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B Tardy

Publications and source records attributed to B Tardy.

At least 73 records · Page 4Linked to original sources

Priming effect of adrenic acid (22:4(n-6)) on tissue factor activity expressed by thrombin-stimulated endothelial cells.

Tissue factor (TF) which initiates clotting process can be expressed by stimulated endothelial cells (EC). TF is an apolipoprotein requiring an association with phospholipids (PL) in order to become active. Also PL constitute an important storage pool of polyunsaturated fatty acids (PUFAs) in EC which can be modulated by diet or cell medium supplementation. In order to test the effect of such manipulation upon TF activity, we have pre-enriched human EC cultures with different fatty acids of nutritional interest. TF was evaluated after 4 h of thrombin stimulation by using a chromogenic method. Without additional stimulating agents, these acids have no effect on the basal level of TF. Eicosapentaenoic and docosapentaenoic acids appeared to be ineffective at the stimulated TF level. Only adrenic acid (22:4(n-6)) has been found to significantly enhance TF activity of thrombin-stimulated endothelial cells. Other TF inducers were also tested after 22:4(n-6) enrichment. An increase tendency of TF expression was found only with tumor necrosis factor, whereas interleukin-1 beta, lipopolysaccharide and especially phorbol myristate acetate stimulations were not significantly modified. The priming effect of adrenic acid on thrombin stimulated TF expression might involve alterations of signal transduction pathways rather than modifications of apolipoprotein III environment. Adrenic acid, which is a prostacyclin inhibitor, appears to be potential prothrombotic agent.

Cells, Cultured↗

Thrombotic thrombocytopenic purpura related to ticlopidine.

4 patients had typical features of thrombotic thrombocytopenic purpura (TTP) after 3 to 8 weeks of ticlopidine therapy. In 2 ticlopidine was the only medication taken before TTP; in another, rechallenge with drugs other than ticlopidine that the patient had been taking did not produce relapse. In all patients the delay between start of ticlopidine and TTP was in the same range as the latent period before ticlopidine-induced neutropenia. No relapse occurred in the 4 to 43 months of follow-up in the 3 surviving patients.

Aged↗

Intravenous prostacyclin in thrombotic thrombocytopenic purpura: case report and review of the literature.

The use of prostacyclin infusion in thrombotic thrombocytopenic purpura is consistent with the hypothesis that patients may lack a plasma factor stimulating prostacyclin production. However, prostacyclin therapy, alone or in combination with aspirin, dipyridamole, steroid and plasmapheresis, failed in many cases. We here describe the case of a patient who responded dramatically to a combination of prostacyclin and plasma infusions, after conventional therapy had failed (plasmapheresis, fresh frozen plasma infusions). Prostacyclin was infused intravenously initially for 120 h from 4 to 9 ng kg min-1 and then continuously for 48 h at 9 ng kg min-1. Despite the scarcity of case reports in the literature, we conclude that the failure of prostacyclin in thrombotic thrombocytopenic purpura appears to be related to insufficient doses and/or duration of therapy.

Adult↗

Circadian dynamics of coagulation and chronopathology of cardiovascular and cerebrovascular events. Future therapeutic implications for the treatment of these disorders?

Arterial thromboembolic disorders are the leading cause of death in most of the advanced nations. The study of epidemiologic relationship of these disorders to biological rhythms may lead to a better understanding and perhaps a better treatment. Chronoepidemiologic studies demonstrated a morning peak for arterial thromboembolic disorders (cerebral and myocardial infarctions) and sudden cardiac deaths. These variations might be explained partially by circadian variations in hemostasis. Indeed chronophysiologic studies have shown that hemostatic variables follow circadian rhythms. The level of platelet aggregation and that of blood coagulation have been found to be increased in the morning whereas fibrinolytic activity is lower at this time of the day. The facts suggest a chronotherapeutic approach in thromboembolic disorders.

Animals↗

[Current indications for inferior vena cava interruption].

Clinical indications of vena cava interruption are reviewed. During the last few years pulmonary embolism frequency remained high and many new percutaneous vena caval filters became available. These facts probably explain the increasing use of these filters reaching about 10,000 filters each year in France. Existing data show that: embolic risk with antithrombotic agents is less than 5%, probably not far greater than embolic risk with cava filters (about 2%); complications encountered with the filters are caval thrombosis in 8%, and more or less than 4% other major complications; there is no controlled study comparing antithrombotic treatment associated with caval filters to antithrombotic treatment alone; there is no controlled study comparing new cava filters among them or to the Greenfield filter; economical implications of caval filters are mostly unknown. The only admitted indications of vena cava interruption, in case of proximal venous thrombosis, are contraindications to anticoagulation. In other situations no data allow to recommend a cava filter; indication will be discussed on a case by case basis. Prospective controlled studies are greatly encouraged.

Heparin↗

[Venous catheterization and congenital abnormalities of the superior vena cava].

Persistent left superior vena cava is encountered in about 0.3 to 0.4% of human beings. It derives from remnants of the left cardinal vein system. This results in either a duplication of the superior vena cava or in a single left vena cava. The diagnosis is easy in case of associated cardiovascular anomalies. Two cases of single left vena cava and one case of duplication of the superior vena cava are described. All were identified owing to repeatedly aberrant courses of central venous catheters. Diagnosis was easily provided by angiography. Clinical course was uneventful. Despite its usual good tolerance, the persistence of a left vena cava, as an isolated anomaly, must not be neglected as it carries many practical implications which are reviewed.

Adult↗

Disseminated intravascular coagulation in Fusobacterium necrophorum septicemia.

A previously healthy 42-year-old man developed, after a neglected tonsillitis, a severe Fusobacterium necrophorum septicemia with disseminated intravascular coagulation. Peripheral, painful, cyanotic and gangrenous lesions appeared on toes, external ears and nose tip. The patient survived. Consumption coagulopathy associated with tonsillitis should suggest F. necrophorum infection. Growth of these bacteria in blood cultures is slow and confirmation of the infection may thus be delayed.

Adult↗

Early versus delayed introduction of oral vitamin K antagonists in combination with low-molecular-weight heparin in the treatment of deep vein thrombosis. a randomized clinical trial. The ANTENOX Study Group.

OBJECTIVE: To compare oral anticoagulant treatment (fluindione) started on either the 1st or the 10th day of a low-molecular-weight heparin (enoxaparin) treatment for deep vein thrombosis confirmed by venography. DESIGN: An open, multicenter, randomized study in two parallel treatment groups. INTERVENTIONS: All patients received enoxaparin, 1 mg/kg s.c. twice daily, and oral fluindione, 20 mg once daily, either beginning on day 1 or on day 10 of the enoxaparin treatment. Enoxaparin was discontinued once the international normalized ratio under fluindione was stable between 2.0 and 3.0 over 2 days. Fluindione treatment was maintained during a 3-month follow-up period. OUTCOME MEASUREMENTS: Specific examinations (venography and/or V/Q lung scanning and/or angiography) were performed only in the event of a clinically suspected recurrence of venous thromboembolism during the 3-month follow-up period. All cases were blindly assessed by an independent Reading Committee. RESULTS: A clinically suspected venous thromboembolism was confirmed by objective tests in 1 of 223 patients (group of delayed introduction of fluindione; n = 111). Equivalence was demonstrated between the two treatment schedules (p < 0.0001) for a maximal difference of 10% (90% confidence interval: -2.42 to 0.58). The mean duration of hospitalization was significantly reduced (p = 0.0001) in the group with early introduction of fluindione. The incidence of hemorrhage was comparable between the two treatment groups. CONCLUSION: Early and delayed introduction of oral anticoagulant treatment in association with subcutaneous enoxaparin in patients with deep vein thrombosis was shown to be equivalent in preventing the recurrence of venous thromboembolism. In patients with early introduction of oral anticoagulant, hospitalization was significantly reduced.

Administration, Oral↗

[Evaluation of the risk of venous thromboembolism in the medical patients].

The venous thromboembolic risk seems to be demonstrated in medical patients since the incidence of symptomatic and asymptomatic deep vein thrombosis (DVT) without any prophylactic methods is respectively about 50 per cent in stroke, 25 per cent in acute myocardial infarction (AMI) and 15 per cent in internal medicine. A synthesis of clinical trials performed in medical patients shows that prophylactic doses of heparins (unfractionated heparin or low molecular weight heparins) reduce the incidence of DVT by 40 to 60 per cent compared with the lack of any antithrombotic agents but without any significant effect on total mortality. Other antithrombotic agents such as antiplatelet agents seem to reduce the incidence of DVT by about 40 per cent associated with a significant decrease in total mortality of stroke or AMI. But the recommendations made on the basis of these results have to be extremely cautious since the number of medical patients included in clinical trials is quite limited compared with the surgical area. Moreover, each of these recommendations is not sufficiently proven. Thus more clinical trials have to be carried out with a placebo control group in internal medicine and an aspirin control group for stroke and AMI.

Anticoagulants↗