Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.6 (thromboplastin)
13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study of coagulation has been performed on 8 chronic renal failure patients receiving carbenicillin therapy. All showed a prolongation of the bleeding, recalcification, partially-activated thromboplastin, prothrombin and thrombin times. These findings suggest the presence of an anticoagulant with an heparin-like mode of action. In vitro tests suggest that carbenicillin may be this factor. We have also shown that the drug produces a disturbance in the normal polymerization process. The implications of these findings for the treatment of (CRF) patients with carbenicillin are discussed.
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PMID:Effects of carbenicillin on blood coagulation: a study in patients with chronic renal failure. 42 53

A pharmacokinetic study of intraperitoneal heparin was undertaken in eleven chronic renal failure patients as a guide for its therapeutic use in peritoneal dialysis. The intraperitoneal heparin was assayed as the activated-partial-thromboplastin time (A-PTT) of peritoneal aspirate or outflow dialyzate added to control plasma. This was noted to decay relatively slowly, the mean t 1/2 of heparin in the peritoneal cavity being 10.8 +/- 0.93 hr. The heparin cofactor antithrombin III determined by both immunological and functional methods was found to be present in low concentration in residual peritoneal fluid aspirated prior to commencing dialysis. Generally this was less than one-third of normal plasma values, and with the repeated dilution and outflow sequences of dialysis the cofactor concentrations rapidly fell to negligible levels that were incapable of activating any heparin present. Systemic blood coagulation was unaffected by single 10000 U doses of heparin administered intraperitoneally in that plasma A-PTT values were not lengthened when measured over the ensuing six hours.
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PMID:Activity of intraperitoneal heparin during peritoneal dialysis. 63 Jul 40

Over a period of 10 months hemodialyses in 20 patients with chronic renal failure were performed with a 40% lower heparin-dose. Blood coagulation was controlled from the activated partial thromboplastin time (APTT). There were no unfavourable side-effects, also the effectivity of the hemodialyses was not changed. However, we measured a significant increase in the hemoglobin-concentration and in the packed cell volume. Bleeding from the punctures was significantly shortened.
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PMID:[Heparin dosage in chronic hemodialysis (author's transl)]. 91 46

A 29-year-old women, who had been treated by hemodialysis for 5 years because of chronic renal failure, developed bleeding tendency in March 1989. Laboratory data showed prolonged activated partial thromboplastin time which was not corrected by addition of normal plasma; factor VIII activity was less than 1% and factor VIII inhibitor 70 Bethesda units/ml. The inhibitor was eluted in the second peak which corresponded to IgG when the plasma was subjected to Sephacryl S 200 column. The further purified IgG fraction by passing through protein A column showed a factor VIII inhibitor activity of 52 Bethesda units/ml. The factor VIII inhibitor epitopes were examined by western blotting technique using factor VIII purified by monoclonal antibody as the antigen. The factor VIII preparation used was composed of a doublet of light chain (Mr 80,000) and three heavy chains (Mr 160,000-200,000) when examined by immunoblotting using anti-factor VIII light and heavy chains monoclonal antibodies after SDS-PAGE. Factor VIII inhibitor that arose in a hemophilia A patient recognized the light chain, and the inhibitor in this case reacted to the heavy chain of factor VIII.
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PMID:[Characterization of the factor VIII inhibitor in a patient with chronic renal failure]. 170 30

A dose finding study of the very low molecular weight heparin CY222 (MW 2500) in patients (n = 8) with chronic renal failure undergoing dialysis has been carried out to (i) establish an effective dose and (ii) determine the relationship between ex vivo anti-factor Xa levels in plasma and the anticoagulant effect (in vivo suppression of FPA levels). Doses of CY222 were compared to a dose (5000 iu bolus + 1500 iu/hr) of unfractionated heparin (UFH) that has been shown to suppress FPA levels during prolonged (greater than 5 hr) dialysis (Ireland et al., J Lab Clin Med 103, 643, 1984). CY222 given iv in increasing doses produced a dose related increase in anti-factor Xa levels (measured as Institute Choay u/ml, with CY222 itself as standard) and suppression of FPA levels. When given in its highest dose, 20,000 Institute Choay u bolus + 1500 Institute Choay u/hr, there was little effect upon KCCT, FPA levels were statistically indistinguishable from those of the UFH regime (indicating comparable anticoagulant effect), but anti-factor Xa levels (expressed in Institute Choay u/ml) were 2-3 times those of UFH (expressed in iu/ml). All samples were also assayed for anti-factor Xa level against the proposed low MW Heparin Standard. Plasma levels of CY222 were then found to be 2.78 times lower, so that the anti-factor Xa levels of CY222 required to produce comparable anticoagulant effect were then indistinguishable from those of UFH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Low molecular weight heparin in haemodialysis for chronic renal failure: dose finding study of CY222. 283 24

There is uncertainty as to which activities of unfractionated heparin (UFH) and low MW heparin are responsible for their anticoagulant and antithrombotic properties. We have sought to answer this question by examining plasma samples taken during a recently conducted dose-finding study of the low MW heparin, CY222, in haemodialysis for chronic renal failure. In this study, in vivo anticoagulant effect was assessed by measurement of plasma FPA levels. UFH was administered as a dose of 5000 iu bolus + 1,500 iu/h maintenance infusion, while the effects of three doses of CY222 were studied (10,000, 15,000 and 20,000 Institute Choay anti-factor Xa u bolus, all with 1,500 Institute Choay anti-factor Xa u/h maintenance infusion). Anti-factor Xa levels were determined by chromogenic substrate assay. Anti-thrombin levels were determined by chromogenic substrate assay and by quantitation of catalysed thrombin-inhibitor complexes (using autoradiography). Analysis of the results indicate that plasma fibrinopeptide A (FPA) levels correlate with anti-factor Xa (r = -0.45) and anti-thrombin (substrate) (r = -0.63) levels of UFH, but only with the anti-factor Xa levels (r = -0.41) of CY222. These results suggest that the anti-factor Xa assay is currently the most suitable assay for monitoring low MW heparins such as CY222 in humans.
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PMID:Relationship between ex vivo anti-proteinase (factor Xa and thrombin) assays and in vivo anticoagulant effect of very low molecular weight heparin, CY222. 284 81

The disappearance of the anticoagulant activities of a standard commercial heparin and of a low molecular weight (LMW) heparin (PK 10169), administered as single intravenous injections, was studied in patients with chronic renal failure. Heparin and LMW heparin anticoagulant activities were determined by activated partial thromboplastin time (APTT) and chromogenic assays of anti-Xa and anti-IIa activities. Following heparin injection, a fast initial decay of anticoagulant activities preceded a slow convex disappearance curve, in semilogarithmic plots. These experimental data are in agreement with a model based on a predominant saturable mechanism of elimination of heparin in patients with renal failure. The disappearance of LMW heparin anti-Xa activity was obviously different, with linear or concave elimination curves, and longer apparent half-life. Taken together, our kinetic data and those previously reported in normal subjects strongly suggest that the mechanism of elimination of the LMW heparin studied is not saturable (at least for the tested dosages), and that the kidneys play a minimal role in the elimination.
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PMID:Pharmacokinetic studies of standard heparin and low molecular weight heparin in patients with chronic renal failure. 371 Feb 92

The heparinoid of natural origin Org 10172 has anti-factor Xa activity but minimal anti-thrombin activity, and little effect upon broad spectrum assays such as the KCCT in vitro. Its anticoagulant effects have been compared to those of commercial heparin in 7 patients undergoing haemodialysis for chronic renal failure. Commercial heparin was administered in a dose (5,000 iu bolus + 1,500 iu/hour continuous iv infusion) previously shown to inhibit fibrin formation during haemodialysis. This produced mean anti-factor Xa levels in plasma between 0.7-1.0 iu/ml and largely suppressed fibrin formation for 5 h dialysis measured as mean FPA levels in plasma. Administration of Org 10172 as a bolus of 1,350 anti-factor Xa u or 2,000-2,400 anti-factor Xa u produced plasma anti-factor Xa levels of less than 0.5 u/ml and allowed fibrin clot and FPA generation during dialysis. Org 10172 administered as a bolus dose of 4,000-4,800 anti-factor Xa u produced mean anti-factor Xa levels of greater than 0.5 u/ml, allowed dialysis of 6 patients for 5 h and appreciably suppressed FPA generation during dialysis, with little effect on the KCCT. It is concluded that the anti-factor Xa activity of Org 10172 may reflect its ability to inhibit fibrin during dialysis and that single bolus injection of Org 10172 may be a useful alternative method of achieving anticoagulation.
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PMID:The anticoagulant effect of heparinoid Org 10172 during haemodialysis: an objective assessment. 371 91

Anticoagulation during haemodialysis for chronic renal failure can be assessed by measurement of plasma fibrinopeptide A (FPA) levels as an objective method of monitoring the initial step in fibrin formation, in conjunction with visual inspection of the dialyser circuit for fibrin clot deposition. Employing this approach, unfractionated commercial heparin administered as an intravenous bolus followed by an intravenous maintenance dose (5,000 IU + 1,500 IU/h) was found to suppress almost completely fibrin formation and deposition during prolonged dialysis. Comparison of a low molecular weight heparin, Kabi 2165, revealed that it can inhibit fibrin formation in the extracorporeal circulation, that this property is largely reflected in its anti-factor Xa activity in plasma, and that a useful and effective dose of Kabi 2165 for haemodialysis may be 4,000 anti-factor Xa U intravenous bolus + 750 anti-factor Xa U/h intravenous maintenance infusion. This dose only minimally alters the KCCT and corresponds to approximately 60% of that of unfractionated heparin, which may be important in the long-term use of heparin in these patients.
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PMID:On the evaluation of heparin and low molecular weight heparin in haemodialysis for chronic renal failure. 374 34

The effects of sequential prostacyclin infusions at 2, 4, and 8 ng/kg/min for 1 hr were determined in six patients with chronic renal failure. Diastolic blood pressure decreased in a dose-dependent fashion from 74 +/- 4 mm Hg (mean +/- SEM) to 70 +/- 4, 66 +/- 5, and 55 +/- 5 during the 2, 4, and 8 ng/kg/min infusions, respectively; systolic blood pressure was not affected by prostacyclin. The fall in diastolic blood pressure was associated with a progressive rise in heart rate from 77 +/- 3 to 91 +/- 4 bpm and lowering of body temperature from 36.7 +/- 0.1 to 36 +/- 0.2 degrees. The threshold concentration of adenosine diphosphate that evoked reversible and irreversible platelet aggregation increased progressively from 1.2 to 2.8 and from 2.8 to 6 microM, respectively, during the prostacyclin infusions. Prostacyclin infusions had no effect on prothrombin time, activated partial thromboplastin time, or platelet count, but template bleeding time increased (not statistically significantly) from 5.8 to 12.3 min. In three of six patients, the 8 ng/kg/min infusion was terminated prematurely due to nausea, vomiting, and/or hypotension. We conclude that platelet aggregability can be inhibited in patients with chronic uremia by infusing 4 ng/kg/min prostacyclin without causing untoward side effects. When infused at hemodynamically tolerable doses, prostacyclin might serve as an in vivo inhibitor of platelet aggregation during hemodialysis or cardiopulmonary bypass.
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PMID:Effects of prostacyclin infusion in uremic patients: hematologic and hemodynamic responses. 701 91


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