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T Lecompte

Publications and source records attributed to T Lecompte.

At least 73 records · Page 4Linked to original sources
PubMed1997

Risk for venous thrombosis related to antiphospholipid antibodies in systemic lupus erythematosus--a meta-analysis.

OBJECTIVE: To describe the relative risk for venous thrombosis (VT) associated with antiphospholipid antibodies (aPL) in systemic lupus erythematosus (SLE). DESIGN: Systematic review and meta-analysis of 26 articles that examined the association between aPL and VT in SLE. SETTING: Mostly secondary and tertiary referral centres. PATIENTS: 2249 patients with SLE, 1120 tested for LA (lupus anticoagulant) and 1563 tested for aCL (anticardiolipin antibodies). MAIN OUTCOME MEASURES: A summary of study characteristics and a critical appraisal of study quality were done. Two statistical combinations of 18 primary studies that examined the association of VT and LA and of 14 studies that examined the association of VT and aCL were performed to estimate the risk for VT associated with aPL. RESULTS: The odds ratios of the risk of VT related to the LA summarized from 18 studies were 5.61 [95% CI; 3.80-8.27] overall, 6.32 [CI; 3.71-10.78] for deep venous thrombosis and pulmonary embolism, 11.6 [3.65-36.91] for recurrent venous thrombosis after the first event. The odds ratios of the risk of VT related to aCL summarized from 14 studies were 2.17 [95% CI; 1.51-3.11] overall, 2.50 [CI; 1.51-4.14] for deep venous thrombosis and pulmonary embolism, 3.91 [1.14-13.38] for recurrent venous thrombosis after the first event. CONCLUSIONS: Patients with SLE and LA are at approximately six times greater risk for VT than patients without LA, whereas patients with SLE and aCL are approximately two times greater risk for VT than patients without aCL. We have identified important methodologic limitations and differences in study characteristics. Other risk factors for VT have not been thoroughly evaluated in these studies. Further studies are needed that provide an accurate estimate of the absolute risk for aPL related VT.

Antibodies, Anticardiolipin↗
PubMed1997

[Reflections on external circulatory assistance. Apropos of 8 patients treated with the MEDOS system].

Mechanical circulatory support is required when cardiogenic shock is unresponsive to well conducted medical therapy. In this hemodynamic situation, when the patient's life is in danger, within hours, several questions should be answered quickly. These questions take into consideration the etiologies of cardiogenic shock and are related to the possibility of improvement of myocardial function, cardiac transplantation, the choice of uni- or biventricular support and surgical techniques of left ventricular assistance (left atrium to aorta or left ventricular apex to aorta). The follow-up of patients with circulatory support is complex. It requires to take into consideration hemodynamic, mechanical and hemobiological parameters as well as the peripheric organ function. We report in this article our clinical experience with eight patients that underwent circulatory support with Medos external ventricular assist device.

Heart-Assist Devices↗
PubMed1997

[Anti-streptokinase antibodies].

The use of thrombolytics has significantly improved the management of patients with acute myocardial infarction but available molecules remains imperfect: restoration of normal coronary patency in about half the cases, risks of reocclusion, risk of bleeding. Streptokinase (SK), which is the least expensive agent, has disadvantages as do the other thrombolytics. SK, an immunogenic bacterial protein, has another feature: administration of SK leads to an immunitory response with the production of specific anti-streptokinase antibodies. These anti-streptokinase antibodies may interfere with the future administration of a compound containing SK either by inducing an allergic response or by neutralising the SK and making it ineffective. Moreover, anti-streptokinase antibodies, the result of previous streptococcal infections, are present in the circulation. Although the prevalence of anti-streptokinase antibodies in the general population, especially coronary patients at risk of myocardial infarction, is not well known and their potentially harmful effects are even less well known. In particular, the platelet aggregant effect in vitro of these antibodies in the presence of SK was not taken into account in the trials studying the influence of anti-streptokinase antibodies in the results of thrombolysis by SK. The anti-lytic effect of anti-streptokinase antibodies is well documented. For this reason, it is not recommended to readminister SK in patients who have previously been thrombolysed with a product containing SK.

Antibodies, Bacterial↗
PubMed1996

Comparative assessment of phospholipid-binding antibodies indicates limited overlapping.

The implication of autoantibodies with anticoagulant and/or so-called antiphospholipid activities, under clinical circumstances with vascular obliteration, has led to the development of various types of tests allowing their detection. The most used tests involve investigation of the presence of an anticoagulant effect and of anticardiolipin IgG. It has also been proposed that the reactivity of patient samples toward other phospholipids or proteins be tested, but it remains difficult to appreciate which tests are redundant or complementary. Here we investigated whether the dissociation or association of anticoagulant and anticardiolipin correlated with specific ELISA reactivity to five other phospholipids: phosphatidylserine, phosphatidylinositol, phosphatidic acid, phosphatidylcholine, and phosphatidylethanolamine. The study was performed with 70 samples, evenly partitioned as positive for either anticardiolipin antibodies or anticoagulant effect, or both. Our data clearly confirm that cardiolipin reactivity is an individual entity, likely to be complementary to other assays. Neither anticardiolipin nor anticoagulant levels correlated with assays investigating antibody levels toward the five other phospholipids, although higher mean levels were noted when both lupus anticoagulant and anticardiolipin antibodies are present. Individual patterns were evidenced in all groups. These data support the interest of current and further studies exploring the clinical relevance of individual reactivities to phospholipids.

Adolescent↗
PubMed1996

[Role of the hemostasis laboratory in the etiologic approach to deep vein thrombosis].

Thrombophilia is characterized by an inherited or acquired defect in the blood coagulation pathway leading to an increased risk for thrombosis. The etiological approach following confirmed venous thrombotic events should rule out medical or chirurgical risk factors. Thrombophilia should be sought by laboratory tests. The recent discovery of a blood coagulation defect: inherited resistance to activated protein C which is found to 20% of patients with former thrombotic events has changed current laboratory approach. Deficiencies of one of the anticoagulant proteins (antithrombin III, protein C, protein S) are found in 10% of the patients, similar to the frequency of antiphospholipid antibodies. These tests may be difficult to interpret immediately after the thrombotic event because of various factors such as inflammatory states or anticoagulant treatments. Therefore this abnormal tests should be confirmed on a later sample analysis far from the event. The discovery of an inherited blood coagulation pathway defect may affect the duration of treatment, prophylaxis in situations with circumstantial risk factors and requires familial analysis. Inherited resistance to activated protein C may be associated with another inherited defect leading to an increased risk for thrombosis.

Antithrombin III Deficiency↗
PubMed1996

[Antiplatelet agents (inhibitors of platelet function) orally administered. Bases for their practical use in coronary artery disease].

Long-term antithrombotic therapy, administered orally, is necessary in all patients with symptomatic coronary artery disease; the most commonly used drugs are those which inhibit platelet aggregation. Aspirin and ticlopidine do not act on the same point of platelet function. They have the common property of inhibiting platelet function irreversibly and of partially inhibiting platelet aggregation. Flurbiprofenee acts like aspirin on thromboxane synthesis but the effect is reversible in 24 hours. The full effect of ticlopidine is only observed after several days' administration. The association of aspirin and ticlopidine is used over short periods after implantation of a stent. The dosage of ticlopidine is 2 tablets per day; that of aspirin is not well established (100 to 330 mg per day in a single dose). Special galenic forms are marketed for this indication in France. Biological monitoring (white cell count) is required with ticlopidine. It has not been shown to be of value to investigate the parameters of primary haemostasis (bleeding time, platelet function--tests of platelet aggregation). However, under certain circumstances, the advice of a haematologist may be useful, especially before an invasive procedure.

Administration, Oral↗
PubMed1996

[Uni- or biventricular circulatory assist devices. Selection criteria and patients' follow-up, choice of device].

Therapy of patients presenting with cardiogenic shock refractory to medical treatment can be undertaken with uni or biventricular circulatory assist devices. Pre implantation evaluation of patients is aimed at defining the etiology as well as the extent of uni versus biventricular heart failure, the possibility of recovery of myocardial function improvement of vital organ function and the possibility of cardiac transplantation. Circulatory assist devices must provide efficient support of the failing ventricles, allow recovery of myocardial function or cardiac transplantation under optimal circumstances. The choice of uni-biventricular support of total artificial heart is discussed as well as criteria useful in defining a therapeutic strategy.

Adult↗
PubMed1995

[Inducible cyclooxygenase. New relationships between non-steroidal anti-inflammatory agents and inhibition of synthesis of prostaglandins].

After a brief history of the main discoveries concerning the research on arachidonic acid and its biologically active derivatives, recent findings related to the identification of 2 isoenzymes of the prostaglandin-H synthase (PGHS) are reviewed. These isoenzymes play different roles within the body, since PGHS-1 is involved in homeostasis when PGHS-2 is mainly expressed during the inflammatory reaction. Non-steroidal anti-inflammatory drugs classically inhibit the biosynthesis of prostaglandins but this inhibitory effect depends on the considered isoenzyme. This discovery may have pharmacological and clinical impact but, at the present time, research is focused more on new pharmacological targets than on improving drug prescription.

Adrenal Cortex Hormones↗
PubMed1995

Hereditary thrombocytopenias in childhood.

Thrombocytopenia is generally known in its most severe form as acquired immunologic disease. However, in some cases thrombocytopenia is constitutional and may or may not be associated with thrombocytopathy. This review focuses on the clinical and biologic diagnostic criteria of genetic thrombocytopenia, with specific emphasis on the clinical value of the platelet life span and wishes to reiterate the necessity of their identification, as an excessively rapid diagnosis of ITP may be a source of treatment failure. As an example of constitutional thrombocytopenia, we report here 83 familial cases with pure genetic macrothrombocytopenia. They are characterized by the absence of significant bleeding disorders, stable thrombocyte counts higher than 50 x 10(9)/l, platelet macrocytosis, normal platelet function, normal or never increased presence of megakaryocytes, and rarely positive immunological abnormalities. In all cases, platelet life span clearly indicated a defect of production with destruction linked to the ageing population (more than 7 days) and no abnormal sequestration in the spleen or liver. Thus, apart from thrombocytopenia with thrombocytopathy, kinetic studies are necessary in thrombocytopenias whenever clinical parameters do not suggest the presence of excessive platelet destruction.

Blood Platelets↗
PubMed1995

Neutrophil degranulation related to the reperfusion of ischemic human heart during cardiopulmonary bypass.

Activation of polymorphonuclear neutrophils (PMNs) during cardiopulmonary bypass (CPB) is a wellknown phenomenon. This study aimed to determine if activated PMNs are sequestered and degranulated within the myocardium at reperfusion in patients undergoing coronary artery bypass grafting (CABG). Nineteen patients undergoing elective CABG were included in a prospective randomized study. Blood samples were obtained simultaneously from the radial artery (RA) and the coronary sinus (CS) at the following times: T0 (5 min after onset of CPB), T1 (2 min after aortic unclamping), and T2 (10 min after aortic unclamping). Neutrophil function was evaluated by PMN count and by elastase and lactoferrin concentrations. All patients survived. Neutrophils increased significantly from T0 to T1 and T2 in both RA and CS (p < 0.001 between T0 and T1 or T2). Pre-ischemia and reperfusion were associated with a significantly lower neutrophil count in CS compared with RA blood (p < 0.001), suggesting that PMNs were trapped within the myocardium at the onset of the CPB. Elastase and lactoferrin concentrations increased significantly from T0 to T1 and from T1 to T2 for each site, with greater concentrations (p < 0.001) in the CS compared with the RA, suggesting that activated neutrophils released their granular content into the plasma milieu only after reperfusion of the ischemic heart. This study establishes that neutrophil sequestration seems to be secondary to PMN activation by CPB but that the ischemia-reperfusion sequence induces specific degranulation of the PMNs trapped within the ischemic myocardium.

Adult↗
PubMed1995

Platelet phenotyping in carriers for Glanzmann's thrombasthenia: a simple screening test for assessment of the molecular defect.

Glanzmann's thrombasthenia (GT) is a recessive autosomal bleeding disorder characterized by the abnormality of aggregation due to a platelet glycoprotein (GP) IIb-IIIa deficiency or a dysfunctional complex. Molecular abnormalities have been localized on the gene coding for GP IIb or IIIa. The aim of our work was an attempt to obtain indirectly information on the putative localization of the molecular defect in patients with GT type I or II by the determination of the HPA-1 (GP IIIa) and HPA-3 (GP IIb) alloantigenic systems' expression in GT carriers. If GT results from a defective GP IIb gene, a GT carrier would appear homozygous for HPA-3 by serology, because the normal gene product will be expressed while the abnormal GP IIb gene product will not be present. Conversely, if the abnormality is in the GP IIIa gene, such an individual would appear homozygous for HPA-1. Therefore, the heterozygous status for HPA would result from the normal expression of the two genes for the considered alloantigenic system. Among the four families studied with informative members, our presumptions were strengthened by the preliminary genetic results in one family showing a mutation in the GP IIb gene. Thus, serology could be a simple screening test for the possible defective gene responsible for GT allowing molecular investigation focusing only on GP IIb or IIIa gene.

Antigens, Human Platelet↗
PubMed1995

[Effects of thrombolysis on platelets and coagulation].

Rupture of an atherosclerotic plaque is often the trigger of the clotting process, via the activation of platelets which immediately adhere, aggregate and initiate coagulation on their surface. The final step of platelet aggregation involves membrane glycoprotein IIB-IIIA which has become available. Antibodies directed against this membrane receptor are currently under evaluation. They possess definite antithrombotic properties. Complex interactions between thrombolysis, leading to generation of plasmin, and platelet functions have been identified. Depending on its concentration and possibly successively, and according to in vitro experimental conditions, plasmin may be a platelet proaggregant or antiaggregant. Correlations have also been recently demonstrated between thrombolytic activity and coagulation, as, paradoxically, it has been shown that plasmin, the final step of thrombolysis, activates the intrinsic pathway of coagulation, predisposing to the formation of thrombin. This activation is involved in the efficacy of heparin therapy following intravenous thrombolysis during the acute phase of myocardial infarction. This paradoxical action of thrombolysis could also play a role in reocclusions after effective thrombolysis during the acute phase of myocardial infarction. A better understanding of the thrombolysis process and its interactions with platelets and coagulation is important in order to improve the results of this treatment, which are correlated with patient survival.

Blood Coagulation↗
PubMed1995

Human anti-streptokinase antibodies induce platelet aggregation in an Fc receptor (CD32) dependent manner.

Exposure to streptokinase (SK) elicits anti-SK antibodies (Abs), which inhibit fibrinolysis and induce platelet aggregation. The mechanism of the latter is not fully understood, although it seems to involve platelet binding by a plasminogen streptokinase and anti-SK ternary complex. Anti-SK Abs were purified by affinity chromatography from serum of patients having received SK for acute myocardial infarction (AMI), and were shown to be of the IgG type. Their effects were studied with (i) human platelets in citrated plasma in the presence of SK or acetylated plasminogen-SK activator complex (APSAC), and (ii) in washed platelets, resuspended in Tyrode buffer after lowering the ionic strength, in the presence of APSAC (which provides both SK and plasminogen). An antibody concentration-response curve was obtained, showing a plateau in the presence of 0.1 mg/ml IgG. By increasing the concentration of APSAC, we obtained a unimodal response curve, the optimal concentration of APSAC being 0.05 U/ml. Aggregation was suppressed by chelating calcium with EDTA, blocking fibrinogen binding by the synthetic peptide Arg-Gly-Asp-Ser (RGDS), and raising intraplatelet cAMP with Iloprost (a prostacyclin analogue). Aggregation required the interaction of the anti-SK Ab Fc domain with the platelet Fc-gamma receptor type II, also known as CD32, since: (i) it was blocked by the monoclonal antibody IV-3 directed against CD32, (ii) it did not occur with F(ab)'2 fragments, which block the response to the intact IgG. The clinical relevance of these platelet-activating anti-SK antibodies remains to be determined.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1994

Myocardial neutrophil sequestration and activation related to the reperfusion of human heart during coronary artery surgery.

OBJECTIVE: The aim was to determine if neutrophils are activated and sequestered as they pass through postischaemic human myocardium. METHODS: The occurrence of neutrophil activation during the reperfusion of the ischaemic myocardium was investigated in 16 selected patients undergoing coronary artery bypass surgery. Neutrophils were counted and elastase and lactoferrin released into the plasma were measured simultaneously in myocardial venous blood and in peripheral venous blood, before aortic cross clamping (T0), and two (T1), 10 (T2), and 20 (T3) min after unclamping. RESULTS: At T0, no statistically significant difference was noted between peripheral and myocardial blood with respect to the three variables studied. Reperfusion was associated with a significantly lower neutrophil count in myocardial blood compared to peripheral blood (p < 0.001), suggesting that neutrophils were trapped within the myocardium during reperfusion. In addition, levels of elastase (T1, T2, and T3), and lactoferrin (T1) were significantly higher in myocardial blood as compared to peripheral blood (p < 0.001), suggesting that activated neutrophils released their granular content into the plasma milieu. CONCLUSION: We provide evidence consistent with local neutrophil activation during myocardial reperfusion in patients undergoing coronary artery bypass surgery, in addition to the well described systemic activation related to cardiopulmonary bypass.

Adult↗
PubMed1994

Heparin-induced thrombocytopenia: a survey of tests employed and attitudes in haematology laboratories. Groupe d'Etude sur l'Hémostase et la Thrombose (GEHT) de la Société Française d'Hématologie.

A survey was carried out of the attitudes adopted in French laboratories with regard to the diagnosis of heparin-induced thrombocytopenia (HIT). The platelet aggregation assay is used in 100% of laboratories, aggregation being measured by light transmission in an aggregometer (3/4). Blood is drawn either in emergency (1/4) or after heparin discontinuation (1/4). The nature of the samples for testing is a fresh citrated plasma (100%) although frozen plasma is occasionally employed, while 40% of laboratories use less than 3 control platelet donors. Platelet response is verified in the presence of a non immune agonist (18%) or an immune challenge (known positive plasma or platelet activating monoclonal antibody) (13%). Heparin is of the same type as received by the patient and is tested at two or more concentrations of approximately 0.5 and 1.0 IU/ml, but rarely at high concentration (100 IU/ml). The platelet count is adjusted to 250-350 x 10(9)/l (18%), the ratio of patient plasma to PRP is 1:1 (59%), the time of observation is about 20 min (50%) and control platelets are tested with heparin to rule out any false positive results (9/10). Standardization is nevertheless required if the platelet aggregation assay is to be considered as a reference test.

Artifacts↗