PubMed Health⌕ Search

Biomedical subjects

F Duckert

Publications and source records attributed to F Duckert.

At least 55 records · Page 3Linked to original sources
PubMed1984

Platelet aggregation, beta-thromboglobulin and platelet factor 4 in diabetes mellitus and in patients with vasculopathy.

We have studied 155 subjects, 48 normals, 36 diabetics without complications, 44 with complications and 27 patients with macroangiopathy. beta-Thromboglobulin (beta-TG) and platelet factor 4 (PF4) are elevated in the patients groups. There is no correlation between the plasma levels of beta-TG and the stages of either retinopathy or macroangiopathy or nephropathy. The difference is more marked between normals and diabetics with neuropathy (p = 0.026). The aggregation response to ADP and platelet activating factor (PAF) is enhanced at lower stimulator concentration. Using the beta-TG, PF4 and aggregation values the discriminant analysis allows a distinction of several subgroups especially with nephropathy and neuropathy (Table 6).

Blood Platelets↗
PubMed1984

Fibrinogen, factor VIII related antigen, antithrombin III and alpha 2-antiplasmin in peripheral arterial disease.

In 306 subjects, 217 without and 89 with peripheral arterial disease (PAD), VIIIR:Ag and alpha 2-antiplasmin are significantly higher in PAD (p less than 0.01). In the PAD negative group the ratio alpha 2-antiplasmin/antithrombin III activity is significantly higher 1.11 +/- 0.3 in the patients with an abnormal exercise ECG typical of coronary disease than in normal subjects 1.02 +/- 0.2 (p less than 0.05). In the PAD positive group antithrombin III concentration is higher in patients with a normal exercise ECG than in patients with abnormal exercise ECG (p less than 0.05). The same is true for alpha 2-antiplasmin but not for the antithrombin III activity. Fibrinogen and VIIIR:Ag are higher in patients with a previous myocardial infarction, however, the age is also significantly different as compared to the group without previous myocardial infarction. Disturbance of the cerebral arterial circulation is characterized by an elevation of VIIR:Ag and of alpha 2-antiplasmin as compared to the values obtained in patients without this complication. There is a general tendency towards higher alpha 2-antiplasmin values with the extension of the arterial disease.

Antigens↗
PubMed1984

Fifteen coagulation and fibrinolysis parameters in diabetes mellitus and in patients with vasculopathy.

Fifteen haemostasis parameters have been measured in 48 normal persons, 36 diabetic without and 44 with complications and 27 with peripheral arterial disease. Since the patient groups are older than normals, part of the differences are due to age. However, the differences are significant between normals and patients. They become highly significant for the diabetics with complications and nephropathy (Table 7). In diabetics without complications factor VIII functions, fibrinogen and thrombin time are related to age whereas there is a negative correlation for the fibrinolytic activity and antithrombin III. The diabetic complications shade off the correlations, which subsist only for VIIIR:CoF, VIIIR:Ag, ATIII and lysis before stasis. With Hbalc as dependent variable VIIIR:CoF is the only significant predictor variable in diabetics (Table 9).

Adult↗
PubMed1984

Heparin cofactor II determination--levels in normals and patients with hereditary antithrombin III deficiency and disseminated intravascular coagulation.

A technique is described to completely remove antithrombin III (AT) from small amounts of human plasma by immunoaffinity chromatography on antibodies against human AT linked to Sepharose 4B. The level of heparin cofactor II (HCII) was not affected by the immunoadsorption. HCII activity was then determined by measuring the rate of human thrombin inhibition by 3 ways: a) activation with heparin in AT-free plasma, b) activation with dermatan sulfate in normal plasma and c) activation with dermatan sulfate in AT-free plasma. The normal range of HCII varied between 0.7-1.5 U/ml, as compared to a normal plasma pool containing by definition 1 U/ml. Highly significant correlations between assays as obtained from 40 normal plasmas proved the suitability of the 3 assays, although the progressive thrombin inhibition by AT, when not removed, contributed about one fifth to the thrombin inhibition by HCII in the presence of dermatan sulfate. There were also highly significant correlations between HCII activity and antigen, as determined by rocket immunoelectrophoresis using specific antibodies against HCII. Levels of HCII and AT were examined in 7 patients with hereditary AT deficiency and 7 patients with disseminated intravascular coagulation (DIC). In hereditary AT deficiency, whereas the AT activity was reduced by half, levels of HCII activity and antigen were in the normal range. In DIC, a parallel decrease of HCII and AT suggests that HCII may participate in the inhibition of thrombin released during DIC and thus provides an inhibitor reserve, once the AT level becomes subnormally low.

Antigens↗
PubMed1984

[Criteria for hemostasis in kidney transplant patients. Comparison of patients undergoing immunosuppression with cyclosporin and azathioprine steroids].

Studies on one-year function conducted by the European Multicenter Trial showed that, after renal allograft transplantation, bleeding complications were only found in patients treated with cyclosporin as compared with those treated with azathioprin/steroids. To investigate a possible relationship between the bleeding tendency and the cyclosporin treatment, 18 parameters of hemostasis were studied in 11 patients, 6 of whom received cyclosporin A and the other 5 conventional treatment with azathioprin/steroids. Bleeding tendency could not be related to any specific coagulation parameter. Of interest is that clot retraction was significantly lower in the cyclosporin group (88 +/- 9% vs. 125 +/- 10%). Considering the fact that the skin bleeding time according to Ivy was normal in all patients, the clinical significance of the lower levels of the clot retraction appears to be minor. Discriminant analysis showed that these significantly lower clot retraction values could not be related to the lower platelet count levels in platelet rich plasma (205 000 +/- 85 000/mm3 vs. 280 000 +/- 67 000/mm3) but were associated with cyclosporin A treatment. All factor-VIII related activities were elevated in both groups. The main difference between the cyclosporin group and the conventionally treated group was significantly elevated levels of factor VIII procoagulant antigen (VIII: CAg) (cyclosporin A treated group: VIII: CAg 435 +/- 145%, conventionally treated group: VIII: CAg 215 +/- 99%). These results suggest hypercoagulability rather than bleeding tendency under cyclosporin treatment.

Adult↗
PubMed1984

Plasmin inhibitors and fibrinogen breakdown during the initial phase of thrombolytic treatment--the problem of the alpha 2-antiplasmin determination.

During the first 3 hr of thrombolytic treatment with porcine plasmin (p-PL) or streptokinase (SK) a rapid decrease of clottable fibrinogen with generation of large amounts of fibrin(-ogen) degradation products (FDP) are found. alpha 2-antiplasmin (alpha 2AP) is rapidly neutralized. Whereas in patients treated with SK more than half of the original plasminogen was consumed, its level remained unchanged during p-PL infusion. When alpha 2AP reaches values below some 20%, spontaneous amidolytic activity towards S-2251 representing either PL-alpha 2-macroglobulin- or SK-plasminogen-complex activity appears. This activity has to be considered in the alpha 2AP assay in order to avoid underestimation of this inhibitor.

Animals↗
PubMed1984

In vitro effects of the acylated streptokinase-plasminogen activator complex BRL 33 575 incubated with normal human plasma.

Thrombolysis with acylated streptokinase-plasminogen complexes is aimed to achieve fibrinolysis without systemic fibrinogenolysis. The p-aminobenzoyl-streptokinase-(Lys)-plasminogen-complex (BRL 33 575) should be particularly useful due to its slow deacylation rate. Unexpectedly, repeated doses of 10 mg of BRL 33 575 (corresponding to 310'000 streptokinase equivalent units) induced systemic effects in patients though less than streptokinase alone. In vitro incubation of normal human plasma with BRL 33 575 at concentrations used in patients resulted in nearly complete consumption of alpha 2-antiplasmin and plasminogen and significant fibrinogenolysis within 3 hr. This demonstrates that - despite of slow deacylation of BRL 33 575 - the small amounts of activator generated are highly efficacious in activating plasma plasminogen under conditions in which no physiological clearance of the free activator takes place. Simulating the calculated activator release from BRL 33 575 by infusing equivalent amounts of streptokinase into plasma resulted in less pronounced effects. This is probably explained by anti-streptokinase antibodies which will neutralize the initially infused streptokinase but will be bound by BRL 33 575. Our in vitro experiments indicate that further clinical studies should be done with lower doses of BRL 33 575 or prolonged dosage intervals.

Fibrinogen↗
PubMed1984

[A frequent problem in the laboratory control of heparinization: contamination of blood specimens with exogenous heparin].

If blood for monitoring of heparin therapy is collected through indwelling catheters it may be contaminated by exogenous heparin. A prospective study comparing thrombin times in plasma obtained by venipuncture and by collection through heparin perfused catheters showed that 26 out of 77 catheter samples were contaminated. In 16 of these 26 cases, overestimation of the heparin effect would have led to incorrect dosage recommendations. It is concluded that blood for laboratory monitoring of heparin treatment should be collected by venipuncture.

Blood Coagulation Tests↗
PubMed1984

Plasma prekallikrein, factor XII, antithrombin III, C1(-)-inhibitor and alpha 2-macroglobulin in critically ill patients with suspected disseminated intravascular coagulation (DIC).

In nine patients with suspected disseminated intravascular coagulation (DIC) and five controls, the following analyses were performed on admission and 7-29 hours later: Routine coagulation studies (fibrinogen, platelet count, fibrin(ogen) degradation products, ethanol gelation, reptilase time, Factor V) providing a semiquantitative DIC score, prekallikrein (PK), Factor XII, antithrombin III (AT-III), C1(-)-inhibitor and alpha 2-macroglobulin. Significant correlations were found: PK or AT III with the DIC-score, PK with AT-III and Factor XII, AT-III with Factor XII. The changes (expressed as a percentage of normal plasma) of PK and AT-III from the first to the second evaluation were nearly identical. The two patients with rapidly fatal irreversible shock showed the highest DIC score and a pronounced decrease of PK and AT-III, whereas in reversible shock stable or increasing PK and AT-III values were found. The other variables showed an overlap between reversible and irreversible shock. DIC in these shock patients, accompanied by a decrease in PK, probably was mediated via Factor XII activation. PK and AT-III might be of prognostic value in patients with (septic) shock.

Aged↗
PubMed1984

Factor VIII (procoagulant activity VIII:C, and antigen VIII:CAg, related antigen VIIIR:Ag and ristocetin cofactor VIIIR:Cof) in intensive care patients with clinically suspected disseminated intravascular coagulation (DIC).

VIII:C, VIII:CAg, VIIIR:Ag and VIIIR:Cof were determined repeatedly in nine shock patients with suspected DIC and in five patients with uncomplicated acute myocardial infarction and compared with the clinical course and the severity of DIC as reflected by a score based on six routine coagulation and fibrinolysis parameters. All shock patients showed high levels of VIIIR:Ag, VIIIR:Cof, and VIII:CAg, averaging fivefold to sixfold the normal level, of VIII:C averaging threefold the normal level. VIIIR:Cof and VIIIR:Ag significantly correlated in both groups of patients. In shock patients, VIII:C values were lower than VIII:CAg and varied between 40-90% of VIII:CAg. There were significant negative correlations between the DIC score on the one hand and ratios of VIII:C/VIIIR:Ag, VIII:C/VIII:CAg, and VIII:CAg/VIIIR:Ag on the other. The two patients who died from irreversible shock had the highest DIC score and lowest ratios of VIII:C/VIIIR:Ag and VIII:CAg/VIIIR:Ag as well as VIII:C/VIIIR:Cof and VIII:CAg/VIIIR:Cof. Released VIIIR:Ag multimers possess the ristocetin cofactor activity. In DIC, VIII:CAg is partially proteolyzed, however, less than VIII:C. The quotient VIII:C/VIIIR:Cof or VIII:C/VIIIR:Ag is a good indicator of the severity of DIC and may have important prognostic value.

Antigens↗
PubMed1983

Controlled multicenter pilot study of urokinase- heparin and streptokinase in deep vein thrombosis.

Thirty-three patients with acute iliofemoral thrombosis were randomly assigned to three treatment groups in a pilot dose-ranging study of thrombolytic therapy in deep vein thrombosis. One group received tissue culture urokinase in a dose of 2,200 I.U./kg/hr, and a second group in a dose of 1,100 I.U./kg/hr following a loading dose of 4,400 I.U./kg given in ten min. Urokinase was administered for 12 hr periods, alternating with 12 hr periods of heparin. A third group received an initial dose of 250,000 I.U. of streptokinase in 20 min, followed by 100,000 I.U./hr. Treatment of all patients continued for three days. At the end of this period little improvement, evaluated by "blinded" interpretation of pre- and post-treatment phlebograms, was found in five out of ten of the higher-dose urokinase patients, seven out of eleven of lower-dosage urokinase patients, and six out of ten of streptokinase patients. Optional treatment for another three days showed little further improvement of urokinase-patients and moderate further improvement in the streptokinase-patients. Neither of the 2 dosage schemes at intermittent application of urokinase appeared to be advantageous. Urokinase treated patients experienced fewer adverse reactions.

Adolescent↗
PubMed1983

The influence of dimethylbiguanide on phenprocoumon elimination and its mode of action. A drug interaction study.

This study was based on the clinical observation of a higher phenprocoumon requirement in these diabetic patients simultaneously treated with phenprocoumon (Marcoumar) and dimethylbiguanide (DMB), and of a drug interaction observed in a patient. These higher requirements of phenprocoumon, suggesting an increased elimination, could have been due to an enhancement of liver microsomal enzyme activity and/or an increase in liver blood flow. Various studies were performed to test this hypothesis. The clinically suggested higher phenprocoumon requirement was proven by a drug observation study. Hence a higher tablet consumption of phenprocoumon and a diminished anticoagulatory effect was found after treatment with DMB in doses of between 1 and 3 g. An increased elimination of phenprocoumon following DMB administration was also found in a pharmacokinetic study. The activity of the liver microsomal enzyme system, investigated in animal and man, showed no changes in the liver microsomal enzymes in animal studies or the in vivo parameters of liver microsomal enzyme activity in patients. Measuring liver blood flow in dogs, utilizing the indocyanine green clearance method, an increased flow of about 33% was observed. As changes in liver blood flow can increase the metabolism of some highly lipid soluble drugs, the increased metabolism of phenprocoumon during DMB treatment could be related to the increase in liver blood flow and not to changes in liver microsomal enzyme activity.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Hydroxycoumarins↗
PubMed1983

Dissociation of factor VIII procoagulant antigen VIII:CAg and factor VIII related antigen VIIIR:Ag by EDTA - influence of divalent cation on the binding of VIII:CAg and VIIIR:Ag.

Assuming 1 U/ml in citrated plasma, the VIII:CAg concentration was found 1.66 U/ml in EDTA-plasma, 1.09 U/ml in heparinized plasma and 0.67 U/ml in serum. Addition of 10 mmol/l EDTA to citrated and heparinized plasmas increased VIII:CAg 1.5fold. There was no increase of VIII:CAg in serum. Gel filtration of plasmas on different anticoagulants showed an elution of VIII:CAg in the void volume Vo and in the later fractions. The VIII:CAg amount detected in the internal volume increased following the series heparin less than citrate less than EDTA. Serum VIII:CAg was eluted at 2.2 Vo. Presence of EDTA in the elution buffer or incubation of plasma with EDTA prior to chromatography caused a displacement of practically all VIII:CAg amount in the internal volume with a peak at 2.2-2.3 Vo. VIIIR:Ag was exclusively detected in the void volume. Removal of divalent cation by chelation likely exposes more antigenic determinants of VIII:CAg, which are otherwise masked by steric hindrance due to VIIIR:Ag in citrated and heparinized milieu. Moreover gel filtration of plasma in the presence of EDTA completely dissociates VIII:CAg from VIIIR:Ag. The VIII:CAg fragment, having an estimated molecular weight of 70,000, might also be present in serum.

Anticoagulants↗
PubMed1983

Assay of Factor XII clotting activity in heparinized plasma.

Clotting tests based upon the activated partial thromboplastin time are disturbed by heparin. This brief communication shows that Factor XII clotting activity in plasma samples heparinized in vitro and in vivo can be measured accurately by means of an aPTT-test using congenitally deficient substrate plasma when the plasma dilution buffer contains hexadimethrine bromide (Polybrene), 15 mg/L. This method of neutralizing heparin obviates more complicated procedures such as heparin adsorption to anion exchange resins.

Blood Coagulation Tests↗
PubMed1982

Sequential treatment of arterial occlusions with porcine plasmin and low dose streptokinase.

Sequential treatment of arterial occlusions of the leg with porcine plasmin and low dose streptokinase results in a strong systemic proteolysis as already seen in deep leg vein thrombosis. In 31 of 45 patients the blood flow through major arterial segments could be restored. Thrombolytic success is possible within the first two treatment days but for the majority of the cases fibrinolytic therapy for 3-6 days is needed. On the average treatment was 1 day shorter than in DVT cases. No statistical relationship between local thrombolysis and systemic proteolysis was detected. The thrombolytic efficacy of this regimen compares favourably with earlier experience on fibrinolytic therapy in arterial occlusions.

Adult↗