Prolonged thrombin time probably no contraindication to kidney biopsy.
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Iopentol is a new non-ionic monomeric intravascular radiologic contrast medium which is undergoing clinical trials. Studies on other iodinated contrast media of various chemical structures, both closely similar to and widely different from iopentol, have shown that some in vitro tests of chemotoxicity correlate very well with clinical systemic toxicity. Some of these tests have been carried out on iopentol and are reported here. Comparison has been made in each case both with a conventional ionic contrast medium, sodium iothalamate, and with another well established medium of low toxicity already in use, iohexol. The results indicate that iopentol will have low clinical toxicity.
This study evaluates and discusses the potential utility (clinical value) of complementary coagulation tests performed in cases with a prolonged aPTT of no obvious etiology from a total of 85,500 routine coagulation tests carried out in our general hospital. aPTT was measured using Actin F.S.L. (Dade, plant-derived and rabbit phospholipids complex with ellagic acid as activator) and Diagen (Biotrol, rabbit phospholipids with kaolin). Tests for acquired anticoagulants and endogenous pathway factors (XII, XI, IX, VIII) were assayed if the aPTT was prolonged by 7 sec or more. 250 abnormal aPTT of previously unknown etiology were found over a 14 months period. 46% of them were without any obvious cause, and were considered "spontaneous" increases: 2/3 of these spontaneous increases were 7-9 (group A), and 1/3 were 10-19 (group B). The diagnoses found in group A were mostly deficits in the contact system, while group B contained mostly cases with acquired anticoagulants and deficits in the contact system. In group C (increases over 20"), an etiology could be established in all cases, with a predominance of acquired anticoagulants and some deficits in factors VIII and XII.
The effects of aspirin (75 mg orally/average-size cat) and propranolol (5 mg orally every 8 hours/average-size cat) alone and in combination on hemostatic determinants in healthy cats were studied. In cats, aspirin alone did not cause a significant effect in platelet numbers, plasma fibrinogen, activated partial thromboblastin time, prothrombin time, thrombin time, or platelet aggregation response to adenosine diphosphate. Aspirin did, however, significantly reduce the degree of aggregation induced by acid soluble collagen. Propranolol alone or in combination with aspirin did not cause a significant effect on platelet numbers, plasma fibrinogen, activated partial thromboblastin time, prothrombin time, thrombin time, or platelet aggregation in response to acid soluble collagen, adenosine diphosphate, or adrenaline. It was concluded that aspirin alone at the recommended dosage of one-quarter of a 5-grain tablet (1.25 grains or 75 mg) every other day will significantly affect platelet function and may be of value in the prevention of thromboembolic disease in the cat.
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In a multicentric study the influence of heparinase (Hepzyme) was evaluated on activated partial thromboplastin time, thrombin clotting time and prothrombin time using the recombinant human tissue factor and synthetic phospholipid (phosphatidylcholine and phosphatidyl-serine reagent). Hepzyme itself does not have any influence on normal coagulation values of activated partial thromboplastin time (aPTT) and prothrombin time (PT) assays whereas thrombin clotting time was prolonged by 10% (n = 60). In patients treated with unfractionated heparin for recent deep vein thrombosis (n = 47), plasma levels of aPTT, PT and thrombin clotting time (TCT) returned to the normal range in 100%, 97% and 91% after treatment with heparinase, respectively. Plasma samples of patients on coumarin were spiked with 2IU heparin/ml (n = 40) and were treated with heparinase. aPTT returned to baseline levels in 97.5%, PT in 99% and TCT in 69% of the samples. Plasma samples of patients receiving both heparin and coumarin were treated with heparinase (n = 18). aPTT and TCT values were shortened substantially and displayed the prolongation due to the effect of oral anticoagulants. PT values in these patients were also shortened. Freezing of plasma samples after treatment with heparinase resulted in a prolongation of the coagulation times in 15% of PT, 7% of aPTT and not of TCT values. The results show that treatment of plasma samples with heparinase abolishes the effect of unfractionated and low molecular weight heparin in vitro and ex vivo in patients during simultaneous treatment with oral anticoagulants. The use of heparinase may be of significance in patients with concomitant treatment of heparin and oral anticoagulants.
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