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At least 253 records · Page 14Linked to original sources
PubMed1997

The use of low-dose aprotinin, epsilon-aminocaproic acid or tranexamic acid for prevention of mediastinal bleeding in patients receiving aspirin before coronary artery bypass operations.

Patients undergoing primary myocardial revascularization were randomized to one of three drug regimens (low-dose aprotinin, epsilon-aminocaproic Acid or tranexamic Acid) to determine which drug regimen would most effectively reduce post-operative bleeding and the need for blood products. All patients had received 325 mg of aspirin within 48 h before operation. All three drug regimens reduced the requirements for blood products and postoperative bleeding after coronary artery bypass operations. There was, however, no significant difference between drug regimens.

Aminocaproic Acid↗
PubMed2001

Comparison of epsilon aminocaproic acid and low-dose aprotinin in cardiopulmonary bypass: efficiency, safety and cost.

BACKGROUND: In this study we compared the clinical efficiency, safety, and economic benefit of low-dose aprotinin with epsilon aminocaproic acid (EACA) in reducing bleeding after cardiopulmonary bypass operation. METHODS: In a double-blind, randomized study, 100 patients received low-dose aprotinin (2 x 10(6) kallikrein inhibitor units) or EACA (20 g). The surgical procedure was single- or double-valve replacement with or without coronary artery bypass grafts. RESULTS: Mediastinal chest drainage and transfusion requirements with both therapies were similar. There were no urgent reoperations to secure hemostasis in either group. Similar levels of D-dimer with both therapies indicate a similar inhibition of fibrinolysis. Release of troponin I was less in the low-dose aprotinin group 1 and 4 hours after bypass, although electrocardiographic measurements did not reflect this difference. Levels of S-100beta and neuron-specific enolase were similar with both therapies, confirming that there was no difference in the occurrence of any adverse neurologic events in either group. CONCLUSIONS: Low-dose aprotinin and EACA showed similar effects on the reduction of intraoperative and postoperative bleeding. The lower cost of EACA with no change in safety outcome suggests it is the preferred treatment.

Aminocaproic Acid↗
PubMed2004

Treatment of acute intracerebral hemorrhage with epsilon-aminocaproic acid: a pilot study.

INTRODUCTION: Up to 40% of primary intracerebral hemorrhages (ICHs) expand within the first 24 hours (natural history). The authors aimed to study the safety and preliminary efficacy of epsilon-aminocaproic acid (EACA) in halting ICH enlargement. METHODS: Consecutive patients with hematoma volumes ranging from 5 to 80 mL were recruited within 12 hours of ICH onset. A total of 5 g EACA was infused during 1 hour and then 1 g/hour for 23 hours. Hematoma volume was compared on baseline, and 24-48-hour brain imaging. Consecutive untreated patients underwent the same imaging protocol. RESULTS: Three of the first five patients treated had HE>33% of their baseline volume. HE occurred in two of the nine untreated patients. The 80% confidence interval for HE in the treated patients was 32-88%. No thrombotic or other serious adverse events were attributed to EACA. CONCLUSION: It is unlikely that the rate of HE in patients given EACA within 12 hours of ICH is less than the natural history rate, although this treatment appears to be safe.

Acute Disease↗
PubMed1999

The effect of prophylactic epsilon-aminocaproic acid on bleeding, transfusions, platelet function, and fibrinolysis during coronary artery bypass grafting.

BACKGROUND: Antifibrinolytic medications administered before skin incision decrease bleeding after cardiac surgery. Numerous case reports indicate thrombus formation with administration of epsilon-aminocaproic acid (epsilon-ACA). The purpose of this study was to examine the efficacy of epsilon-ACA administered after heparinization but before cardiopulmonary bypass in reducing bleeding and transfusion requirements after primary coronary artery bypass surgery. METHODS: Seventy-four adult patients undergoing primary coronary artery bypass surgery were randomized to receive 125 mg/kg epsilon-ACA followed by an infusion of 12.5 mg x kg(-1) x h(-1) or an equivalent volume of saline. Coagulation studies, thromboelastography, and platelet aggregation tests were performed preoperatively, after bypass, and on the first postoperative day. Mediastinal drainage was recorded during the 24 h after surgery. Homologous blood transfusion triggers were predefined and transfusion amounts were recorded. RESULTS: One patient was excluded for surgical bleeding and five patients were excluded for transfusion against predefined criteria One patient died from a dysrhythmia 2 h postoperatively. Among the remaining 67, the epsilon-ACA group had less mediastinal blood loss during the 24 h after surgery, 529+/-241 ml versus 691+/-286 ml (mean +/- SD), P < 0.05, despite longer cardiopulmonary bypass times and lower platelet counts, P < 0.05. Platelet aggregation was reduced in both groups following cardiopulmonary bypass but did not differ between groups. Homologous blood transfusion was similar between both groups. CONCLUSIONS: Prophylactic administration of epsilon-ACA after heparinization but before cardiopulmonary bypass is of minimal benefit for reducing blood loss postoperatively in patients undergoing primary coronary artery bypass grafting.

Adult↗
PubMed1978

Quantitative determination of the binding of epsilon-aminocaproic acid to native plasminogen.

The binding of epsilon-amino[14C]caproic acid (6-aminohexanoic acid, EACA) to native human plasminogen was determined using the ultrafiltration technique of Paulus (Paulus, H. (1969) Anal. Biochem. 32, 91-100) at free ligand concentrations ranging from 2 micrometer to 16 mM. One strong binding site (Kd = 0.009 mM) and approximately five weaker ones (Kd = 5 mM) were found. The constants were obtained by fitting the experimental points to the simple assumption of two sets of noninteracting sites. The distinct separation of the two kinds of sites allowed the correlation of the well known epsilon-aminocaproic acid-induced conformational transition in plasminogen with the saturation of the weaker group of binding sites by this ligand. The conformational transition was monitored by measurements of the sedimentation coefficient, as was done by others earlier. The midpoint of the transition occurred at approximately 3.3 mM free ligand. A dissociation constant of 0.32 mM was also obtained for L-lysine by measurements of the competition between this compound and labeled epsilon-aminocaproic acid for the strong binding site. The correlation between epsilon-aminocaproic acid binding and effects of the compound on various physical and functional properties is discussed. A discussion of the possible sources of error encountered in the technique used is also included.

Aminocaproates↗
PubMed2004

Effects of epsilon-aminocaproic acid and aprotinin on leukocyte-platelet adhesion in patients undergoing cardiac surgery.

BACKGROUND: The administration of aprotinin during cardiopulmonary bypass (CPB) is hypothesized to decrease activation of leukocytes and platelets and possibly reduce their adhesion. Although epsilon-aminocaproic acid (EACA) shares the ability of aprotinin to inhibit excessive plasmin activity after CPB, its effect on leukocyte and platelet activation and leukocyte-platelet (heterotypic) adhesion is largely unknown. This study was performed to determine the relative effectiveness of the antifibrinolytics, aprotinin and EACA, at reducing leukocyte and platelet activation and leukocyte-platelet conjugate formation in patients undergoing CPB. METHODS: Thirty-six patients scheduled to undergo cardiac surgery with CPB were randomized in a double-blind fashion to receive EACA, aprotinin, or saline (placebo). Markers of plasmin activity (D-dimer concentrations), platelet activation (CD62P), leukocyte activation (CD11b), and leukocyte-platelet adhesion (monocyte- and neutrophil-platelet conjugates) were measured before, during, and after CPB. RESULTS: Platelet CD62P (P-selectin), monocyte CD11b, and monocyte-platelet conjugates were all significantly increased (compared with baseline) in the saline group during and after CPB. Despite equivalent reductions in D-dimer formation in patients receiving EACA (P < 0.0001) and aprotinin (P < 0.0001), decreases in platelet CD62P and monocyte CD11b expression were incomplete (not significantly different from saline control). In contrast, peak monocyte-platelet conjugate formation was significantly reduced by both EACA (P = 0.026) and aprotinin (P = 0.039) immediately after CPB. CONCLUSIONS: EACA seems to be as effective as aprotinin at reducing peak monocyte-platelet adhesion after CPB. Furthermore, inhibition of excessive plasmin activity seems to influence monocyte-platelet adhesion. The findings suggest that monocyte-platelet conjugate formation may be a useful marker of monocyte and platelet activation in this clinical setting.

Aged↗
PubMedDate not supplied

[Comparative effectiveness of epsilon-aminocaproic acid and contrical in preventing complement activation on immune complexes].

Experiments on formation of circulatory immune complexes followed by activation of the complement components were made on sensitized guinea-pigs after intravenous injection of human gamma-globulin as specific antigen. epsilon-Aminocaproic acid did not affect the formation of circulatory immune complexes but significantly inhibited complement activation. Contrykal did not alter the formation of the immune complexes but slightly inhibited activation of the complement components.

Aminocaproates↗
PubMed2003

Excessive fibrin after cataract surgery associated with aminocaproic acid use.

A 78-year-old woman developed a severe fibrinous anterior chamber reaction 1 day after uneventful clear corneal incision cataract extraction with intraocular lens implantation. There was no history of uveitis or diabetes, and the fibrin responded immediately to topical steroids. The patient was followed closely to rule out endophthalmitis. The only risk factor identified was the use of systemic aminocaproic acid as prophylaxis for bleeding in chronic leukemia.

Aged↗
PubMed1975

Aminocaproic acid and menstrual loss in women using intrauterine devices.

A controlled study of the effect of aminocaproic acid 3 g six-hourly taken by mouth during menstruation was carried out on 56 women for eight months from the time of insertion of a Lippes D intrauterine device (IUD). Thirty-five women presenting with menorrhagia in association with an IUD were also treated during three out of six consecutive menses. A highly significant reduction in menstrual loss was observed during treatment in both groups.

Aminocaproates↗
PubMed1998

A multicenter trial of 6-aminocaproic acid (Amicar) in the prevention of bleeding in infants on ECMO.

BACKGROUND/PURPOSE: Intracranial hemorrhage (ICH), is a major source of morbidity and the leading cause of death in neonates treated with extracorporeal membrane oxygenation (ECMO). Anecdotal reports have suggested that epsilon-aminocaproic acid (EACA) can decrease the risk of ICH. The purpose of this study was to evaluate, in a multiinstitutional, prospective, randomized, blinded fashion, the effect of EACA on the incidence of hemorrhagic complications in neonates receiving ECMO. METHODS: All neonates (except congenital diaphragmatic hernia) who met criteria for ECMO at three institutions were eligible for enrollment. EACA (100 mg/kg) or placebo was given at the time of cannulation followed by 25 mg/kg/h for 72 hours. Bleeding complications, transfusion requirements, and thrombotic complications were recorded. Post-ECMO imaging included head ultrasound scan computed tomography (CT) scan, and duplex ultrasound scan of the inferior vena cava and renal vessels. RESULTS: Twenty-nine neonates were enrolled (EACA, 13 and placebo, 16). Five (17.2%) patients had a significant (grade 3 or larger) ICH. There was no statistical difference in the incidence of significant ICH in patients who received EACA (23%) versus placebo (12.5%). Septic patients accounted for all of the ICH in the EACA group. Thrombotic complications (aortic thrombus and SVC syndrome) developed in two patients from the placebo group. There was no difference in thrombotic circuit complications between groups. CONCLUSIONS: Our results suggest that the use of EACA in neonates receiving ECMO is safe but may not decrease the overall incidence of hemorrhagic complications.

Aminocaproic Acid↗
PubMed2002

The effects of ultrafiltration on e-aminocaproic acid: an in vitro analysis.

Blood conservation strategies have become a standard of practice in cardiac surgery, with the use of antifibrinolytic agents and ultrafiltration two popular techniques. The purpose of this study was to evaluate the effects of continuous ultrafiltration on e-aminocaproic acid (EACA) utilizing functional coagulation analysis. A fibrinolytic assay was developed to detect EACA using the thromboelastograph (TEG) and urokinase (0.138 units 0.360 mL(-1)). Fresh bovine blood (23 +/- 1% hematocrit) was pumped (100 mL min(-1)) through an ultrafiltrator (HPH 400) at 37 degrees C with a transmembrane pressure of 280 mmHg. EACA (0.065 mg mL(-1)) was circulated for 10 minutes before initiating ultrafiltration. Samples (pre- and postultrafiltrator) were obtained at baseline, 5, and 10 min of ultrafiltration and analyzed via the fibrinolytic assay for EACA determination. TEG profiles significantly decreased from concentrations of 0.065 mg to 0.0325 mg of EACA mL(-1) blood (maximum amplitude MA, 75.4 +/- 4.0 versus 63.3 +/- 2.9, p < .05, TEG index 5.4 +/- 0.7 versus 4.0 +/- 0.3, p < .05). Fibrinolysis at 30 min increased as EACA concentrations declined (0.065 mg, 0% versus 0.032 mg, 16.4 +/- 2.8%, p < .05). During ultrafiltration the MA increased significantly from baseline to 10 min postultrafiltrator (68.2 +/- 3.0 versus 75.8 +/- 10.0, p < .05) and from 5 min pre- to 10 min postultrafiltrator (69.7 +/- 4.2 versus 75.8 +/- 10.0, p < .05). The TEG index showed no significant change, and no fibrinolysis was detected at 30 min from any datapoint during ultrafiltration. In conclusion, this study demonstrates that the antifibrinolytic properties of EACA are maintained during ultrafiltration with a 25% reduction in total circulating volume.

Aminocaproic Acid↗
PubMed2006

Effects of Tissucol and epsilon aminocaproic acid in the healing process following dental extraction in dehydrated rats.

A histological study was conducted of the alveolar bone healing process following tooth extraction of dehydrated rats after the implantation of fibrin adhesive (TISSUCOL) associated to previous irrigation of the wound with a 5% epsilon aminocaproic acid solution (EACA). Seventy two rats were used, divided into three groups receiving different treatments after the surgical procedure. In group I, the gingival mucosa was sutured after extraction of the right upper incisor. In groups II and III, chronic dehydration was produced by water deprivation for 9 days (3 days in the preoperative period and 6 days in the postoperative period). In the animals of Group II, after tooth extraction, the gingival mucosa was sutured in the same way as performed in group I. In group III, after extraction, the dental socket was irrigated with 5% EACA, followed by implantation of the fibrin adhesive (TISSUCOL). The mucosa was sutured in the same way as performed in the other groups. At 3, 7, 15 and 21 postoperative days, the animals were sacrificed in number of 6 for each group. Specimens containing the dental socket were removed and fixed in 10% formalin and decalcified in an equal part formic acid and sodium citrate solution. After routine processing, the specimens were embedded in paraffin for microtomy. We obtained 6 microm semi-serial slices that were stained with hematoxylin and eosin for histological evaluation. The results showed that the water deprivation in the pre- and postoperative periods caused a delay in the alveolar bone healing process. The use of the fibrin adhesive (TISSUCOL) produced an improvement in the fibrinolytic picture caused by dehydration.

Aminocaproic Acid↗
PubMed1996

Effect of antiproteolytic drugs: epsilon-aminocaproic acid (EACA) and aprotinin on experimental anti-GBM nephritis.

BACKGROUND: Given the evidence accrued by other authors on beneficial effect of protease inhibitors on experimental immune nephritis, and following our preliminary report on abrogation of immune glomerulopathy in the rat by antifibrinolytic and antiproteolytic drug, epsilon-aminocaproic acid (EACA), we investigated the effect of this drug on the rat autologous anti-GBM nephritis. Along with the EACA we evaluated another protease inhibitor, aprotinin, an antagonist of serine proteases. METHODS: EACA (0.3g/kg) or aprotinin (5000 kallkrein inhibition units, KIU/kg) was administered intraperitoneally (t.i.d.) from day 0 (preventive protocol) or day 3 (therapeutic protocol) of autologous anti-GBM nephritis induced in Wistar rats. Proteinuria, creatinine clearance and renal histopathology were assessed as markers of disease activity, while glomerular fibrin deposits (immunoperoxidase staining) and standard parameters of coagulation/fibrinolysis of peripheral blood enabled insight into local and systemic haemostatic mechanisms. Glomerular binding of anti-GBM antibodies (immunofluorescence) and serum titres of autologus nephrotoxic antibodies (haemagglutination assay) represented conditions of immune induction of glomerulopathy. RESULTS: Our experiments indicated that EACA, and to a lesser extent also aprotinin, are capable of preventing proteinuria (EACA, reduction by 57.6%; aprotinin, reduction by 26.8%, compared to untreated nephritic rats, day 3 post-induction) and glomerular histopathological changes, without affecting endogenous creatinine clearance, otherwise depressed in this model of glomerulonephritis. More importantly, both drugs significantly ameliorated glomerular lesions and proteinuria, even when the treatment was initiated on day 3 post-induction, after the injury has begun (EACA reduced proteinuria by 32.0%, and aprotinin reduced it by 20.9% day 7). Administration of EACA and aprotinin at doses reducing glomerular injury did not cause appreciable fibrin deposition in glomeruli of nephritic rats, nor did it modify parameters of systemic coagulation and fibrinolysis in these animals, EACA and aprotinin did not interfere with serum titres of nephrotoxic antibody, nor with the intensity of its binding to the glomerular basement membrane in vivo. CONCLUSIONS: Antiproteolytic drugs utilized in our studies exert their beneficial effect on autologous anti-GBM nephritis through interference with inflammatory phase of the disease, while sparing its immune induction and mechanisms of coagulation/fibrinolysis.

Aminocaproic Acid↗
PubMed2003

Analysis of 6-hydroxy-2-aminocaproic acid (HACA) as a specific marker of protein oxidation: the use of N(O,S)-ethoxycarbonyl trifluoroethyl ester derivatives and gas chromatography/mass spectrometry.

An alteration of low density lipoprotein (LDL) apolipoprotein (apo) B-100 structure by direct oxidative modification is an important mechanism involved in atherogenesis. There is difficulty in quantifying this type of modification because a lack of specific assays. The use of N(O,S)-ethoxycarbonyl trifluoroethyl amino acid esters for a rapid and sensitive determination of 6-hydroxy-2-aminocaproic acid (HACA), a highly specific marker of metal catalyzed protein oxidation, by using standard gas chromatography/electron impact mass spectrometry, is discussed. The derivatives are formed by the unlabored reaction of amino acids with ethylchloroformate plus trifluoroethanol plus pyridine. Femtomole levels of HACA can be reproducible measured in different LDL preparations subjected to oxidative damage in the presence of iron or copper. HACA determination compares well with the measurement of carbonyl groups that are generally accepted as a nonspecific index of protein oxidation. Thus, the method could prove to be a sensitive assay for studying specific apoB-100 modification.

Aminocaproates↗
PubMed2005

Aprotinin and epsilon aminocaproic acid are effective in reducing blood loss after primary total hip arthroplasty--a prospective randomized double-blind placebo-controlled study.

A prospective randomized double-blind placebo-controlled study was undertaken to determine the efficacy and mechanism of action of two antifibrinolytic drugs aprotinin and epsilon aminocaproic acid (EACA) in reducing blood loss in primary unilateral total hip arthroplasty (THA). Aprotinin was administered as a bolus of 2 x 10(6) kallikrein inhibitor units (KIU) followed by 0.5 x 10(6) KIU h(-1) for 3 h, EACA was given as 10 g over 30 min followed by 5 g over 3 h. The median postoperative blood loss 24 h postoperatively was reduced from 450 mL in the placebo group to 180 mL for aprotinin (60% reduction, P < 0.001) and to 210 mL for EACA (53% reduction, P < 0.01). In this population, there was no reduction in the perioperative transfusion requirements. The mechanism of both drugs was independent of platelets as indicated by flow cytometric measurement of change of their expression of P-selectin, platelet-monocyte aggregates, V/Va and CD40 ligand. There were no thrombotic or infective complications and no adverse events were attributable to use of either drug. Infusion of either aprotinin or EACA at the doses described is a safe and effective means of reducing blood loss after THA. These therapies provide a means of reducing blood loss in THA patients.

Aged↗
PubMed1986

Aminocaproic acid (AMICAR) in advanced colorectal carcinoma.

We treated 20 patients with measurable histologically confirmed colorectal adenocarcinoma with aminocaproic acid (AMICAR). There were 11 males and 9 females with a median age of 63 years. All 20 patients had received prior chemotherapy. The majority of monitoring lesions were distributed between lung and liver. We evaluated 12 patients in this series for response. Three patients had stable disease and nine patients had progressive disease. All patients were evaluable for toxic effects, the most common being nausea and vomiting. AMICAR given orally at 210 mg/kg of actual body weight/day is not an effective single agent in the treatment of metastatic colorectal carcinoma. In view of previously published animal data the role of AMICAR in the adjuvant setting for colorectal carcinoma still needs to be determined.

Adenocarcinoma↗
PubMed1985

A monoclonal antibody to the epsilon-aminocaproic acid binding site on the kringle 4 region of human plasminogen that accelerates the activation of Glu1-plasminogen by urokinase.

A monoclonal antibody, 10-F-1, previously shown [V. A. Ploplis, H. S. Cummings, and F. J. Castellino (1982) Biochemistry 21, 5891-5897] to interact with a particular epsilon-aminocaproic acid (EACA)3 binding site on the kringle 4 (K4) region of human Glu1-plasminogen (Glu1-Pg), has been employed to assess the contribution of this particular EACA site toward the enhancement, by EACA and its analogs, of the urokinase (UK)-catalyzed activation of Glu1-Pg. As is the case with EACA-like compounds, the presence of antibody 10-F-1 accelerates the activation of Glu1-Pg by UK, but does not enhance the similar activation of Lys77-plasminogen. In the presence of concentrations of antibody 10-F-1 which saturate its binding site on Glu1-Pg, the Km of Glu1-Pg activation by UK is raised from 1.4 +/- 0.2 microM, a value obtained in the absence of antibody, to 17.0 +/- 2.0 microM. On the other hand, the kcat for this activation, 0.038 +/- 0.005 s-1, is elevated to 2.45 +/- 0.2 s-1 at saturating concentrations of antibody 10-F-1. The kcat/Km for activation under these conditions is 0.027 s-1 microM-1 in the absence of antibody, and 0.144 s-1 microM-1 in the presence of saturating levels of antibody 10-F-1. This demonstrates that the interaction of this antibody with its epitope results in a fivefold stimulation of the activation rate of Glu1-Pg by UK. The availability of antibody 10-F-1 allows for a specific means of probing the function of one of the four to five thermodynamically equivalent weak EACA sites on human plasminogen. From this particular study, it is concluded that the weak binding site for EACA on the K4 domain of Glu1-Pg is either in-part or in-whole responsible for the enhancing effect of EACA on human Glu1-Pg activation by UK.

Aminocaproates↗