Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AMINOCAPROIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 1,045 records · Page 58Linked to original sources
PubMed1981

Activated factor IX complex in treatment of surgical cases of hemophilia A with inhibitors.

Three patients with severe hemophilia A with inhibitors to factor VIII were treated with activated factor IX complex. Bleeding was controlled adequately during surgical procedures involving each of the three. Partial thromboplastin times showed a variable shortening and prothrombin times were significantly shortened to values less than normal. Hemostasis was substantiated by the use of epsilon aminocaproic acid. Neither anamnestic responses nor thrombotic complications were observed. A transient hypertension developed in two patients shortly after infusion with the activated factor IX complex.

Adult↗
PubMed1985

Fibrinolysis and acquired alpha-2 plasmin inhibitor deficiency in amyloidosis.

A patient with plasma cell myeloma and amyloidosis presented with a severe bleeding disorder. There was laboratory evidence of fibrinolysis and severe deficiency of alpha-2 plasmin inhibitor. Treatment with epsilon aminocaproic acid was associated with diminished bleeding and marked increase in the plasmin inhibitor level. This is the first report of acquired alpha-2 plasmin inhibitor deficiency in the fibrinolytic state associated with amyloidosis.

Aged↗
PubMed1988

Characterization of the interaction of human plasmin with its specific receptor on a group A streptococcus.

Certain Group A beta-hemolytic streptococci express a receptor that is capable of specifically binding the human plasma protease plasmin. Once bound, plasmin remains enzymatically active and is unregulated by its naturally occurring inhibitor alpha-2-antiplasmin (Lottenberg, R., C. C. Broder and M. D. P. Boyle, 1987. Infect. Immun. 55: 1914-1918). In this study certain characteristics of the interaction between plasmin and the receptor expressed on a group A beta-hemolytic streptococcus, strain 64/14, were examined. Binding occurred optimally at physiologic pH and ionic strength. The KD was 5 x 10(-11) M and there were approximately 800 receptors per bacterium. Mouse passage of strain 64 had no significant effect on the KD of the receptor. Binding of plasmin to the bacteria was inhibited by lysine and epsilon-aminocaproic acid in a concentration dependent manner. Similarly these amino acids would displace pre-bound plasmin from the bacteria. These findings suggest a role for plasmin's high affinity lysine binding site in the interaction of plasmin with the bacteria.

Aminocaproic Acid↗
PubMed1985

Lathyrism: mini-review and a comment on the lack of effect of protease inhibitors on osteolathyrism.

Lathyrism has been reviewed in respect to four overlapping phases: finding an animal model for neurolathyrism, characterizing osteolathyrism in respect to its possible use as an animal model for human diseases, such as Marfan's syndrome, idiopathic juvenile scoliosis, etc., use of beta-aminopropionitrile (BAPN) as a tool to study collagen, and use of BAPN as a therapeutic agent in man. Because it has been suggested that the lathyrogen, BAPN, may stimulate the release of proteases, the protease inhibitors Trasylol and epsilon-aminocaproic acid (EACA) were given alone or in combination to BAPN-treated rats. The protease inhibitors did not reduce the effects of BAPN as measured by exostosis formation or collagen extractability.

Aminocaproates↗
PubMed1977

Biological behavior of higher molecular weight products of fibrinolysis.

We have examined the consequence of infusions into rabbits of the products of limited plasmin hydrolysis of fibrin (early fibrin degradation products, or early fdp) containing defined quantities of fibrin fragment X. For comparison, early fibrinogen degradation products (early FDP) and late fibrin degradation products (late fdp) consisting almost exclusively of core fragments D and E were infused into separate groups of animals. Components of early fdp, probably fibrin fragment X, behaved in many respects like fibrin monomer. Infused unlabeled early fdp produced circulating soluble fibrin complexes with 125I-labeled fibrinogen. 125I-labeled early fdp rapidly accumulated in the spleen and liver and also to a significant degree in the lungs as insoluble, nonextractable tissue-bound protein; in contrast, only minimal quantities of early FDP and late fdp accumulated in organs. When 125I-labeled early fdp were administered to animals given continuous infusions of epsilon-aminocaproic acid to block fibrinolysis, substantial amounts of radioisotope also accumulated in the kidneys. These observations suggest a possible pathophysiological role for the products of lysing fibrin encountered in clinical states associated with disseminated intravascular coagulation.

Aminocaproic Acid↗
PubMed1988

Antifibrinolytic therapy in the management of the Kasabach Merritt syndrome.

The Kasabach Merritt syndrome consists of thrombocytopenia, microangiopathic hemolytic anemia, and a localized consumption coagulopathy that develops within the abnormal vascular channels of a hemangioma. In general, these patients demonstrate only mild abnormalities of screening clotting tests, but they can potentially develop life-threatening complications. We present a patient who developed a severe anemia that was refractory to erythrocyte transfusions. Treatment with epsilon-aminocaproic acid to inhibit fibrinolysis and cryoprecipitate to replenish his deficient circulating fibrinogen interrupted the cycle of his systemic coagulopathy and enabled us to transfuse him to a normal hematocrit.

Adult↗
PubMed1979

Biting activity by Aedes egypti mosquitoes in guinea-pigs. An experimental model for screening the effect of some systemically administered compounds.

The Aedes egypti mosquito fed consistently on guinea-pigs in a 2-hour period (n = 61), the mean percent feeding rate (+/- S.D.) being 88.84 +/- 9.32. Of a total of 34 different compounds systematally administered in guinea-pigs and tested for their effect on the mosquito biting rate using the above model, five: heparin, sodium fluoride, aminocaproic acid, thiourea and dithiocarb partially reduced the biting rate. The results are consistent with the view that certain aminoacids or proteins of blood or tissues serve as 'pheromones' attracting the mosquito to guinea-pigs.

Aedes↗
PubMed1985

Gross hematuria in a patient with sickle cell trait.

Sickle cell trait must be included in the differential diagnosis of hematuria in black patients. Therefore, diagnostic workup should include hemoglobin electrophoresis, urine culture, coagulation studies, intravenous pyelography, cystoscopy, renal ultrasonography, and renal arteriography. If the patient is found to have hemoglobin AS and no other abnormality, initial therapy consists of bed rest and intravenous fluids, with transfusion of red cells if needed. Intravenous epsilon-aminocaproic acid (EACA) has been used effectively to reverse hematuria in patients who do not respond to conservative management. In the case reported here, gross hematuria in a 24-year-old black woman resolved with use of EACA therapy.

Adult↗
PubMed1993

Factor VIII and DDAVP reverse the effect of recombinant desulphatohirudin (CGP 39393) on bleeding in the rat.

The infusion of a high dose of recombinant desulphatohirudin HVI (CGP 39393) for 40 min at 30 micrograms/kg/min, resulted in a prolongation of bleeding time in the rat when evaluated using transection of the tail. The prolonged bleeding was evident both immediately, and 30 min after cessation of the infusion of hirudin (CGP 39393). Bleeding time returned to normal after 60 min. The effect of several agents, reported to be successful in reducing bleeding tendencies in man, were evaluated in this rat model. The agents were administered immediately following cessation of the CGP 39393 infusion and their ability to normalize the prolonged bleeding-time, observed at 30 min after cessation of the CGP 39393 infusion, determined. Desmopressin (DDAVP), recombinant factor VIII and Vueffe reduced the bleeding time to the control range but did not exert any significant effects on the bleeding time in rats which did not receive CGP 39393. Epsilon-aminocaproic acid (EACA) and recombinant factor VII were ineffective, at the doses used. In conclusion, DDAVP, factor VIII and Vueffe are effective in reversing the effect of direct thrombin inhibition on bleeding in the rat.

Aminocaproic Acid↗
PubMed1984

Modulators of plasma fibronectin response during sepsis.

Plasma fibronectin (PFN) depletion has been associated with poor outcome in patients with sepsis or those who have experienced trauma; restoration of normal levels appears beneficial. PFN synthesis is increased after cecal ligation even in malnourished animals with sepsis, implying that stimulation of endogenous PFN synthesis is possible. One hundred rats received either a single therapeutic agent (gelatin, heparin, indomethacin, urokinase, captopril, or endotoxin) or the combination of a cecal ligation and a single agent (cimetidine, methylprednisolone, epsilon-aminocaproic acid (EACA), or transaminomethyl cyclohexane carboxylic acid. PFN levels were measured by enzyme-linked immunosorbent assay at 0, 24, and 48 hours. Only endotoxin alone caused significant PFN elevation at 24 to 48 hours (p less than 0.01); however, its multiplicity of effects precludes localization of regulatory pathways. Methylprednisolone results in an accelerated rise in PFN levels after operation (p less than 0.05), probably through an intracellular augmentation PFN synthesis. EACA attenuates the postoperative response while transaminomethyl cyclohexane carboxylic acid augments the PFN rise. This effect of EACA implies the existence of a proteolytic fragment capable of stimulating PFN synthesis. If a nontoxic factor can be identified, the use of exogenous PFN may be avoided.

Aminocaproic Acid↗
PubMedDate not supplied

Traumatic hyphema.

Multiple modalities of treatment for traumatic hyphema have been advocated in the past. Therapy should be directed at reducing the risk of secondary hemorrhage and the potentially devastating complications of corneal blood staining and optic atrophy. Therapeutic regimens proven successful include: a patch and shield to the traumatized eye; daily visual acuity and slit-lamp biomicroscopy, including intraocular pressure, evaluation of corneal clarity, and size of hyphema; topical atropine; the systemic administration of aminocaproic acid; and topical and systemic antiglaucomatous medications with elevated intraocular pressure. Surgical intervention should generally be avoided in hyphemas of less than 50%. In larger hyphemas, there are definite indications for surgical intervention. Preferred surgical methods include: irrigation and aspiration, and hyphema evacuation by vitrectomy instrumentation.

Aminocaproic Acid↗
PubMedDate not supplied

[2-stage microsurgical autoneuroplasty under pharmacologic effects (experimental research)].

It is shown in experiments on 36 dogs that two-stage microsurgical autoneuroplasty with subsequent administration of an inhibitor of proteolytic enzymes (aminocaproic acid), an antioxidant (tocopherol acetate) and heparin makes it possible to realize more fully the histoblastic potencies of tissues which are components of the injured nerve and the graft. This circumstance leads to the improvement of the morphofunctional results of sciatic nerve restoration after its experimental injury.

Aminocaproates↗
PubMed1988

Modification of cyclophosphamide-induced pulmonary toxicity in normal mice.

The effects of fractionated doses, in vivo thiol modulation, and antifibrinolytic therapy on the expression of lung damage induced by cyclophosphamide (Cy) were evaluated in C3H mice. The protein content of lung lavage samples taken 4 days after Cy treatment was used as an early indicator of damage. In fractionation studies, little difference in lung protein was observed when 200 mg of Cy/kg was administered as a single dose or as two or four equal doses given daily, suggesting that little sparing effect occurred with fractionated doses of Cy. In experiments that tested the effects of exogenous thiol administration, mice treated with WR-2721 before Cy were protected against lung damage, whereas the use of sodium thiosulfate or mesna did not give this protection. Treatment with epsilon-aminocaproic acid, which inhibits the breakdown of fibrin clots, did not result in enhanced Cy damage as measured by lung lavage or breathing rate; this suggests that the extended presence of fibrin per se did not contribute to Cy-induced pulmonary damage.

Aminocaproic Acid↗
PubMed1987

[Recurrent macroscopic hematuria and heterozygote drepanocytosis].

The sickle cell trait may result in recurrent macroscopic haematuria which can cause severe anaemia. Despite normal intravenous urography and CAT, the haemorrhage probably occurs in the renal medulla due to the operative physiopathogenic conditions. A proliferative mesangial glomerulonephritis with IgG, IgA, IgM and complement deposits, which has a controversial relationship with sickle cell disease, may be discovered by renal biopsy. The severity of the anaemia may necessitate treatment with epsilon-aminocaproic acid which cures the haematuria but may provoke rhabdomyolysis. This case report is followed by a review of the literature of the different types of renal involvement in sickle cell trait and sickle cell anemia.

Adult↗
PubMed1990

Plasma cross-linked fibrin degradation product (XLFbDP) assays in an in vivo model of fibrinolysis.

Assumptions regarding the elaboration of plasma cross-linked fibrin degradation products (XLFbDPs) in vivo were tested using an experimental model in which particulate human fibrin was infused into rabbits and the products of lysis monitored with an immunoassay utilizing DD-3B6/22, a monoclonal antibody to human cross-linked derivatives. XLFbDPs were generated following the infusion of a suspension of cross-linked fibrin, attaining a peak between 40 and 60 min, then falling at a rate approximating a plasma half-life of 2 h. The major in vivo products of lysis of cross-linked fibrin, identified by SDS-PAGE of immunoextracted plasma, were D-dimer and high-molecular-weight moieties. Peak levels of XLFbDPs achieved correlated with the amount of fibrin administered. Since XLFbDP levels were no higher when fibrin infusion was followed by infusions of streptokinase and human plasminogen, it is concluded that endogenous mechanisms of lysis were already maximally stimulated. Infusions of non-cross-linked (NXL) fibrin or of fibrinogen led to much smaller, but measurable, rises in XLFbDP. In the latter group, XLFbDP levels rose further following fibrinolytic therapy. Treatment with epsilon aminocaproic acid (EACA) caused partial (greater than 50%) inhibition of lysis while pre-treatment with nitrogen mustard, inducing leucopenia, virtually abolished the appearance of XLFbDPs in the circulation. This implies that fibrinolytic responses are substantially dependent upon cellular functions sensitive to nitrogen mustard.

Aminocaproic Acid↗
PubMedDate not supplied

Chronic angioedema. Three relevant cases.

Three cases of clinical angioedema are reported in which the etiopathogenetic involvement of qualitative and quantitative complement disorders was demonstrated. The first patient had a functional deficit in C1 inhibitor, the second had a decrease in CH50, and the third, a reduction in the C1q, C3, and C4 fractions. The cases are interesting because of occasional difficulties in the causal diagnosis, the severity of the symptoms, which can include laryngeal edema, and, finally, the favorable outcome achieved with correct medication, which did not include antihistamines or steroids. The clinical picture of hereditary angioedema is characterized by the familial occurrence of the process, although this apparently was absent in these cases. Two patients experienced laryngeal edema and none had abdominal manifestations. The treatment of choice for angioedema of these characteristics is antifibrinolytic agents, which achieve good results in 70% of the patients. Epsilon-aminocaproic acid and tranexamic acid inhibit the formation of plasmin and fragments of the Hageman factor, thus inhibiting kallikrein and bradykinin production. The androgens danazol and stanazolol have been used since the 1970s, and stanazolol proved to be very effective in two of our patients.

Adult↗
PubMed1992

Case report: successful use of antifibrinolytic therapy in acquired factor VIII deficiency.

Acquired factor VIII deficiency is a rare immunologic disorder characterized by severe bleeding due to an antibody inhibitor directed against factor VIII. Treatment of this coagulopathy often is ineffective and costly. The authors report a case of acquired factor VIII deficiency in a patient who developed severe recurrent epistaxis. Antifibrinolytic therapy with epsilon aminocaproic acid (EACA) was used to control the epistaxis with excellent results. To the authors' knowledge, this is the first report of the efficacy of EACA therapy in acquired factor VIII deficiency. Use of antifibrinolytic therapy may represent a relatively safe, effective, and inexpensive approach to treating factor VIII inhibitors.

Aged↗
PubMed1977

Reference values for fibrinogen concentration and inhibitors of fibrinolysis.

epsilon-Aminocaproic acid and tranexamic acid when added to whole blood will dissolve in the plasma and draw water from the cells in accordance with their concentration. When these compounds are added to whole blood in recommended amounts (10 mg/ml), the osmotic dilution of the plasma must be taken into consideration when concentrated solutions or dry substances are used.

Aminocaproic Acid↗