Results for “Tranexamic Acid” — Page 40

PubMedDate not supplied

Some drug effects on the activity of erythrocyte hexokinase and glucose 6-phosphate dehydrogenase enzymes in vitro and in vivo.

Effects of theophylline, lidocaine, cyclophosphamide, hyoscine N-butyl bromide, tranexamic acid and cytarabine on hexokinase (HK) from human erythrocytes have been investigated in vitro. In addition, in vivo effects of theophylline and lidocaine were investigated in rats. HK was purified from human red blood cells by DEAE-Sephadex A50 ion exchange chromatography. HK activity was measured spectrophotometrically at 25 degrees C in a system coupled with glucose 6-phosphate dehydrogenase, according to Beutler's method at 340 nm. Cyclophosphamide, hyoscine N-butyl bromide, tranexamic acid and cytarabine had no effects on human erythrocyte HK activity in in vitro conditions. On the other hand, human erythrocyte HK was inhibited by theophylline, but activated by lidocaine. IC50 value for theophylline was 0.013 M. In the case of in vivo studies, 6 mg kg(-1) of theophylline inhibited the rat HK activity by 43% at the first 1.5 h (p < 0.001). A dose of 5 mg kg(-1) of lidocaine activated the rat HK activity by 41% (p < 0.001), 22% (p < 0.001), and 11% (p < 0.05), at 1.5, 3 and 6 h, respectively.

Animals↗

PubMed1991

Streptokinase-induced platelet aggregation. Prevalence and mechanism.

BACKGROUND: Streptokinase (SK) is a bacteria-derived protein and one of the plasminogen activators that is currently available for therapeutic use. Exposure to SK induces synthesis of specific antibodies that may initiate platelet aggregation and paradoxical clot propagation during treatment. METHODS AND RESULTS: Using platelet-rich plasma (PRP), we found that SK (5,000 units/ml) but not urokinase (2,500 units/ml) or recombinant tissue-type plasminogen activator (2,500 units/ml) caused platelet aggregation in PRP from 14 of 100 normal volunteers. In 13 consecutive patients treated with SK for acute myocardial infarction, SK-mediated platelet aggregation was induced in five patients within 1 week after treatment. SK-mediated platelet aggregation was associated with significantly increased titers of both anti-SK antibodies and SK-neutralizing activity in plasma; it was partially inhibited by aspirin (1 mM) and by aprotinin (500 kallikrein inhibitor units/ml) and completely inhibited by tranexamic acid (1 mM) and by prostaglandin E1 (9 microM). Addition of SK (1,000 or 5,000 units/ml) induce a statistically significant dose-dependent thromboxane B2 release in mixtures of PRP with plasma from subjects with SK-induced aggregation but not in samples of PRP mixed with plasma from nonresponders; addition of recombinant tissue-type plasminogen activator (1 or 50 micrograms/ml) did not induce thromboxane B2 release. Mixing experiments with PRP and immunoglobulin G from reactive and nonreactive donors revealed that SK-induced aggregation requires the presence of anti-SK antibodies. When 125I-SK (50 nM) was used, platelets preincubated with plasminogen (0.5 microM) bound 9,500 +/- 600 (mean +/- SEM, n = 6) molecules SK/platelet, which increased to 25,000 +/- 3,100 molecules/platelet after thrombin stimulation. Tranexamic acid (1 mM) blocked specific binding of SK to resting platelets. CONCLUSIONS: These data demonstrate that SK-induced platelet aggregation is initiated by the binding of anti-SK antibodies to the SK-plasminogen complex located on the platelet surface. SK-induced platelet activation may limit the therapeutic effectiveness of the drug, and in view of the high prevalence of aggregation in a normal population, prospective evaluation of the effects of platelet aggregation during treatment with SK is warranted.

Adult↗

PubMed1999

Technologies to minimize blood transfusion in cardiac and orthopedic surgery. Results of a practice variation survey in nine countries. International Study of Peri-operative Transfusion (ISPOT) Investigators.

OBJECTIVES: Due to the discovery in the 1980s that blood transfusion can transmit HIV, there has been increased interest in technologies that reduce the amount of allogeneic blood used during and after surgery. These technologies include drugs (aprotinin, tranexamic acid, epsilon-aminocaproic acid, erythropoietin), devices (cell salvage), and techniques (acute hemodilution, predeposited autologous donation). The purpose of this study was to ascertain the degree of practice variation, if any, that exists for eight technologies in nine countries in orthopedic and cardiac surgery. METHODS: In each country, either all hospitals or a random sample of hospitals with medical/surgical beds were surveyed between 1995 and 1997. Two instruments were used. The first instrument was a postcard that asked recipients whether the technologies were currently being used in their hospital for orthopedic and/or cardiac surgery to reduce perioperative allogeneic transfusion. The second questionnaire elicited information regarding the degree of use both in qualitative and quantitative terms. Data were collected, entered, and analyzed in each country, with summary results submitted to the Canadian coordinating center on a standardized data collection form. RESULTS: Pharmaceuticals were generally used in a much smaller proportion of hospitals in orthopedic than in cardiac surgery. Aprotinin and tranexamic acid were the drugs most frequently used in cardiac surgery. Nonpharmacological technologies were used to a greater degree than drugs in orthopedic surgery, although there was wide variation among technologies and countries. Acute hemodilution and cell salvage were used in a greater proportion of hospitals for cardiac surgery than orthopedic surgery. CONCLUSIONS: The results of this survey indicate that there is considerable practice variation in the use of technologies to minimize exposure to perioperative allogeneic transfusion within and between countries.

Antifibrinolytic Agents↗

PubMed2006

Gynaecological and obstetric management of women with inherited bleeding disorders.

OBJECTIVE: The prevalence of bleeding disorders, notably von Willebrand disease (vWD), among adult women with objectively documented menorrhagia is consistently reported to be 10% to 20% and is even higher in adolescents presenting with menorrhagia. This consensus document has been developed by a multidisciplinary committee consisting of an anesthesiologist, 2 hematologists, and an obstetrician/gynaecologist and has been endorsed by their relevant specialty bodies. It has been prepared with the express purpose of providing guidelines for both women with inherited bleeding disorders and for their caregivers regarding the gynaecological and obstetric management of these women, including appropriate anesthesia support where indicated. OPTIONS: Diagnostic tools and specific medical and, where appropriate, surgical alternatives to management are reviewed and evidence-based recommendations presented. EVIDENCE: A MEDLINE search of the English literature between January 1975 and November 2003 was performed using the following key words: menorrhagia, uterine bleeding, pregnancy, von Willebrand, congenital bleeding disorder, desmopressin/DDAVP, tranexamic acid, oral contraceptives, medroxyprogesterone, therapy, hysterectomy, anesthesia, epidural, spinal. Recommendations from other society guidelines were reviewed. RECOMMENDATIONS: 1. Inherited bleeding disorders should be considered in the differential diagnosis of all patients presenting with menorrhagia (II-2B). The graphical scoring system presented is a validated tool which offers a simple yet practical method that can be used by patients to quantify their blood loss (II-2B). 2. Because underlying bleeding disorders are frequent in women with menorrhagia, physicians should consider performing a hemoglobin/hematocrit, platelet count, ferritin, PT (INR) and APTT in women with menorrhagia. In women who have a personal history of other bleeding or a family history of bleeding, further investigation should be considered, including a vWD workup (factor VIII, vWF antigen, and vWF functional assay) (II-2B). 3. Treatment of menorrhagia in women with inherited bleeding disorders should be individualized (III-B). 4. An inherited bleeding disorder is not a contraindication to hormonal therapy (oral contraceptives [II-1B], depot medroxyprogesterone acetate (DMPA) [II-3B], danazol [II-2B], GnRH analogs [II-3B]) or local treatments (levonorgestrel-releasing IUS [II-1B]) and non-hormonal therapy (antifibrinolytic drug tranexamic acid [II-1B]) as well as desmopressin (II-1B). These therapies represent first line treatment. Blood products should not be used for women with mild bleeding disorders (III-A). 5. In women who no longer want to preserve their fertility, conservative surgical therapy (ablation) and hysterectomy may be options (III-B). Clinicians may consult the "SOGC Clinical Practice Guideline: Guidelines for the Management of Abnormal Uterine Bleeding" for an in-depth discussion of the available therapeutic modalities, both medical and surgical. To minimize the risk of intraoperative and post-operative hemorrhage, coagulation factors should be corrected preoperatively with post-operative monitoring (II-1B). 6. Girls growing up in families with a history of vWD or other inherited bleeding disorders should be tested pre-menarchally to determine whether or not they have inherited the disease to allow both the patient and her family to prepare for her first and subsequent menstrual periods (III-C). 7. In adolescents presenting with menorrhagia, an inherited bleeding disorder should be excluded (III-B). When possible, investigation should be undertaken before oral contraceptive therapy is instituted, as the hormonally induced increase in factor VIII and vWF may mask the diagnosis (II-B). 8. Pregnancy in women with inherited bleeding disorders may require a multidisciplinary approach. A copy of their recommendations should be given to the patient and she should be instructed to present it to the health care provider admitting her to the birthing centre. Women with severe bleeding disorders or with a fetus at risk for a severe bleeding disorder should deliver in a hospital (level three) or where there is access to consultants in obstetrics, anesthesiology, hematology, and pediatrics (III-C). 9. Vacuum extraction, forceps, fetal scalp electrodes, and fetal scalp blood sampling should be avoided if the fetus is known or thought to be at risk for a congenital bleeding disorder. A Caesarean section should be performed for obstetrical indications only (II-2C). 10. Epidural and spinal anesthesia are contraindicated if there is a coagulation defect. There is no contraindication to regional anesthesia if coagulation is normalized. The decision to use regional anesthesia should be made on an individual basis (III-C). 11. The risk of early and late postpartum hemorrhage is increased in women with bleeding disorders. Women with inherited bleeding disorders should be advised about the possibility of excessive postpartum bleeding and instructed to report this immediately (III-B). 12. Intramuscular injections, surgery, and circumcision should be avoided in neonates at risk for a severe hereditary bleeding disorder until adequate workup/preparation are possible (III-B). The quality of evidence reported in this document has been described using the Evaluation of Evidence criteria outlined in the Report of the Canadian Task Force on the Periodic Health Exam (Table 1).

Journal Article↗

PubMed2005

Gynaecological and obstetric management of women with inherited bleeding disorders.

OBJECTIVE: The prevalence of bleeding disorders, notably von Willebrand disease (vWD), among adult women with objectively documented menorrhagia is consistently reported to be 10% to 20% and is even higher in adolescents presenting with menorrhagia. This consensus document has been developed by a multidisciplinary committee consisting of an anesthesiologist, 2 hematologists, and an obstetrician/gynaecologist and has been endorsed by their relevant specialty bodies. It has been prepared with the express purpose of providing guidelines for both women with inherited bleeding disorders and for their caregivers regarding the gynaecological and obstetric management of these women, including appropriate anesthesia support where indicated. OPTIONS: Diagnostic tools and specific medical and, where appropriate, surgical alternatives to management are reviewed and evidence-based recommendations presented. EVIDENCE: A MEDLINE search of the English literature between January 1975 and November 2003 was performed using the following key words: menorrhagia, uterine bleeding, pregnancy, von Willebrand, congenital bleeding disorder, desmopressin/DDAVP, tranexamic acid, oral contraceptives, medroxyprogesterone, therapy, hysterectomy, anesthesia, epidural, spinal. Recommendations from other society guidelines were reviewed. RECOMMENDATIONS: 1. Inherited bleeding disorders should be considered in the differential diagnosis of all patients presenting with menorrhagia (II-2B). The graphical scoring system presented is a validated tool which offers a simple yet practical method that can be used by patients to quantify their blood loss (II-2B). 2. Because underlying bleeding disorders are frequent in women with menorrhagia, physicians should consider performing a hemoglobin/hematocrit, platelet count, ferritin, PT (INR) and APTT in women with menorrhagia. In women who have a personal history of other bleeding or a family history of bleeding, further investigation should be considered, including a vWD workup (factor VIII, vWF antigen, and vWF functional assay) (II-2B). 3. Treatment of menorrhagia in women with inherited bleeding disorders should be individualized (III-B). 4. An inherited bleeding disorder is not a contraindication to hormonal therapy (oral contraceptives [II-1B], depot medroxyprogesterone acetate (DMPA) [II-3B], danazol [II-2B], GnRH analogs [II-3B]) or local treatments (levonorgestrel-releasing IUS [II-1B]) and non-hormonal therapy (antifibrinolytic drug tranexamic acid [II-1B]) as well as desmopressin (II-1B). These therapies represent first line treatment. Blood products should not be used for women with mild bleeding disorders (III-A). 5. In women who no longer want to preserve their fertility, conservative surgical therapy (ablation) and hysterectomy may be options (III-B). Clinicians may consult the "SOGC Clinical Practice Guideline: Guidelines for the Management of Abnormal Uterine Bleeding" for an in-depth discussion of the available therapeutic modalities, both medical and surgical. To minimize the risk of intraoperative and post-operative hemorrhage, coagulation factors should be corrected preoperatively with post-operative monitoring (II-1B). 6. Girls growing up in families with a history of vWD or other inherited bleeding disorders should be tested pre-menarchally to determine whether or not they have inherited the disease to allow both the patient and her family to prepare for her first and subsequent menstrual periods (III-C). 7. In adolescents presenting with menorrhagia, an inherited bleeding disorder should be excluded (III-B). When possible, investigation should be undertaken before oral contraceptive therapy is instituted, as the hormonally induced increase in factor VIII and vWF may mask the diagnosis (II-B). 8. Pregnancy in women with inherited bleeding disorders may require a multidisciplinary approach. A copy of their recommendations should be given to the patient and she should be instructed to present it to the health care provider admitting her to the birthing centre. Women with severe bleeding disorders or with a fetus at risk for a severe bleeding disorder should deliver in a hospital (level three) or where there is access to consultants in obstetrics, anesthesiology, hematology, and pediatrics (III-C). 9. Vacuum extraction, forceps, fetal scalp electrodes, and fetal scalp blood sampling should be avoided if the fetus is known or thought to be at risk for a congenital bleeding disorder. A Caesarean section should be performed for obstetrical indications only (II-2C). 10. Epidural and spinal anesthesia are contraindicated if there is a coagulation defect. There is no contraindication to regional anesthesia if coagulation is normalized. The decision to use regional anesthesia should be made on an individual basis (III-C). 11. The risk of early and late postpartum hemorrhage is increased in women with bleeding disorders. Women with inherited bleeding disorders should be advised about the possibility of excessive postpartum bleeding and instructed to report this immediately (III-B). 12. Intramuscular injections, surgery, and circumcision should be avoided in neonates at risk for a severe hereditary bleeding disorder until adequate workup/preparation are possible (III-B). The quality of evidence reported in this document has been described using the Evaluation of Evidence criteria outlined in the Report of the Canadian Task Force on the Periodic Health Exam (Table 1).

Blood Coagulation Disorders↗

PubMed2006

[Effects of different durations of thromboembolism on blood gases, hemodynamics, pulmonary arteriography and thrombo-pathology in a canine model with selective embolization of pulmonary lobar arteries].

OBJECTIVE: To investigate the effects of different durations of thromboembolism on blood gases, hemodynamic parameters, pulmonary arteriography and thrombo-pathology in an animal model mimicking chronic pulmonary thromboembolism (PTE). METHODS: Sixteen dogs were embolized with five thrombi developed by autologous blood into the left lower pulmonary artery (n = 15) and the right lower pulmonary artery (n = 1, used to confirm the available method of selective embolization). The 15 dogs were divided into three groups: sham group (n = 5), one-week group (n = 5) and two-week group (n = 5) according to the different durations of embolization. Swan-Ganz catheter was used to guide a plastic duct, through which the thrombi were injected selectively into the left or right lower pulmonary artery by X-ray fluoroscopy. Local pulmonary arteriography of lower pulmonary arteries was taken. Blood pressure (BP), and blood gases were measured. Central venous pressure (CVP), mean pulmonary arterial pressure (MPAP), pulmonary arteriole wedge pressure (PAWP), and cardiac output (CO) were recorded, and pulmonary vascular resistance (PVR) was calculated. Each dog underwent muscular injection with tranexamic acid for one or two weeks to prevent thrombolysis. The lower lung lobe was dissected to confirm the thromboembolism after one or two weeks. The lung sections were stained with phosphotungstic acid hematoxylin (PTAH) to observe thromboemboli with optical microscopy. RESULTS: In the PTE group, PaO(2)/FiO(2), MPAP and PVR changed significantly as compared to baseline values (P < 0.05) after one hour of embolization, with MPAP increasing from (15 +/- 3) mm Hg to (21 +/- 4) mm Hg, PVR increasing from (178 +/- 114) mm Hg.s/L to (404 +/- 260) mm Hg.s/L, and PaO(2)/FiO(2) decreasing from (508 +/- 58) mm Hg to (395 +/- 100) mm Hg; these parameters returned to the baseline values one or two weeks later. After embolization, pulmonary arteriography demonstrated lower lobar artery cut-off perfusion defects. One week later, pulmonary arteriography demonstrated irregularities and stiffness of the arterial wall, enlarged proximal part of lower pulmonary artery and cut-off perfusion defects. Poor filling at embolus site was evident after embolization for two weeks. In the 1-week PTE group, organized tissue covered with the blue-purple fibrin nest was observed in the thrombus with PTAH stain. In the two-week group, the well organized thrombi were partially recanalized and surrounded and invaded by hyperplastic tissues from pulmonary artery wall. CONCLUSIONS: A canine model mimicking chronic PTE can be established by the use of fibrinolytic inhibitor tranexamic acid. Different manifestations on pulmonary arteriography and varied degree of organization of thrombi are evident at different times after embolization.

Angiography↗

PubMed2006

Phosphorylcholine coating may limit thrombin formation during high-risk cardiac surgery: a randomized controlled trial.

BACKGROUND: During cardiopulmonary bypass, blood contact with the large nonendothelial surfaces of the extracorporeal circuit induces activation and consumption of platelets and plasma coagulation factors. Phosphorylcholine (Pc) coating of oxygenators has been designed to improve surface biocompatibility. We evaluated the effects of a Pc-coated oxygenator on blood coagulation in patients undergoing high-risk open heart surgery and receiving tranexamic acid. METHODS: Thirty-nine patients undergoing reoperative valvular or combined procedures were randomized to the use of an oxygenator treated with Pc coating (Pc group) or of a standard oxygenator (control group). Platelet count, soluble CD40 ligand, fibrinogen, antithrombin, D-Dimer, prothrombin fragment 1.2 (F1.2), and free plasma hemoglobin levels were measured at baseline, at aortic unclamping, and at arrival in the intensive care unit. RESULTS: Postoperative bleeding, need for blood products, and clinical outcomes were similar in the two groups. At unclamping, F1.2, a marker of in vivo thrombin formation, increased to a greater extent in control patients than in Pc patients (p = 0.02), and in the latter group of patients was positively correlated with aortic cross-clamp times (r = 0.70). Relative to baseline values, the percent decrease in platelet count, fibrinogen, and antithrombin levels was not significantly different in Pc patients and in control patients after adjustment for multiple comparisons, but the percent decrease in platelet counts was negatively correlated with F1.2 levels in the entire series of patients (r = -0.62, p < 0.0001). All the evaluated parameters were similar in the two groups of patients at arrival in the intensive care unit. CONCLUSIONS: For patients undergoing high-risk open heart surgery and receiving tranexamic acid, a phosphorylcholine-coated oxygenator may reduce intraoperative thrombin formation and the associated consumption of platelets, fibrinogen, and antithrombin.

Aged↗

PubMed2000

Antifibrinolytic therapy for aneurysmal subarachnoid haemorrhage.

BACKGROUND: Re-bleeding is an important cause of death and disability in people with aneurysmal subarachnoid haemorrhage. This is probably due to dissolution of the clot by natural fibrinolytic activity. OBJECTIVES: The objective of this review was to assess the effect of antifibrinolytic treatment in patients with aneurysmal subarachnoid haemorrhage. SEARCH STRATEGY: We searched the Cochrane Stroke Group trials register and reference lists of articles. We also contacted drug companies. SELECTION CRITERIA: Randomised trials comparing oral or intravenous antifibrinolytic drugs (tranexamic acid, epsilon amino-caproic acid or an equivalent) with control in people with confirmed subarachnoid haemorrhage. DATA COLLECTION AND ANALYSIS: Two reviewers independently selected trials for inclusion and extracted the data. All five reviewers assessed trial quality. MAIN RESULTS: Eight trials involving 937 patients were included. Based on 579 patients in two trials, antifibrinolytic treatment did not show any benefit for poor outcome (death, vegetative state or severe disability) with an odds ratio of 1.05, 95% confidence interval 0.76 to 1.46. Death from all causes was not significantly influenced by treatment across all eight trials (odds ratio 0.96, 95% confidence interval 0.72 to 1.26). Antifibrinolytic treatment reduced the risk of re-bleeding reported at the end of follow-up, with some heterogeneity between the trials (odds ratio 0.59, 95% confidence interval 0.42 to 0.81). Treatment increased the risk of cerebral ischaemia in four trials (odds ratio 2.03, 95% confidence interval 1.40 to 2.94). Antifibrinolytic treatment showed no effect on the reported rate of hydrocephalus in four trials (odds ratio 1. 05, 95% confidence interval 0.71 to 1.56). REVIEWER'S CONCLUSIONS: Antifibrinolytic treatment does not appear to benefit people with aneurysmal subarachnoid haemorrhage. However, the trials were all done more than 10 years ago. New strategies may counteract the ischaemia-inducing potential of antifibrinolytic treatment and lead to improved outcome. A trial of combined antifibrinolytic and anti-ischaemia treatment is underway.

Antifibrinolytic Agents↗

PubMed2003

Spectrum of dysfunctional uterine bleeding and its conservative management.

OBJECTIVE: To find out the proportion of dysfunctional uterine bleeding (DUB) and the response of patients of DUB to medical treatment at Abbasi Shaheed Hospital. DESIGN: Cross sectional and comparative study. PLACE AND DURATION OF STUDY: The study was conducted in Gynaecology Unit II of Abbasi Shaheed Hospital, Karachi, from December 1999 to December 2000. PATIENTS AND METHODS: The study included 210 Gynae patients between the age group 13-50 years presenting with DUB. These patients were divided into adolescent, reproductive and perimenopausal group. They were initially assessed by general and pelvic examination, ultrasound of pelvis, Pap smear, hysteroscopy and diagnostic curettage. Results were recorded. The efficacy of treatment was assessed in terms of reduction in the amount of blood loss. RESULTS: Two hundred and ten out of 1300 patients were diagnosed as having DUB with the proportion of 16.1%. Response rate was 20 30 % with oral mafenamic acid, 50% with capsule tranexamic acid, 60% and 50% respectively with oral contraceptive pills containing ethinylestradiol and norethisterone, and norethisterone alone. The response rate with capsulated micronised flavonoid and derivative of ethinyltestosterone was 90% and 75% respectively. CONCLUSION: The patients in adolescent age group are good responders to conservative treatment. Most of the patients preferred micronised flavonoid over derivative of ethinyltestosterone for some misconceptions regarding this medicine. The former was better tolerated with less side effects.

Adolescent↗

PubMedDate not supplied

The inhibitory effect of DL-alpha-tocopheryl ferulate in lecithin on melanogenesis.

Oral vitamin E (alpha-tocopherol) supplementation has been reported to improve facial hyperpigmentation. The compound of alpha-tocopherol and ferulic acid, also an antioxidant connected with an ester bond, alpha-tocopheryl ferulate (alpha-TF) can absorb ultraviolet (UV) radiation and thus maintain tocopherol in a stable state. Our aim was to determine whether alpha-TF can be applied to improve and prevent facial hyperpigmentation induced by UV as a whitening agent as well as an antioxidant. In this study, the effects of alpha-TF on melanogenesis were examined using cultured human melanoma cells and normal human melanocytes in vitro. alpha-TF solubilized in 0.5% lecithin inhibited melanization significantly at the concentration of 30 micrograms/ml compared with arbutin (100 micrograms/ml), kojic acid (100 micrograms/ml), ascorbic acid (600 micrograms/ml), and tranexamic acid (600 micrograms/ml). alpha-TF had no effect on the protein amounts of tyrosinase, TRP (tyrosinase related protein)-1, and TRP-2 of human melanoma cells exposed to UV radiation, but inhibited tyrosine hydroxylase activity. alpha-TF neither directly inhibited tyrosinase activity of the large granule fraction extracted from melanoma cells, nor modulated glycosylation of tyrosinase. These results suggest that alpha-TF may be a candidate for whitening agent which suppresses melanogenesis, possibly by inhibiting tyrosine hydroxylase activity in an indirect manner. Further, alpha-TF decreased the amount of 8-hydroxydeoxyguanosine produced indirectly through active oxygen species (AOS) in guinea pig skin exposed to 2 times the minimal erythema dose of UVB radiation, but did not suppress the direct formation of cyclobutane pyrimidine dimers and (6-4) photoproducts. Thus alpha-TF may reduce AOS-induced DNA damage and thereby contribute at least in part to suppressing or retarding skin cancer development.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed1977

Bullous keratopathy (Fuchs' endothelial dystrophy) treated systemically with 4-trans-amino-cyclohexano-carboxylic acid.

Twenty patients with bullous keratopathy (Fuchs' endothelial dystrophy) were treated systemically with the antifibrinolytic drug tranexamic acid. The effect was evaluated by slit-lamp biomicroscopy, measurement of central corneal thickness and determination of visual acuity. The patients subjective complaints were also registered. The duration of the treatment varied from 3 to 16 months. In most cases the treatment was given over several periods with intervening free intervals. In all cases the central corneal thickness decreased and slit-lamp biomicroscopy revealed an improvement. The visual acuity improved and all patients became free of pain. A possible mechanism involving the complement system is discussed and preliminary studies on the composition of the aqueous humour in cases of bullous keratopathy are mentioned.

Aged↗

PubMed1981

Influence of omega-aminoacids on the activation of the first component of complement at low ionic strength.

Cl, is the first component of human complement, was activated to Cls by diluting human plasma in a solution of low ionic strength. The addition of lysine and its related aminoacids to plasma resulted in inhibition of Cl activation, alpha, omega-diaminoacids such as lysine and ornithine were most effective and omega-aminoacids such as 6 aminohexanoic acid were far less effective. Tranexamic acid which is most potent in inhibition of fibrinolysis among those aminoacids was least effective in the inhibition of Cl activation. omega-aminoacids or their analogues hardly inhibited Cls which had already been activated.

Amino Acids↗

PubMed1985

A bleeding disorder due to deficiency of alpha 2-antiplasmin.

The investigation of a 33 year old man with a lifelong bleeding tendency is described. Defective fibrinolysis was suspected in 1968, when clinical bleeding was corrected by administration of aminocaproic acid. The paper establishes the diagnosis as alpha 2-antiplasmin deficiency and describes its management with oral tranexamic acid.

Adult↗

PubMed1979

Complications of antifibrinolysis therapy after prostatectomy.

As part of a trial to compare the effectiveness of various agents which have been claimed to reduce blood loss after prostatectomy, tranexamic acid (AMCA) was given pre-operatively and post-operatively to 6 patients having routine transurethral resections. Three of these developed indissoluble intravesical blood clots which persisted until they were evacuated surgically 5 to 17 days after cessation of AMCA therapy. AMCA cannot be recommended for routine use after prostatectomy.

Cyclohexanecarboxylic Acids↗

PubMed2001

A new vascular sealant (Sealgel) to achieve rapid hemostasis after percutaneous angioplasty in anticoagulated patients: clinical feasibility and preliminary results.

The aim of this study was to assess the feasibility of a new vascular sealant (Sealgel) to provide rapid hemostasis in anticoagulated patients after percutaneous transluminal angioplasty (PTA). Sealgel was designed with ancrod (10 mg) and tranexamic acid (80 mg) dissolved in a hyaluronic acid gel (3 ml). Fifty anticoagulated patients (heparin, aspirin, ticlopidin) who underwent PTA of coronary artery were enrolled in the study. Sealgel (3 ml) was delivered under manual compression through a 9-F cannula at the arterial puncture site after the introducer sheath removal at the end of PTA procedure. Hemostasis time as well as complications were recorded. Sealgel was successfully delivered in 98 % of patients. Hemostasis occurred within 15 mn of manual compression in 82 % of patients, within 25 mn in 98 %, and failed in 1 patient (2 %). Hematoma (6-cm diameter) was observed in 1 patient and late bleeding in another one. There were no clinical signs of embolism, inflammatory swelling, local infection, vascular fistula, or pseudoaneurysm. No surgery or blood transfusion was required. Sealgel application after PTA in anticoagulated patient is feasible and secure. Preliminary results suggest that the Sealgel brought about rapid hemostasis; however further studies are needed to determine its clinical efficacy.

Aged↗

PubMed1989

Effect of plasmin inhibitors on gastric mucosal permeability in rats.

We examined the protective effect of plasmin inhibitors on gastric mucosal vascular permeability in rats. Tranexamic acid and aminocaproic acid significantly inhibited the increase in vascular permeability and macroscopic gastric mucosal lesions induced by 50% ethanol and 1% ammonia. The protective effect afforded by plasmin inhibitors was not affected by pretreatment with indomethacin. Our results show that plasmin inhibitors inhibit the increase in gastric vascular permeability and suggest that plasmin may play an important role in the pathogenesis of gastric mucosal damage.

Aminocaproates↗

PubMed1978

The use of antifibrinolytic drugs in aneurysmal subarachnoid hemorrhage.

Antifibrinolytic drugs have been investigated in a series of 58 patients with recent aneurysmal subarachnoid hemorrhage. It is concluded that tranexamic acid (AMCA) provides a rational method for reducing the frequency of recurrences, and that antifibrinolytic treatment is a preliminary to surgical intervention. In the present series, ischemic complications, which often follow aneurysmal hemmorrhage, seem to be of a more serious nature. There is evidence also that hydrocephalus due to adhesive arachnoiditis is a rare occurrence. The last 20 patients of the present series have been treated with very low doses of AMCA associated with parotid kallikrein inhibitor (Trasylol); this dosage has been effective in preventing recurrence and has appeared to be freer from severe side effects.

Adolescent↗

PubMed1982

The initial phase of the dextran-induced anaphylactoid reaction in the rat: a comparison of inhibitors of the blood pressure fall.

The histamine H2-receptor antagonist cimetidine (25-100 mg/kg) caused a partial inhibition of the pronounced blood pressure fall induced by dextran (Macrodex, 40-100 mg/kg) in the rat. The inhibition by cimetidine could not be distinguished from the inhibition achieved by the serotonin D-receptor antagonist bromolysergic acid diethylamide (BOL, 1-4 mg/kg). Doses of cimetidine and BOL that gave submaximum inhibitory effects separately, showed approximately additive effects when combined. The combined effect of these drugs never exceeded the maximum effects of the drugs separately, whereas injection of tranexamic acid (AMCHA, 100-300 mg/kg) together with cimetidine or BOL, increased the total inhibition. Previous works showed that dextran injected intravenously into rats reduced the level of plasminogen (PG) and plasminogen proactivator (pro-PGA) in plasma (Briseid et al. 1979; Berstad 1980a; Berstad & Briseid 1982). High doses of AMCHA (200 mg/kg) did not inhibit these effects, but significantly increased the lowering caused by dextran of the capacity of high molecular weight kininogen (HMWK) to function as a cofactor in the activation of factor XII. BOL (1-4 mg/kg, Berstad 1981) and cimetidine (50-100 mg/kg) also reduced the cofactor capacity of HMWK in the doses that were required to provide a manifest inhibition of the dextran-induced blood pressure fall. It is suggested that the early phase of the state of shock induced by dextran in the rat can be counteracted at different sites, correlated with histamine and serotonin receptors on the one hand, and with an effect antagonized by AMCHA, on the other. The lowest effective doses of cimetidine and BOL were rather high, suggesting a less specific mechanism for their effects than inhibition at selective receptor sites.

Anaphylaxis↗