Haematologica 2004;89: supplement no. 8 - Supplements ...

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XVIII Congress of the Italian Society for Hemostasis and Thrombosis Research, Rome, Sept. 30-Oct. 3, 200459CO-076THE PROTHROMBIN G20210A MUTATION ATTENUATES THEANTICOAGULANT BUT NOT THE FIBRINOLYTIC ACTIVITY OFACTIVATED PROTEIN CBinetti BM,* Asti D,° Tripodi A,° Semeraro N,*Colucci M**Dipartimento di Scienze Biomediche, Sezione diPatologia Generale, Università di Bari, °Centro diEmofilia e Trombosi A. Bianchi Bonomi, Dipartimentodi Medicina Interna, Università di Milano, ItalyHyperprothrombinemia associated with the prothrombingene mutation G20210A is a common riskfactor for thrombosis and has been reported to causeAPC resistance. The inhibition of thrombin formationby APC, however, not only limits fibrin formation butalso stimulates fibrinolysis by reducing TAFI (thrombinactivatable fibrinolysis inhibitor) activation. Weevaluated the influence of prothrombin G20210Amutation on the anticoagulant and fibrinolytic activitiesof APC. Thirty-two heterozygous carriers and 32non carriers were studied. APC anticoagulant activitywas assessed by aPTT prolongation whereas APCfibrinolytic activity was determined by a microplateclot lysis assay. APC-induced aPTT prolongation wasmarkedly less pronounced in carriers than in non carriers,resulting in APC sensitivity ratios of 2.11±0.41and 3.15±1.37, respectively (p
60Oral Communicationswith G20210A allele and 5G/5G polimorphism ofgene PAI-I (OR= 2.3, C.I. 0.87-6, p=0.09). Our resultsshow that 4G/4G genotype is a mild independent riskfactor for VTE but it may be of clinical impact whenassociated with prothrombin mutation. Moreover,we found the lack of interaction between G1691Amutation and 4G/5G polymorphism. Factor V Leiden,as independent risk, play alone a crucial role in determiningthrombotic events. On the other hand, themechanism by which the G20210A mutation canlead to a thrombotic event is still not well understood.Probably, it needs the concomitantly presenceof an hypofibrinolytic state, induced by 4G allele, toconfer patients an higher thrombotic risk. In conclusionwe think that, to stratify the patient risk forVTE, the 4G/5G polymorphism of the gene PAI-1could to be searched in patients carrying the prothrombinmutation but it is not necessary when thefactor V Leiden is present, since the 4G/5G polymorphismof the gene PAI-1 does not significantly affectthe risk in patients carrying the G1691A mutation.Oral CommunicationsANTICOAGULANT THERAPY:CLINICAL & LABORATORY PROBLEMSCO-078EVALUATION OF BLEEDING RISK FROM THE ASSOCIATION OFANTIAGGREGANTS AND ORAL ANTICOAGULANTSFrigerio L,° Frigerio G,* Bianchi M,* Beretta A*°Centro Sorveglianza Anticoagulati,*DivisioneMedicina I, Ospedale Valduce, Como, ItalyThe association of antiaggregants and anticoagulantshas always been a difficult therapeutic choicebecause of the possibility of increasing the risk ofhemorrhage in the patients. The aim of our studywas to evaluate the incidence of major and minorbleeding events in patients treated with both thesetypes of drugs. We selected 80 patients (58 males –73%, 22 females – 27%), aged between 30 and 90yr old (mean 71, median 73), who were attendingour anticoagulant clinic. All the patients were beingtreated with oral anticoagulants and contemporaneouslywith antiaggregants. A computer programwas used to calculate the total days of therapy andthe number of days that anticoagulation was withinthe therapeutic range for each patient. A total of36881 days (corresponding to 101 yr) of treatmentwere considered; of these about 66% were passedwith the patient in the correct therapeutic range.During the follow up 6 adverse events occurred (4males and 2 females): 1 death because of cancer(1.3%, unrelated event), 1 AMI (1.3%) and 4 eventsrelated to the therapy (95% CI :0.014-0.123 – in 3patients with ischemic heart disease and in 1 patientwith peripheral arterial disease, of which 2 majorbleeding events (2.5%- severe hematoma followedby death and a sudden death) and 2 minor bleedingevents (2.5%, hematoma and epistaxis), equivalentto 4.0% of events per patient per year. The INR waswithin the therapeutic range at the time of the hemorrhagicevent. The doses of antiaggregant were: ASA160 mg for AMI event; 100 and 300 mg for the twominor bleeding events; ASA 50 mg or ticlopidine inthe two major events. Although this is a limitedseries, our results suggest that in the context of continuosand punctual monitoring of anticoagulanttherapy, the association of antiaggregants with anticoagulantsdoes not seem to lead to an increasedrisk of bleeding.haematologica vol. 89(suppl. n. 8):september 2004
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haematologicaThe origin and power o
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XVIII Congress of the Italian Socie
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XVIII Congress of the Italian Socie
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2Educational Sessionssurgery. In av
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4Educational Sessionsclinical relev
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6Educational SessionsTREATMENT OF S
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114Postersprostanoide intravenously
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124Posters§Department of Nephrolog
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126PostersPostersWOMEN'S HEALTH ISS
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128Postersexcess of the anticoagula
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130PostersC (APC- Resistance). The
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132Postersgene substitution may be
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134Postersof LMWH or OA for the tre
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136Postersthe increased DVT risk as
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138Postersinternal jugular vein thr
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140PostersPostersANTIPLATELET THERA
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