Tranexamic Acid for Hip Socket Surgery
Recruiting in Palo Alto (17 mi)
Age: 18+
Sex: Any
Travel: May Be Covered
Time Reimbursement: Varies
Trial Phase: Phase < 1
Recruiting
Sponsor: University of Cincinnati
Disqualifiers: Polytrauma, Thromboembolic disease, Bleeding disorder, others
Approved in 5 Jurisdictions
Trial Summary
What is the purpose of this trial?This multi-center, prospective study will evaluate the use of topical tranexamic acid (TXA - Cyklokapron; Pfizer, New York, NY) on pre-operative and post-operative hemoglobin (Hb)/hematocrit (Hct) in patients undergoing operative repair of isolated posterior wall (PW) acetabular fractures.
Will I have to stop taking my current medications?
The trial information does not specify whether you need to stop taking your current medications. It's best to discuss this with the trial coordinators or your doctor.
Is Tranexamic Acid (TXA) generally safe for use in humans?
Tranexamic Acid (TXA) is generally considered safe for use in humans, but there are rare cases where it can cause serious side effects if accidentally injected into the spine, leading to heart and nerve problems. It has been used safely in various surgeries and for treating skin conditions like melasma, with studies showing it is well-tolerated.
12345How does the drug Tranexamic Acid differ from other treatments for hip socket surgery?
Tranexamic Acid (TXA) is unique because it helps reduce bleeding during surgeries by preventing the breakdown of blood clots, which is particularly useful in orthopedic surgeries like hip socket surgery. Unlike other treatments, TXA works by blocking enzymes that dissolve clots, making it effective in managing surgical bleeding.
12678Eligibility Criteria
This trial is for adults with isolated, closed posterior wall acetabular fractures needing surgery within a week of injury. It's not for those with multiple injuries requiring several surgeries, pre-existing blood clots, bleeding disorders, kidney issues, or who can't consent.Inclusion Criteria
I have a non-operative fracture in my arm that doesn't affect my ability to bear weight.
I had surgery for a specific hip fracture within a week of the injury.
My bones have stopped growing.
Exclusion Criteria
I was admitted for injuries to internal organs from a severe accident.
I had a blood clot before my surgery.
I need several surgeries.
+8 more
Trial Timeline
Screening
Participants are screened for eligibility to participate in the trial
2-4 weeks
Pre-operative
Pre-operative hemoglobin and hematocrit levels are drawn to establish baseline levels
1 day
1 visit (in-person)
Treatment
Participants undergo surgery with either topical TXA or placebo applied; intraoperative transfusion requirements and estimated blood loss are recorded
1 day
1 visit (in-person)
Post-operative Monitoring
Hemoglobin and hematocrit values are obtained on postoperative day one and two; post-operative transfusion requirements are recorded
2 days
2 visits (in-person)
Follow-up
Participants are monitored for safety and effectiveness after treatment, including standard DVT prophylaxis for four weeks post-operatively
4 weeks
Participant Groups
The study tests if applying tranexamic acid (TXA) directly to the fracture site before and after surgery affects hemoglobin/hematocrit levels compared to using normal saline in patients with specific hip fractures.
2Treatment groups
Experimental Treatment
Placebo Group
Group I: Topical TXA TreatmentExperimental Treatment1 Intervention
2 gm TXA/100 ml of normal saline
Group II: No Topical TreatmentPlacebo Group1 Intervention
Normal saline
Tranexamic Acid is already approved in United States, European Union, Canada, Japan, Australia for the following indications:
πΊπΈ Approved in United States as Tranexamic Acid for:
- Heavy menstrual bleeding
- Prevention of excessive bleeding during surgeries
πͺπΊ Approved in European Union as Tranexamic Acid for:
- Heavy menstrual bleeding
- Prevention of excessive bleeding during surgeries
- Hereditary angioedema
π¨π¦ Approved in Canada as Tranexamic Acid for:
- Heavy menstrual bleeding
- Prevention of excessive bleeding during surgeries
π―π΅ Approved in Japan as Tranexamic Acid for:
- Heavy menstrual bleeding
- Prevention of excessive bleeding during surgeries
π¦πΊ Approved in Australia as Tranexamic Acid for:
- Heavy menstrual bleeding
- Prevention of excessive bleeding during surgeries
Find a Clinic Near You
Research Locations NearbySelect from list below to view details:
University of Cincinnati College of MedicineCincinnati, OH
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Who Is Running the Clinical Trial?
University of CincinnatiLead Sponsor
Foundation for Orthopedic TraumaCollaborator
References
Ventriculolumbar perfusion and inhalational anesthesia with sevoflurane in an accidental intrathecal injection of tranexamic acid: unreported treatment options. [2022]Tranexamic acid (TXA) decreases hemorrhage-related mortality in trauma patients and is increasingly being used during obstetric and orthopedic surgeries. Inadvertent intrathecal injection of TXA is a rare, potentially lethal event leading to dose-dependent cardiotoxicity and neurotoxicity. TXA enhances neuronal excitation by antagonizing inhibitory Ξ³-aminobutyric acid type A and glycine receptors. Until now, mechanistic-based pharmacological treatments targeting multiple central nervous system receptors have been advocated for use in such cases, with no data on intrathecal TXA elimination techniques.
Synthesis of [17,18-3H] trans-13-azaprostanoic acid. A labeled probe for the PGH2/TXA2 receptor. [2019]Because of its highly unstable nature, TXA2, produced by platelet metabolism of arachidonic acid, does not lend itself to use as a receptor probe for its own receptor. As such, the stable TXA2/PGH2 antagonist, trans-13-azaprostanoic acid (trans-13-APA, 12b), was prepared as the [17, 18 3H] derivative [( 3H] trans-13-APA, 12c) to study this receptor and to better evaluate the mechanism of action of these azaprostanoids. Tritiated trans-13-APA, 12c, was prepared in nearly theoretical specific activity (57 Ci/mmole) from (17Z)-trans-13-azaprost-17-enoic acid (11b) by catalytic tritiation. The unsaturated 11b was prepared by condensation of cis-7-amino-3-heptene (8) with 2-(6-carboxyhexyl) cyclopentanone (9), NaBH4 reduction, chromatography, and hydrolysis of the trans isomer so isolated. The olefins 11a and b were also of biochemical interest because of the unsaturation in the lower side chain. The presence of similar unsaturation in PGH3(4) and TXA3 (3) renders these prostaglandins inactive as proaggregatory agents. Evaluation of the antiaggregatory activity of 11a and b indicated it to be about the same potency in inhibiting human platelet aggregation as the parent cis and trans-13-APAs, suggesting that introduction of a double bond at the 17 position in platelet prostaglandin antagonists is unlikely to result in enhanced antiplatelet activity.
Antiplatelet and anticoagulant effects of "HN-11 500," a selective thromboxane receptor antagonist. [2019]The antiplatelet and anticoagulant effect of a thromboxane receptor (TX receptor) antagonist developed by Nycomed (Linz) has been studied in a placebo-controlled double-blind phase I study. Sixteen healthy male volunteers received different single oral doses of "HN-11 500" (C(14)H(15)NO(5)S(2); 1, 10, 100, 200, and 400 mg). Eight volunteers received placebo. The washout period between each dosage applied was at least 12 days. Platelet aggregation induced by the thromboxane mimetic "U 46 619" (C(21)H(34)0(4)) and platelet adhesion to siliconized glass were significantly and dose-dependently inhibited. The effect lasted between 3 and 4 h (10 mg) and 8 h (400 mg), respectively, and correlated well with the pharmacokinetic data. Platelet aggregation seems to be more sensitive to monitor the effects of HN-11 500 on platelet function than platelet adhesion. Plasma levels of 300 ng/ml HN-11 500 probably leads to >90% inhibition of platelet aggregation. The template bleeding time slightly increased but did not exceed the normal range. Furthermore, there was a wide variation of results. There were no significant changes in platelet counts, platelet-induced thrombin generation time (PITT), and blood coagulation parameters. All doses of HN-11 500 were well tolerated. HN-11 500 is a potent TX receptor antagonist (TXRA), which inhibits either platelet aggregation or platelet adhesion, which has not yet been described. In clinical routine, TXRAs have to demonstrate the effectiveness in large clinical trials for different clinical indications and to compete with single or combined administrations of cyclooxygenase (COX) inhibitors, thienovridines, thromboxane synthase inhibitors, and GIIb/IIIa inhibitors.
Oral Tranexamic Acid for the Treatment of Melasma: Evidence and Experience-Based Consensus Statement from Indian Experts. [2023]Melasma, a chronic pigmentary skin condition mainly affecting the face, remains a challenge despite the availability of several options for treatment. Many melasma patients are not satisfied with treatment outcomes. Tranexamic acid (TXA), an anti-fibrinolytic drug has shown promising results in patients with melasma. Evidence from several clinical studies has surfaced on efficacy and tolerability of TXA in these patients. It can be used as monotherapy or adjuvant with other therapies. Currently, there is no published consensus or guideline document for its use in the treatment of melasma. TXA is available for oral use, topical use as well as an injection. In this article, a consensus of Indian experts is prepared based on the available literature and experience with use of oral TXA in melasma. This review article might help clinicians for use of oral TXA appropriately while treating melasma.
MC-002 exhibits positive effects against platelets aggregation and endothelial dysfunction through thromboxane A2 inhibition. [2014]Thromboxane A2 (TXA2) induces platelet aggregation and vasoconstriction, and agents that inhibit TXA2 production or interaction with receptors may exert potential application in stroke therapy.
Discovery of potent, efficacious, and orally bioavailable inhibitors of blood coagulation factor Xa with neutral P1 moieties. [2014]The bicyclic dihydropyrazolopyridinone scaffold allowed for incorporation of multiple P1 moieties with subnanomolar binding affinities for blood coagulation factor Xa. The compound 3-[6-(2'-dimethylaminomethyl-biphenyl-4-yl)-7-oxo-3-trifluoro-methyl-4,5,6,7-tetrahydro-pyrazolo[3,4-c]pyridine-l-yl]-benzamide 6d shows good fXa potency, selectivity, in vivo efficacy and oral bioavailability. Compound 6d was selected for further pre-clinical evaluations.
3-Substituted imidazo[1,2-d][1,2,4]-thiadiazoles: a novel class of factor XIIIa inhibitors. [2014]A new class of selective FXIIIa inhibitors with a bicyclic [1,2,4]-thiadiazole pharmacophore is described. At 160 muM, compound 8 caused 50% reduction in fibrin gamma-chain cross-linking and suppressed the polymerization of alpha chains in platelet-depleted human plasma clots. Fibrinolysis rates in response to tissue plasminogen activator were directly proportional to the concentration of 8 in plasma at the time of clotting.
Pharmacological characterization of 2NTX-99 [4-methoxy-N1-(4-trans-nitrooxycyclohexyl)-N3-(3-pyridinylmethyl)-1,3-benzenedicarboxamide], a potential antiatherothrombotic agent with antithromboxane and nitric oxide donor activity in platelet and vascular preparations. [2013]Thromboxane (TX) A(2), prostacyclin (PGI(2)), and nitric oxide (NO) regulate platelet function and interaction with the vessel wall. Inhibition of TXA(2), implemented synthesis of PGI(2), and supply of exogenous NO may afford therapeutic benefit. 2NTX-99 [4-methoxy-N(1)-(4-trans-nitrooxycyclohexyl)-N(3)-(3-pyridinylmethyl)-1,3-benzenedicarboxamide], a new chemical entity related to picotamide, showed antithromboxane activity and NO donor properties. 2NTX-99 relaxed rabbit aortic rings precontracted with norepinephrine or U46619 (9,11-dideoxy-9alpha,11alpha-methanoepoxy-prosta-5Z,13E-dien-1-oic acid; EC(50), 7.9 and 17.1 microM, respectively), an effect abolished by 10 microM 1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one (ODQ). 2NTX-99 inhibited arachidonic acid (AA)-induced washed platelet aggregation (EC(50), 9.8 microM) and TXB(2) formation (-71% at 10 microM), and its potency increased in the presence of aortic rings (EC(50), 1.4 microM). In whole rabbit aorta incubated with homologous platelets, AA caused contraction and TXA(2) formation, reduced by 2NTX-99 (10-40 microM): contraction, -28 and -47%, TXA(2) formation, -37 and -75.4%, respectively, with concomitant increase in PGI(2). 2NTX-99 (20-40 microM) inhibited U46619-induced aggregation in rabbit platelet-rich plasma (PRP) (-74 +/- 6.7 and -96 +/- 2.4%, respectively) and inhibited collagen-induced aggregation in human PRP (-48.2 +/- 10 and -79.2 +/- 6%), whereas ozagrel was ineffective. In human embryonic kidney 293 cells transfected with the TXA(2) receptor isophorm alpha receptor, 2NTX-99 did not compete with the ligand, [(3)H]SQ29,548 ([(3)H][1S-[1alpha,2beta(5Z),3beta,4alpha]]-7-[3-[[2-(phenylamino)-carbonyl]hydrazino]methyl]-7-oxabicyclo[2,2,1]-hept-2-yl]-5-heptanoic acid), or prevent inositol phosphate accumulation. After oral administration (50-250 mg/kg), 2NTX-99 inhibited TXA(2) production in rat clotting blood (-71 and -91%); at 250 mg/kg, an area under the curve, 0 to 16 h, of 149.5 h/microg/ml and a t(1/2) of 6 h were calculated, with a C(max) value of 31.8 +/- 8.2 microg/ml. An excellent correlation between plasma concentrations and TXA(2) inhibition occurs. 2NTX-99 controls platelet function and vessel wall interaction by multifactorial mechanisms and possesses therapeutic potential.