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At least 19 recordsLinked to original sources
PubMed1975

Plasminogen-plasmin system IX. Specific binding of tranexamic acid to plasmin.

Interactions between tranexamic acid and protein were studied in respect of the antifibrinolytic actions of tranexamic acid. Tranexamic acid did neither show any interaction with fibrinogen or fibrin, nor was incorporated into cross-linked fibrin structure by the action of factor XIII. On the other hand, tranexamic acid bound to human plasmin with a dissociation constant of 3.5 X 10-5 M, which was very close to the inhibition constatn (3.6 X 10-5 M1 for this compound in inhibiting plasmin-induced fibrinolysis. The binding site of tranexamic acid on plasmin was not the catalytic site of plasmin, because TLCK-blocked plasmin also showed a similar affinity to tranexamic acid (the dissociation constant, 2.9-4.8 x 10-5m). in the binding studies with the highly purified plasminogen and TLCK-plasmin preparations which were obtained by affinity chromatography on lysine-substituted Sepharose, the molar binding ratio was shown to be 1.5-1.6 moles tranexamic acid per one mole protein. On the basis of these and other findings, a model for the inhibitory mechanism of tranexamic acid is presented.

Antifibrinolytic Agents↗
PubMed1976

Failure of tranexamic acid to influence the ellagic acid-induced hypercoagulable state.

Tranexamic acid in a dose of 50 mg/kg b.w. was unable to alter the ellagic acid induced hypercoagulable state. No change in the hypercoagulability pattern was observed regardless of the time of administration of the compound (before or after the ellagic infusion). The silicone clotting times after the infusion of ellagic acid were markedly shortened and remained so for about 60 minutes. The results observed in two control groups treated with saline were similar. The euglobulin lysis times were clearly prolonged after the administration of tranexamic acid, whereas no changes were observed after the administration of saline. These results indicate that tranexamic acid has no anti-factor XII activity.

Animals↗
PubMed1978

A double-blind study of the influence of tranexamic acid on the central corneal thickness after cataract extraction.

A double-blind study of the influence of systemic tranexamic acid on the central corneal thickness after cataract extraction was performed in 17 pairs of patients. Apart from the cataract, no were present. A sequential statistics was used to show that the increase in central corneal thickness after operation was significantly less in the tranexamic acid treated group than in the placebo group. There was no significant difference in intraocular pressure between the tranexamic acid and the placebo treated group. The possible influence of tranexamic acid on the thickness controlling mechanism of the cornea is discussed, and studies concerning the fibrinolytic system, the complement system and the aqueous humour amino acid treated patients are mentioned.

Aged↗
PubMed1978

Treatment of subarachnoid hemorrhage from ruptured intracranial aneurysm with tranexamic acid: a double-blind clinical trial.

A double-blind clinical trial of tranexamic acid was carried out on 39 patients with fresh subarachnoid hemorrhage from a ruptured aneurysm. Twenty patients received tranexamic acid, 6 gm daily for 14 to 21 days, while 19 patients received conventional therapy of bedrest and dexamethasone when cerebral edema developed, plus isotonic saline. Rebleeding and mortality were reduced by one-fourth and one-fifth, respectively (p less than 0.001). No side-effects were observed. Tranexamic acid is valuable in the treatment of subarachnoid hemorrhage caused by ruptured intracranial aneurysms.

Adult↗
PubMed1978

A double-blind study on the influence of tranexamic acid on the intraocular pressure and the central corneal thickness after trabeculectomy for glaucoma simplex.

The influence of tranexamic acid on the intraocular pressure and central corneal thickness has been examined by means of a double-blind trial in patients with glaucoma simplex. The material comprised 28 patients (14 pairs) who had all been operated on for glaucoma in one eye by trabeculectomy. Tranexamic acid was found not to influence the intraocular pressure, neither in the operated eye nor in the opposite eye. The possible antifibrinolytic effect on the outflow of the aqueous humour is discussed. As in previous studies an effect of tranexamic acid on the central corneal thickness was found in both the operated and in the non-operated eye. A possible mechanism behind this is discussed.

Aged↗
PubMed1978

Tranexamic acid in the preoperative management of ruptured intracranial aneurysms.

A randomized, controlled clinical trial was carried out to study the effect of tranexamic acid (AMCA, trans-AMCHA) in prevention of early rebleeding after proven rupture of an intracranial aneurysm. The series comprises 46 patients admitted to the hospital within three days after the first bleeding. Twenty-three were treated with tranexamic acid and 23 were controls. Nine patients in the control group and one in the group treated with tranexamic acid had confirmed rebleeding. The incidence of vasospasm, cerebral ischemia and hydrocephalus as well as mortality and morbidity is discussed.

Adult↗
PubMed1979

Tranexamic acid in massive haemorrhage from the upper gastrointestinal tract: a double-blind study.

In a double-blind trial of tranexamic acid in massive upper gastrointestinal haemorrhage, 76 patients were treated with the active drug and 73 patients with placebo. The doses were 1 g intravenously six times daily for a maximum of 3 days, followed by 1.5 g orally four times daily for a maximum of 4 days. The treatment group and the placebo group were comparable with respect to mean age, diagnoses and laboratory tests but differed slightly with respect to sex and alcohol consumption. The transfusion requirement in the treatment group was less than in the placebo group during the first days after admission, the difference being significant on the second day after admission. Ten patients in the treatment group and 18 patients in the placebo group were operated on. Eleven patients in the treatment group and 12 patients in the placebo group died. In the tranexamic-acid-treated group fewer operations were performed and significantly less blood was needed. It therefore seems highly likely that tranexamic acid has a beneficial effect, although small.

Aged↗
PubMed2026

Tranexamic acid protects human dermal fibroblasts from D-galactose-induced senescence via the GPR30/MAPK pathway.

BACKGROUND: Tranexamic acid (TXA) is widely used for pigmentary disorders, but its anti-ageing potential remains unclear. This study aimed to evaluate whether topical 3% TXA improves early periorbital wrinkles in women with facial melasma and to investigate whether TXA protects human dermal fibroblasts from D-galactose-induced senescence via the GPR30/MAPK pathway. METHODS: Fifty women with melasma were randomized to 3% TXA serum plus moisturizer or moisturizer alone for 8 weeks, with follow-up to week 12. Periorbital wrinkles were graded using a modified Fitzpatrick Wrinkle Scale (MFWS). Separately, D-gal-induced senescence in HDFs was assessed via viability, SA-β-gal activity, senescence markers, ROS, antioxidant enzymes, SASP/ECM gene expression, and MAPK activation. GPR30 involvement was examined using antagonist G15, shRNA knockdown, and molecular docking. RESULTS: Topical TXA produced significantly greater MFWS reductions versus moisturizer alone at weeks 4, 8, and 12, with benefit persisting post-treatment. In HDFs, TXA preserved viability, reduced SA-β-gal positivity, attenuated p21/p16, restored Lamin B1, decreased ROS, and rescued antioxidant activities. TXA downregulated IL-6, IL-8, MMP1, and MMP3, and suppressed D-gal-induced ERK, JNK, and p38 phosphorylation. These effects were weakened by G15 or GPR30 knockdown; docking supported a stable TXA-GPR30 interaction. CONCLUSIONS: TXA showed clinical anti-wrinkle activity in melasma patients and protected HDFs from D-gal-induced senescence, partly via GPR30-dependent modulation of oxidative stress, SASP/ECM expression, and MAPK signalling. TXA is a promising candidate for skin ageing intervention.

Humans↗
PubMed1978

Human leucocyte response to migration inhibitory activity from lymphocytes. Modification by aprotinin, Tranexamic acid and phenylmethyl sulfonylfluoride.

Human lymphokines can elicit several effects associated with inflammation, e.g. leucocyte migration inhibition and fibrinolysis. These effects can be assessed in vitro by the leucocyte migration agarose technique (LMAT) and the leucocyte migration fibrinolysis technique (LMFT). The present study shows that preincubation of normal leucocytes with aprotinin, tranexamic acid and phenyl-methyl-sulfonylfluoride (PMSF) reduces or abolishes their migration inhibition response to leucocyte migration inhibition factor. The compounds exert this effect at non-toxic concentrations, which do not otherwise interfere with migration or fibrinolysis, and are non-toxic as estimated by PHA stimulation of lymphocytes. The LMFT is more sensitive to the modifying effect than the LMAT. The effect of aprotinin and tranexamic acid is reversible, the effect of PMSF is irreversible.

Aprotinin↗
PubMed2026

Tranexamic acid in spontaneous intracerebral hemorrhage: an updated systematic review and meta-analysis of randomized controlled trials.

BACKGROUND: Tranexamic acid (TXA) is a well-established antifibrinolytic medication in the general population. However, its efficacy and safety for patients with spontaneous intracerebral hemorrhage (ICH) remain inconclusive. Consequently, we conducted a systematic review and meta-analysis to assess the effectiveness and safety of TXA for spontaneous ICH. METHODS: We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) following established methodological standards. Our search encompassed eight electronic databases from inception to April 25, 2024. The primary outcome was a reduction in all-cause mortality. The secondary outcomes included improvements in functional independence, neurological impairment, activities of daily living, and reduction in hematoma expansion (HE). Fixed-effects or random-effects model were performed for pooled data where eligible. RESULTS: A total of 9 RCTs that initially enrolled 3,124 patients were included. There were no significant differences observed concerning all-cause mortality (RR, 1.03; 95% CI [0.89-1.18]), hematoma expansion (RR, 0.90; 95% CI [0.80-1.00]), improvement of functional independence (RR, 1.02; 95% CI [0.92-1.12], neurological impairment (MD, -0.88 [95% CI, -2.22-0.45]), or activities in daily living (MD, -0.83 [95% CI, -29.25-12.59]). The pooled data indicated that TXA for ICH was associated with a decrease in hematoma volume from baseline (MD, -1.74; 95% CI [-2.47 to -1.02]). No significant difference in adverse events was observed between the TXA group and the control group. CONCLUSIONS: In summary, TXA does not affect all-cause mortality, functional outcomes, or neurological impairment, nor does it reduce HE, despite reducing hematoma volulume. TXA use for ICH requires careful clinical consideration.

Humans↗
PubMed1976

Treatment of hereditary angioneurotic edema with tranexamic acid and cinnarizine.

Six out of 7 Finnish patients suffering from hereditary angioneurotic edema were helped during attacks, by treatment with tranexamic acid (AMCA, Cyklokapron, Kabi) in doses of 1.5 g 3 times daily, follow-up time 3-25 months. 3 of these patients also had continuous AMCA treatment, in the course of which 2 remained nearly symptom-free on a dosage of 1 g 2-3 times daily. Even the third one had shorter and milder attacks. One patient, however, had to stop taking AMCA after 6 weeks' treatment, because of fatigue and nausea. Follow-up time for the others was 9-11 months. For comparative purposes, 3 patients were given continuous treatment with an antihistamine, cinnarizine in a dosage of 20-30 mg daily. Two of the patients were helped by it, one becoming nearly symptom-free and the other having fewer and milder attacks; follow-up time 9-10 months.

Adult↗
PubMed1979

Effect of p-hydroxyphenyl-propionic ester of tranexamic acid hydrochloride (Cetraxate) on peptic ulcer. Multi-center clinical study.

The therapeutic effects of a new antiulcer drug, a p-hydroxyphenyl-propionic ester of tranexamic acid (cetraxate, CET) hydrochloride, were investigated in 234 patients with gastric ulcer by double blind controlled study using trans-3,7-dimethyl-2,6-octadienyl-5,9,13-trimethyltetradeca-4,8,12-trienoate (gefarnate) as the standard drug in 18 medical institutions. The cure rates confirmed by endoscopic examination in CET-treated patients were 28, 61 and 73% each after 4, 8 and 12 weeks of medication, while those in gefarnate-treated patients were 23, 47 and 55%, respectively, with statistical significance after 8 and 12 weeks. Global utility rate based on the judgement by the physician in charge also supported the results with cure rate. Stratified analysis again confirmed the superiority of CET hydrochloride against gefarnate in the hospitalized patients in terms of both cure rate and global utility rate. However, there was no significant difference between the two drugs as to the effects in the out-patients. Among the symptoms, there was also a significant difference between the improvement rate of epigastralgia with the two drugs in favour of CET hydrochloride. No serious side effects were reported throughout the study.

Adolescent↗
PubMed1977

Acute gastrointestinal haemorrhage. Experience with early panendoscopy and tranexamic acid in a rural hospital.

One hundred and fifty-nine consecutive patients admitted to a small rural hospital because of acute gastrointestinal haemorrhage were studied. Patients with haematemesis and/or melaena were treated with antacids and tranexamic acid from the very beginning and were examined by means of early panendoscopy. All patients were closely observed on a general medical ward by a staff especially trained to deal with acute gastrointestinal bleeding. Eight patients required acute surgery. The overall mortality rate was 4.4%. It is concluded that acute gastrointestinal haemorrhage can be successfully handled with modern diagnosis and treatment even in a small hospital.

Acute Disease↗
PubMed2026

Intravenous Tranexamic Acid Reduces Perioperative Blood Loss in Reduction Mammoplasty With Immediate Implant-Based Reconstruction: A Randomized, Triple-Blinded, Placebo-Controlled Trial.

BACKGROUND: Postoperative hematoma and oozing can compromise outcomes after reduction mammoplasty with immediate reconstruction. Intravenous (IV) tranexamic acid (TXA) is antifibrinolytic, but prospective evidence in this setting is limited. OBJECTIVES: The aim of this study was to determine whether a single pre-incision dose of IV TXA reduces perioperative blood loss and fibrinolytic activation vs placebo. METHODS: In this randomized, triple-blinded, placebo-controlled trial, 60 women (American Society of Anesthesiologists I/II, 18-75 years) undergoing bilateral reduction mammoplasty with immediate implant-based reconstruction received TXA 10 mg/kg in 100 mL saline or placebo 10 min before incision. The primary outcome was total blood loss within 24 h (intraoperative suction + swab plus drain output). Secondary outcomes were perioperative changes in hemoglobin, D-dimer and fibrinogen, and complications within 30 days. Intention-to-treat analyses were performed. RESULTS: All patients completed follow-up. Total blood loss was lower with TXA than with placebo (mean ± standard deviation: 221.1 ± 72.4 vs 298.1 ± 90.6 mL; mean difference -77.0 mL; 95% CI, -122.4 to -31.6; P = .001). Intraoperative loss and 24 h drain output were also reduced. Postoperative D-dimer rise was attenuated with TXA (0.31 ± 0.15 vs 0.49 ± 0.22 µg/mL; P = .002); hemoglobin decline was smaller. No thromboembolic, neurologic, or allergic events occurred; no skin-flap necrosis was observed. CONCLUSIONS: Pre-incisional IV TXA safely reduces perioperative bleeding and fibrinolytic activity after reduction mammoplasty. These findings support incorporation of IV TXA into perioperative protocols. LEVEL OF EVIDENCE: 2 (THERAPEUTIC): For image description, please refer to the figure legend and surrounding text.

Humans↗