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T H Tran

Publications and source records attributed to T H Tran.

At least 55 records · Page 3Linked to original sources
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

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

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↗
PubMed1981

Rabbit antibodies against the procoagulant activity (VIII:C) of human factor VIII. Some theoretical and practical considerations on the human factor VIII molecule using heterologous antibodies.

The procoagulant activity VIII:C was separated from factor VIII antigen (VIIIR:Ag) by gel filtration in the presence of 0.25 mol/l calcium chloride. Antibodies (anti-VIII:C) were obtained by immunization of rabbits with VIII:C. The last step of the purification procedure of antibodies consists of an adsorption on VIIIR:Ag-Sepharose 2 BCL as immunoadsorbent to remove contaminating traces of antibodies against VIIIR:Ag. The anti-VIII:C titer remains unchanged during this adsorption (29 Bethesda units per mg). In solution, anti-VIII:C neutralizes factor VIII activity (in plasma, cryoprecipitate or in purified form) and the fragment VIII:C without reacting with VIIIR:Ag. Once immobilized on a solid matrix, i.e. 2% agarose, it loses over 95% of its inhibitory capacity. The immobilized anti-VIIIR:Ag binds stoichiometrically the antigen and the activity of plasma factor VIII. These results together suggest that factor VIII is composed of 2 different entities, but undissociated under physiological conditions. Immunophysical analyses as a function of pH and temperature of anti-VIII:C and its complex with factor VIII show properties similar to those of homologous antibodies. The antigen determinants of VIII:C (VIII:CAg) are destroyed at low pHs or high temperatures, and VIII:C can no more form a complex with anti-VIII:C. Purified anti-VIII:C is also used in a two-stage assay to detect VIII:CAg or cross-reacting material in some severe haemophiliacs.

Animals↗
PubMed1980

Reactivity of a hereditary abnormal antithrombin III fraction in the inhibition of thrombin and factor Xa.

Two different AT-III fractions were purified from the plasma of a patient with recurrent superficial thrombophlebitis. The abnormal AT-III fraction (A-AT) was compared to the normal AT-III fraction (N-AT) in the inhibition of thrombin and factor Xa. Without heparin, both inactivate proteases in a similar manner and at the same rate. However, at low heparin concentration the thrombin inhibition proceeds more slowly with A-AT than with N-AT. At high heparin concentration the difference between A-AT and N-AT becomes very small. The inhibition of factor Xa follows a similar pattern. It is suggested that the heparin binding site of A-AT differs from that of N-AT resulting in a decreased heparin cofactor activity.

Antithrombin III↗
PubMed1979

[Dissociation of human factor VIII and recombination of the fragments VIII-C and VIII-AG].

Human factor VIII has been dissociated into fragment VIII-C and fragment VIII-AG in the presence of calcium chloride (0.25 M). After removing the calcium, recombination of the molecule is obtained. Fragment VIII-C can be activated by thrombin in a similar manner to the coagulant activity of whole factor VIII. This activation is calcium-dependent. In rabbits immunized against purified F VIII, VIII-C and VIII-AG specific antisera against these three entities were obtained.

Blood Coagulation Tests↗
PubMedDate not supplied

A randomized comparative study of artemisinine (qinghaosu) suppositories and oral quinine in acute falciparum malaria.

In adult patients with acute falciparum malaria in Ho Chi Minh City, Vietnam, a more rapid reduction in parasite count (50% clearance in 11.3 h) and complete clearance (41.8 h) was obtained in 32 adult patients randomly assigned to received artemisinine suppositories than was obtained with 30 patients receiving oral quinine (20.8 h and 68.1 h). There were higher degrees of resistance (RII, 3 cases; RI early, 1 case) with quinine than with artemisinine but in a subgroup of patients quinine reduced parasitaemia as rapidly as artemisinine (50% clearance 13.6 h and 10.1 h respectively). Recrudescence (RI, delayed), occurred in 16 patients receiving artemisinine compared with 6 receiving quinine. Artemisinine suppositories, because of ease of administration, efficacy, and lack of side effects or risk of overdose, have advantages for the early treatment of falciparum malaria by possibly reducing the morbidity and mortality associated with a high or sustained parasitaemia.

Acute Disease↗