[The determination of heparin].
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Biomedical subjects
Publications and source records attributed to M Aiach.
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Sixty nine patients were treated with local intra-arterial urokinase (37,500 U/CTA. hr-1) for recent severe ischemia of lower limbs: 27 (40%) ultimately required amputation. The difference of amputation rate between the groups with and without thrombolysis was not significant (33% v. 42%). A biological study in 6 patients showed that local arterial plasminemia occurred in only 1 patient. Local urokinase does not strongly stimulate "endogenous" thrombolysis and enhances "exogenous" thrombolysis only very inconstantly. A better adaptation of urokinase dosage or the use of an agent with higher affinity for fibrin might improve the efficiency of local thrombolytic therapy.
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The use of heparin by continuous infusion from a electric pump gives very good immediate results in the treatment of venous thromboses. In 58 patients, there was a constant improvement in clinical signs and recurrence of the venous thrombosis was exceptional (2%), pulmonary embolism rare (3.5%) and well tolerated. Constant flow and the surveillance of treatment led to the method ensuring stable blood heparin levels. Mid-term results (8 months) in 43 patients appeared to be less favourable, the prevalence of venous sequelae reaching 50% for iliac phlebitis, 28% for sural phlebitis. The respective advantages and disadvantages of heparin and fibrinolytic agents are discussed.
Selective intra-arterial urokinase (UK) is effective in treating recent arterial thromboembolism. However, usually only partials lysis is achieved and this treatment seems less effective than intravenous streptokinase. At a dose of 37,500 UCTA/hour it does not produce systemic fibrinolysis. This protocol substantially reduces the risk of systemic bleeding and embolism and extends its applicability to operative patients. The combination of surgery and UK seems particularly promising in patients with atherosclerotic arterial thrombosis.
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Thrombosis of the visceral veins is an extremely rare condition in cases of congenital and hereditary deficiency of antithrombin III, associated with recurring venous thorbosis of the limbs. The authors report such a case in a man of 40 years of age, who had this deficiency, associated with thrombosis of the portal and superior mesenteric veins and a portal cavernoma. They stress the frequent association of recurring peripheral vein thrombosis, portal vein thrombosis in adults, and thrombosis of the mesenteric vein, and the importance of systematic measurements of antithrombin III levels in these pathological conditions.
Thrombolysis occurred in five out of eleven patients treated with intra-arterial urokinase for recent raterial obliteration. These positive results were accompanied by perfect tolerance and absence of systemic fibrinolysis. In some cases, therefore, surgical revascularization can be associated with fibrinolytic treatment.
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Systemic streptokinase has shown its effectiveness in the treatment of recent arterial obstruction of the limbs. The haemorrhagic and embolic complications of this type of treatment nevertheless limit its indications. Streptokinase should be reserved for acute thromboses present for less than two months, and responsible for severe ischaemia without the possibility of surgical treatment. The intra-arterial administration of urokinase limits the risks of systemic fibrinolysis, though the effectiveness of the therapeutic protocols proposed has yet to be demonstrated.
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The electrophoretic mobility of several forms of antithrombin III in an agarose gel has been compared with the mobility in a gel containing heparin. When a serum was studied, three different compounds were observed. The inactige antithrombin III with higher molecular size, separated by gel filtration, was found to be homogenous even if there was heparin in the gel. A purified antithrombin III, prepared by affinity chromatography, contained an immunoreactive material of higher molecular size which has no activity and a higher mobility in agarose gel. When heparin is incorporated in the agarose plate, the electrophoretic mobility of this polymerized antithrombin III is not modified.
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