Biomedical subjects
Publications and source records attributed to M Roncato.
Eight patients with heparin associated thrombocytopenia (HAT) were treated by a low molecular weight heparin derivative (LMW). Biological and clinical improvement occurred in all patients. This efficiency confirms the antithrombotic activity of LMW and allows its use in patients with HAT.
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Thirty-five patients hospitalized for recent angiographically documented arterial occlusion in the legs (27 femoropopliteal arteries and eight grafts) benefited from local fibrinolytic therapy delivered at the site of the occlusion with a 4- or 5-F catheter. This therapy combined a continuous urokinase (UK) infusion of 1,000 U/kg/hour and a lysyl plasminogen (LYS-PLG) infusion of 15 microkatals every 30 minutes. Angiographically confirmed lysis was obtained in 85% of the cases. Only 3% of the patients had major and 6% had minor groin hematomas. Only two patients had concentrations of fibrinogen as low as 100 mg/dl. Intravascular infusion of UK-LYS-PLG is as effective as streptokinase. Its excellent tolerance makes it a good alternative in the treatment of acute ischemia in the lower limbs.
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The authors report the case of a 26-year-old man with Von Recklinghausen neurofibromatosis and hereditary plasminogen deficiency. A hypothesis of a relationship in the inheritance of these abnormalities is discussed.
Thirty-five patients with peripheral arterial occlusions were treated by intraarterial infusion of low-dose urokinase associated with bolus of lys-plasminogen. Thrombolysis was achieved in 26 cases (74%), but only 10 patients (28.5%) experienced sustained improvement. Complications of thrombolysis occurred in 11 patients: Five patients developed groin hematoma, five had distal emboli, and one experienced macroscopic hematuria. Catheter-related thrombosis was observed in 14 patients (40%) despite intravenous heparin. Nine patients suffered from recurrent thrombosis and three from proximal emboli. A patient died from catheter-related infection. Limited fibrinolysis could increase pericatheter thrombosis, and further work will be necessary to assess the local risk of intraarterial thrombolysis.
Interaction of low molecular weight heparin (LMW-Hep) along with coagulation system is characterized through an increase of the proportion between activity anti-Xa and anticoagulation activity. In animals, their antithrombotic role can be compared with the heparin one. Longer life of the biological effect (close to 100 p. 100) enables to act subcutaneously as well as to reduce posology: only one injection is then required so as to prevent from post-operative thrombosis. There are neither method nor international standard to control preparations efficacy. At the moment, posologies are better to be expressed in mg. Trials are assessed in the treatments of thrombosis with results increasing therapeutic efficacy. Too high posologies did supply hemorrhagic syndromes in surgical patients. A biological survey is thus required. As usual tests, such as "time" of cephalin are slightly sensible to LMW-Hep, only anti-Xa activity can be used. LMW-Hep with a low anticoagulant action thus demonstrate a new concept of antithrombotic therapy.
Thirty patients with acute severe lower limb arterial obstruction were treated with local administration of low dose Urokinase associated with Lysyl Plasminogen. Fifty-three per cent primary and 40 p. 100 secondary successes were obtained with few complications but one death due to cerebral embolism related to the catheterisation procedure. This intra-arterial therapeutic association seems to be as effective as local streptokinase infusion, but it is much better tolerated than other forms of treatment. It could be the treatment of choice in acute occlusive arterial disease of the lower limbs providing the therapeutic indications are strictly respected.
Antithrombin III is a well-known coagulation inhibitor. Its heterozygous deficit is demonstrated through concentrations reduced about by 50 p. 100. On a clinical level, about 40 p. 100 to 70 p. 100 patients present with deep venous thrombosis (visceral on the whole) and pulmonary embolisms from puberty. There are both qualitative and quantitative deficits, these appearing to be mostly frequent. Only calculation of activity in the presence of heparin (co-factor of heparin) enables to diagnose these two types of deficits. Treatment performed includes both AT III concentrated agents and heparin in severe cases. Recurrences prevention is performed thanks to antivitamins K. If surgical treatment or delivery, a prevention of any incidents thanks to a vicarious therapy (AT III concentrated agent) is to be used.
An antithrombin III (AT III) functional defect (AT III Charleville) was discovered in a patient presenting with recurrent venous thrombosis. Both anti-activated factor X (anti Xa) and antithrombin activity were decreased, in the absence and in the presence of heparin, while protein concentration was normal in an immunological assay. The abnormal AT III copurified with functional AT III using insolubilized heparin affinity chromatography. Polyacrylamide gel electrophoresis (PAGE) and high pressure liquid chromatography (HPLC) on a TSK column suggest that AT III Charleville forms unstable complexes with thrombin from which a modified protein is rapidly released.
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The authors study the biological variations which accompany an oral, thrombolytic treatment in which urokinase and lysyl-plasminogen are combined. Fibrinogen, the products of degradation of fibrinogen or fibrin, plasminogen and rapid alpha 2 antiplasmin are studied as a function of time. Two dimensional electrophoreses were carried out at precisely determined times. The combination of the two therapeutic agents causes the appearance of plasmin in the circulation, but it is neutralised by its rapid inhibitor. This therapeutic protocol entails moderate circulating fibrinolysis and may easily be monitored by determination of the circulating fibrinogen.
35 patients with acute arterial occlusions [27] and graft thromboses [8], responsible for severe and recent ischemia, were treated by fibrinolytic therapy (Urokinase: 1 000 units/kg/hour, and Lys Plasminogen). These drugs were delivered at the site of occlusions using a 5 French catheter. Angiographically, initial success was obtained in 30 patients (85%) and a significant clinical benefit persisted 5 months later, in 20 patients (57%). 4 distal embolisms during the treatment were noted, and one woman died a few hours after the withdrawal of an axillary catheter of a cerebellar infarction. Only two minor (6%) and one severe (3%) groin hematoma were encountered. No patient had at any moment a fibrinogen concentration lower than 1 g/l. Thus, the thrombolytic treatment used in the study appears as effective as locally administered Streptokinase but better tolerated.
17 patients admitted to an intensive coronary care unit for premonitory syndrome or acute myocardial infarction were divided into four groups (premonitory syndrome, non-transmural infarction, transmural infarction with and without inflammation) on the basis of electrocardiographic findings and total CK activity. Serum levels of CK and CK2, myoglobin, ASAT and ALAT, LDH, haptoglobin, CRP and alpha-1 acid glycoprotein were determined daily for ten days. Patients with premonitory syndrome had no significant increase in markers of cytolysis or myoglobin. In acute myocardial infarction, regardless of clinical type, time course of peak values for biologic factors assayed was as follows: D0: myoglobin; D1: CK and CK2; D0 to D2: ASAT; D2 to D5: LDH and CRP; D5 to D6: ALAT; D4 to D7: haptoglobin and alpha-1 acid glycoprotein. These parameters may increase with size of myocardial necrosis and association with an inflammatory syndrome (CK, LDH, CRP and alpha-1 acid glycoprotein). They may be predictive of poor prognosis (LDH at peak CK concentrations). Some determinations, both more difficult to perform and less specific, have a particular value: prompt diagnosis of myocardial necrosis and detection of early repeat infarction by myoglobin assay, retrospective diagnosis by inflammatory protein assays when total CK has returned to normal.
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