are used to reduce surgical bleeding. This series of studies tested whether these drugs (aprotinin, desmopressin, tranexamic acid, epsilon-aminocaproic acid) could reduce bleeding due to traumatic injuries in two models of uncontrolled hemorrhage in rats. In the first phase of each study, a nonlethal tail bleeding model was used that incorporated limited fluid resuscitation (lactate Ringer's solution). Four doses of vehicle or the test substance were given successively with bleeding time and blood loss measured after each dose. In the second phase of each study, a lethal liver injury was produced by excising a section of the median lobe (approximately 0.8% of body weight) and an infusion of either vehicle or the test substance was immediately begun. This model included aggressive fluid resuscitation and a severe dilutional coagulopathy. Blood loss, survival time and mortality rate were recorded. Three studies were performed, testing each of the drugs singly and in combination. None of the drugs significantly reduced either bleeding time or blood loss in the tail bleeding model, nor were blood loss, survival time or mortality rate altered in the liver injury model. Taken together, these results suggest that these FDA-approved drugs, when used either singly or in combination, are not efficacious in these models of traumatic uncontrolled hemorrhage.

Aminocaproic Acid↗

PubMedDate not supplied

Oral management of a patient with a plasminogen activator inhibitor (PAI-1) deficiency: case report.

Plasminogen activator inhibitor-1 (PAI-1) deficiency causes a rare bleeding disorder by allowing excessive fibrinolysis to occur. Knowledge of the specific type and severity of the bleeding disorder is crucial in planning a safe and appropriate treatment sequence in conjunction with a hemophilia team. This article reports the oral management of a 9-year-old female with PAI-1 inhibitor deficiency using tranexamic acid (Cyclokapron).

Anesthesia, Dental↗

PubMed1997

trans-4-(Aminomethyl)cyclohexane carboxylic acid (T-AMCHA), an anti-fibrinolytic agent, accelerates barrier recovery and prevents the epidermal hyperplasia induced by epidermal injury in hairless mice and humans.

Because wounding the epidermis increases proteolytic activity and because disorders associated with barrier dysfunction have elevated protease activity, we studied the effect of protease inhibitors on the time course of barrier recovery and on the development of epidermal hyperplasia induced by repeated injury. After injuries to the epidermis produced by tape stripping, acetone treatment, or detergent (SDS) treatment that disrupt the barrier, a single application of 5% tranexamic acid [4-(aminomethyl)cyclohexane carboxylic acid, t-AMCHA], a well known anti-plasmin reagent, accelerated barrier recovery in both hairless mouse and human skin. In contrast, neither aminocaproic acid nor aminobutyric acid, inactive analogs of t-AMCHA, affected the time course of barrier recovery. Several trypsin-like serine protease inhibitors, e.g., leupeptin, TLCK, and PMSF, also accelerated barrier repair. In contrast other types of protease inhibitors, e.g., EDTA, pepstatin, N-ethylmaleimide, chymostatin, and TPCK, did not accelerate barrier recovery. We next evaluated the effects of daily topical application of t-AMCHA on epidermal hyperplasia, induced by repeated tape stripping or acetone treatment for 7 d. The degree of hyperplasia, quantified by the measurement of epidermal thickness, was reduced in both models by repeated applications of t-AMCHA. Finally, proteolytic activity in both human and mouse epidermis increased 1-2 h after epidermal injuries that disrupt the barrier. These results demonstrate that the inhibition of plasmin, a serine protease, accelerates barrier recovery and inhibits the epidermal hyperplasia induced by repeated barrier disruption, perhaps by decreasing the extent of attendant epidermal injury.

Animals↗

PubMed1999

[Patient with recurrent gastrointestinal hemorrhage in acquired von Willebrand disease].

A 61-year-old female without prior history of bleeding experienced several symptomatic episodes of gastrointestinal bleeding in the last few years. A source of gastrointestinal bleeding could not be found although several tests of occult blood in the stool were positive. Diagnostically, a significant deficiency of von Willebrand factor could be found due to a shortened half-life of the von Willebrand factor. This acquired von Willebrand factor deficiency most likely can be explained by an immunological mechanism (e.g. antibodies against von Willebrand factor). Neither an immunosuppressive therapy with steroids nor cyclophosphamide could normalize the von Willebrand factor and the bleeding continued. Only tranexamic acid (inhibiting fibrinolysis) could at last stop the symptomatic episodes of gastrointestinal bleeding despite the fact of decreasing von Willebrand factor.

Autoantibodies↗

PubMedDate not supplied

Glanzmann's thrombasthenia: the use of autologous fibrin glue in tooth extractions.

Three teeth were extracted in three sessions in a 15-year-old girl with Glanzmann's thrombasthenia who suffered in the past severe bleeding and required platelet transfusions. The extraction sites were treated locally with autologous fibrin glue in adjunct of tranexamic acid swish and swallow rinses. No systemic platelet infusion was employed as a preventive measure. No postoperative bleeding occurred.

Adolescent↗