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Biomedical subjects

K Andrassy

Publications and source records attributed to K Andrassy.

At least 181 records · Page 10Linked to original sources
PubMed1979

Isolation and renal localisation of urokinase.

Physico-chemical characteristics of urokinase in urine were studied by immunological and chemical methods. By agar zone electrophoresis, commercial urokinase preparations could be separated into an anodic and cathodic fraction. The latter reacted with urokinase antibodies with two precipitation bands. Band I displayed the major part of urokinase activity and migrated as a beta-globulin with a molecular weight of 32,000 daltons. Band II showed immunological identity with human serum, human albumin, alpha-2-macroglobulin and alpha-2-HS-glycoprotein. The specific activity of the cathodic fractions was up to 80,000 ploug units/mg protein. The ratio esterase/fibrinolytic activity did not change during the purification procedure. Further purification of the fractions with higher specific activity by affinity chromatography was unable to eliminate material cross reacting with human antisera (Band II). These findings permit the conclusion, that urokinase activity in urine is not confined to a homogeneous protein fraction. Activity is found both in a low molecular weight fraction and in a high molecular weight complex which contains serum proteins. These cannot be removed by exhaustive purification procedures and may play an important role in stabilizing and/or protecting urinary urokinase against proteolytic degradation. With Todd's technique diffuse fibrinolytic activity could be demonstrated in the kidney in the iuxtamedullary border region, (venae arcuatae, venae interlobulares, vasa recta) and in the epithelium of the calyces. Urokinase activity was specifically blocked by highly purified urokinase antibodies and could thus be distinguished from nonspecific proteolytic activity. The topographic relationship to medulla and uroepithelium may point to a role of urokinase in maintaining patency in slow flow systems.

Endopeptidases↗
PubMed1978

The effect of bezafibrate on the fibrinolytic enzyme system and the drug interaction with racemic phenprocoumon.

The influence of a new hypolipidaemic agent, bezafibrate, on anticoagulant requirements and fibrinolysis was studied in 15 patients with hyperlipidaemia on long-term treatment with racemic phenprocoumon. Our results suggest a dose-dependent augmentation of the anticoagulant response to the coumarin drug. Treatment with bezafibrate at 450 and 600 mg daily required a reduction of the phenprocoumon dose by 18.5 and 33.5%, respectively. Correspondingly, the serum level of phenprocoumon decreased by 11.6 and 35.3%. No evidence for an altered drug elimination of racemic phenprocoumon could be found during treatment with bezafibrate. The results support the hypothesis that bezafibrate and analogous hypolipidaemic drugs enhance the response to oral anticoagulant drugs by increasing the affinity of the receptor site for coumarins or the rate of degradation of the vitamin-K-dependent clotting factors. The investigation of the fibrinolytic enzyme system demonstrated an increase of the fibrinolytic activity by enhancing the activity of the plasminogen activator. The lysis time for euglobulin clot was reduced significantly, plasma fibrinogen only moderately. The antiplasmin activity could not be altered substantially by a decrease of alpha1-antitrypsin and a slight increase of alpha2-macroglobulin. In contrast with the inhibition of platelet function the effect of bezafibrate on the fibrinolytic enzyme system showed no dose dependence.

4-Hydroxycoumarins↗
PubMed1978

Antibody coating of urinary bacteria in transplanted patients.

24 patients with renal transplants were studied beyond the immediate postoperative period (greater than 8 weeks p.o.) for a period of 6 months in three weekly intervals. Quantitative bacteriology (dip slide method) and immunofluorescence microscopy (antibody coating of urinary bacteria) of the urine were regularly performed. Urinary tract infection was found in 13 of 24 patients, being permanent in 9 and episodic in 4 of the patients. There was no correlation between presence of urinary tract infection and deterioration of renal function. Mixed infection was found in 7 of the 13 patients and monoinfection in the others. In 7 out of these 13 patients, antibody coating of urinary bacteria could be demonstrated by immunofluorescence microscopy. In 3 of the 7 cases with antibody coating, this was permanently positive, in the other 4 it was intermittently positive. In only 1 case could conversion to positive antibody coating be attributed to urological complications (pyelostomy). Both IGG and IGA were demonstrable in 6 of 7 cases with positive antibody coating and IGG exclusively was demonstrable in 1 more case. IGM was questionably positive in 1 case and complement (beta1C) could not be demonstrated in any of the patients. This investigation shows that despite immunosuppression patients with renal transplants are able to mount an immune response against urinary tract infections.

Adolescent↗
PubMed1977

[Carbenicillin induced disturbance of platelet function: a study in patients with normal renal function (author's transl)].

After therapeutic doses of carbenicillin (3X10 g/24 h) prolongation of bleeding time, measured according to Ivy, was observed (median time prior to therapy 4 min 08 s-4 min 18 s; 24 h after therapy 15-20 min; 72 h after therapy greater than 30 min) in 5 patients with normal renal function and 2 patients with slight impairment of renal function (Ccr60-70 mlX1.73 m(2)). Prolongation of bleeding time was observed at serum concentrations between 13 and 180 microgram/carbenicillin/ml. After carbenicillin was withdrawn, prolongation of bleeding time was demonstrable for 4 days, i.v. even after the drug had been eliminated completely by urinary excretion. Higher doses of carbenicillin caused more severe disturbances of platelet function. The finding of prolonged bleeding time after carbenicillin may have clinical relevance (e.g. interaction with other anticoagulants, p.o. wound bleeding, gastro-intestinal hemorrhage, thrombopenia).

Adult↗
PubMed1977

Preparation (agar zone electrophoresis) and immunological characterisation of urokinase.

Urokinase was highly purified by electrophoretical and immunological methods starting with a commercial urokinase preparation (UK-Leo). Contaminating serum proteins and enzyme activities migrated into opposite directions in agar gel electrophoresis which proved to be a valuable preparative method. The final purification achieved was 80,000 Ploug units/mg protein. Traces of albumin, alpha2HS-glycoprotein and alpha2-macroglobulin migrated towards the cathode together with UK in a multimolecular complex. Urokinase antibodies (rabbit) gave with the cathodic fraction 2 precipitation lines (Ouchterlony technique): the one precipitation line corresponded to urokinase (molecular weight on gel chromatography 32,000 daltons), the other corresponded to UK complexed with serum proteins. Urokinase antibodies completely suppressed UK activity in various commercial preparations. All these preparations showed immunological identity; on disc electrophoresis pure urokinase (32,000 daltons, 80,000 Ploug units/mg protein) still gave 2--3 bands suggesting the presence of isoenzymes.

Antigen-Antibody Reactions↗
PubMed1977

[Oral anticoagulants and platelet function in hypolipemic therapy using a new clofibrate analog (BM 15.075) (author's transl)].

When testing the effect of a new clofibrate analogue (BM 15.075) on oral anticoagulation and blood clotting in 15 patients for over four weeks it was demonstrated that, depending on the dose of the drug, there was an increase in anticoagulation. The dose of phenprocoumon had to be reduced by 20.6 or 28.7%, respectively, when BM 15.075 was given at a dose of 450 or 600 mg. There was an inhibition of collagen-induced platelet-aggregation. In parallel there was an increase in bleeding time. Fibrinogen concentration was slightly but statistically not significantly decreased. Euglobulin lysis was shortened, especially if previously abnormally long. There was no direct influence on other plasmatic clotting factors.

Aged↗
PubMed1976

Penicillin-induced coagulation disorder.

A coagulation disorder was seen after penicillin-G administration (10 million units/day) in uraemic patients and after high-dose penicillin G (40 million units/day) in patients with a normal glomerular filtration-rate (5 patients after cardiac surgery). This disorder was characterised by: prolongation of bleeding-time, appearing immediately after penicillin-G administration and persisting until 4 days after withdrawal of therapy; disturbance of collagen-induced and ristocetin-induced platelet aggregation; increase of antithrombin-III activity; and inhibition of factor-xa activity. The inhibition of factor-xa activity corresponded to that seen after low-dose-heparin prophylaxis. The clinically latent coagulation disorder, when super-imposed upon pre-existing coagulation abnormalities (uraemia, treatment with anti-coagulants) may cause severe bleeding, as observed in 1 patient with acute renal failure on haemodialysis.

Abscess↗
PubMed1976

Bleeding in uremic patients after carbenicillin.

Hemorrhagic diathesis was observed in patients with renal insufficiency after carbenicillin at serum levels greater than 300 mug/ml. Normal coagulation factors (F. I, II, V, VII, VIII, X), normal PTT, normal platelet counts, negative ethanol gelation test (fibrin monomers) were found as well as a prolongation of thromboplastin time (Quick), thrombin time, reptilase time and thrombin coagulase time. Platelet function was disturbed. In addition, the plasmatic system was involved: inhibition of fibrinogen-fibrin conversion (Belitser assay) and enhanced antithrombin III activity; in vivo the latter was ascribed to a heparin-like activity. In vitro, abnormal III was seen: however an enhanced antithrombin III activity in vitro was not found with carbenicillin and various penicillin derivatives. This study demonstrates that carbenicillin, in addition to its known effect on platelet function, also disturbs the plasmatic coagulation system. This additional effect of carbenicillin is clinically important since protamin chloride effectively blocks bleeding without interfering with antibacterial activity. Both penicillin and penicillin derivatives have been shown to interfere with hemostasis and to cause clinically manifest hemorrhagic diathesis (Fleming and Fish 1947, Lurie et al. 1970a, b, McClure et al. 1970, Yudis et al. 1972, Demos 1971, Waisbren et al. 1971). Carbenicillin interferes with ADP-, collagen- or thrombin-induced platelet aggregation and with the release reaction both in vivo (McClure et al. 1970, Cazenae et al. 1973) and in vitro (McClure et al. 1970, Cazenave et al. 1973). In addition Lurie and colleagues (1970b) concluded that an inhibition of the conversion of fibrinogen to fibrin is involved although no experimental details were given. Later Brown and colleagues (1974) concluded that carbenicillin at usual dose levels "only affects the platelet component of hemostasis and has little effect on fibrin formation or other phases of coagulation in patients with normal renal function".

Adult↗
PubMed1976

[Longtime therapy of congenital factor XIII deficiency using factor XIII concentrate].

Factor XIII was determined by enzymatic and immunochemical methods in 3 patients with congenital factor XIII deficiency. Factor XIII activity measured by trans-glutaminase assay was below 1% of normal value in each of these cases. Immunelectrophoresis determination revealed the absence of the functionally active subunit A, whereas subunit S was only slightly diminished (30 to 50% of the normal value). Substitution with factor XIII concentrate caused a parallel increase of factor XIII activity and subunit A concentration. No uptake of factor XIII activity or of subunit. A by platelets could be demonstrated. Despite discontinuous substitution over a period of six years no antibody against factor XIII activity could be demonstrated in one patient with congenital factor XIII deficiency.

Antibodies↗
PubMed1976

Topography of human urokinase activity in renal tissue.

Frozen sections of human kidneys were studied with a modified technique after TODD [22] )fibrinogen slides). Urokinase activity could be demonstrated in the juxtamedullary region (venae arcuatae, venae interlobulares, vasa recta) and in the epithelium of the calyces. Urokinase activity was specifically blocked by highly purified urokinase antibodies.

Animals↗
PubMed1976

Sexual behaviour of hemodialyzed patients.

18 married men on home dialysis and 10 of their wives were interviewed (structured interview) to evaluate sexual adjustment. The frequency of intercourse prior to the onset of their disease was reported to be 3.4/week by the patients and 2.4/week by their wives. During maintenance hemodialysis, frequency was reported to be 1.7/week by the patients and 1.0/week by their wives. If libido prior to the disease was rated 100%, the patients reported their libido at the time of the interview as 66+/-34%; only 5 rated their libido as less than 50% of their libido prior to the onset of their disease. After the start of dialysis, considerable time was required before a stable state of sexual activity was reached (13.9+/-7.4 months), presumably reflecting the time required for adaptation to the procedure, loss of anxiety and restoration of physical well-being. Except in older patients, there was good agreement between the feeling of physical fitness as reported by the patients and sexual performance as reported by both the patient and his spouse.

Adult↗