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Biomedical subjects

J Conard

Publications and source records attributed to J Conard.

At least 145 records · Page 8Linked to original sources
PubMed1985

A multicenter study on amidolytic factor X evaluation in oral anticoagulant therapy.

For laboratory control of oral anticoagulation, amidolytic factor X (F X) determination may offer an alternative to standardization difficulties of prothrombin time (PT). In order to validate this amidolytic assay on a large scale, a multicenter study was undertaken in 6 French laboratories using the same chromogenic substrate (Stachrom X Stago) and different automated instruments. Intra and between laboratory reproducibility of factor X was estimated on fresh and lyophilized patients plasmas and was found to be highly satisfactory. Standardization of the method did not seem to depend on the chromogenic substrate used, as investigated in two different centers. Results of PT and factor X were compared in over 500 patients on a long-term stabilized oral anticoagulant treatment: there was a strong positive correlation between the 2 tests in each center. The therapeutic range for factor X was evaluated from therapeutic PT values reported by Duckert and Marbet for the different thromboplastin reagents: the estimated mean range was 21 to 32%. Pooling the results of the six different centers a concordant information for prothrombin time and factor X amidolytic assay was found in 76% of patients and a fully discordant response was present in 0.6%. The results suggest that amidolytic factor X may be suitable for monitoring long-term anticoagulation. However, prospective trials are needed to evaluate its usefulness as compared to conventional methods.

Administration, Oral↗
PubMed1984

Congenital protein C deficiency and thrombotic disease in nine French families.

Investigation of 118 patients for protein C deficiency using an immunological and a functional assay, and subsequent investigation of those (nine) found to be deficient, identified 22 patients (14 women, eight men) with protein C deficiency, of whom six were asymptomatic, 15 had histories of venous thromboembolism, and one had a history of arterial thromboembolism. Protein C deficiency was associated in the nine probands with young age at first episode of thromboembolic disease (mean 24.1 (SD 11.9) years), absence of a precipitating condition (five (56%], and a family history of thromboembolic disease (six (66%]. Investigation of the nine families suggested autosomal dominant transmission of the defect. Thromboembolic episodes were seen in patients with protein C antigen concentrations below 0.6 U/ml. Mean (SD) protein C antigen concentrations were 0.48 (0.12) U/ml in 18 patients not receiving oral anticoagulant treatment and 0.28 (0.05) U/ml in four receiving such treatment. One patient with severe protein C deficiency (0.16 U/ml) developed skin necrosis soon after starting oral anticoagulant treatment.

Adolescent↗
PubMed1984

Plasma beta-thromboglobulin in patients with valvular heart disease with or without valve replacement: relationship with thromboembolic accidents.

Plasma beta-thromboglobulin (BTG) was measured in 132 patients with valvular heart disease: 43 were studied before, 89 after surgery (78 mechanical valves and 11 bioprostheses). In this group of 89 selected patients, a history of thromboembolism was present in 53 (5 of them had bioprosthesis). Some abnormalities have been observed in patients with valvular heart disease as compared with controls: decreased platelet count and retention on glass column, and increased BTG. There is no statistically significant difference in BTG level between patients with (m +/- SD: 62.4 +/- 42.0 ng ml-1), or without (59.5 +/- 41.0 ng ml-1) a prosthesis; in the small series of 11 patients with a bioprosthesis, BTG was slightly lower than in other patients (44.5 +/- 14.1 ng ml-1), but still higher than in controls (26.8 +/- 13.3 ng ml-1). In the patients with a history of thromboembolism, BTG was significantly higher (66.7 +/- 47.9 ng ml-1 than in patients without this complication (49.9 +/- 21.0 ng ml-1). Thus, BTG evaluation may have some value in valvular heart disease but, at present, it should be confined to systematic research including prospective studies.

Adult↗
PubMed1984

Spontaneous platelet aggregation in heparin-treated patients.

To evaluate the influence of heparin on spontaneous platelet aggregation (SPA) two groups of patients, one treated with heparin and the other without heparin, were compared. The frequency of SPA is highly increased in patients with prosthetic heart valves treated with heparin as compared to patients not treated with heparin. Thus, the high frequency of SPA in prosthetic heart valve carriers treated with heparin might be due either to the prosthesis itself or to heparin. In contrast, in patients with thromboembolic disease, SPA does not seem to be more frequent in heparin-treated than in untreated patients.

Adult↗
PubMed1984

Studies of the pathophysiology of acquired von Willebrand's disease in seven patients with lymphoproliferative disorders or benign monoclonal gammopathies.

In seven patients with acquired von Willebrand's disease (AvWD) associated with lymphoproliferative disorders or benign monoclonal gammopathies, the platelet contents of von Willebrand factor antigen and ristocetin cofactor (vWF:Ag and vWF:RiCof, respectively) were normal. All the multimers of vWF:Ag could be seen in the 1.6% SDS-agarose gel electrophoresis patterns of plasma and platelet lysates. Infusion of 1-deamino-8-D-arginine vasopressin (DDAVP) augmented plasma levels of vWF:Ag and vWF:RiCof of all patients and corrected prolonged bleeding times (BT). However, compared with patients with congenital vWD type I and comparable degrees of baseline abnormalities treated in the same way, vWF:Ag and vWF:RiCof were increased less and cleared more rapidly from plasma and the BT remained normal for a shorter period of time. These studies provide evidence that these AvWD patients have qualitatively normal vWF in plasma, but at lower concentrations, that vWF in platelets is normal both qualitatively and quantitatively, and that cellular vWF can be rapidly released into plasma by DDAVP to correct the hemostatic abnormalities. However, vWF is removed rapidly from plasma, making the correction more transient than in congenital vWD type I.

Adult↗
PubMed1984

[Recurrent abortions and circulating anticoagulant. Relation to lupic disease: 6 cases].

Six women, aged 16 to 27 years old at the beginning of their illness suffered recurrent spontaneous abortion (two to eight episodes) and three of them had arteriolar venous thrombosis. These symptoms led to the finding of an antiprothrombinase type of circulating anticoagulant. In two cases, positive dissociated syphilitic serology was observed and all patients presented other haematological abnormalities: thrombocytopaenia and/or autoimmune haemolysis. The diagnosis of disseminated lupus erythematosis was established after an average period of 11 years (range 1 to 27 years) based on at least 4 of the ARA criteria (five out of six cases) and/or characteristic immunological abnormalities (five out of six cases). Thrombosis is more common in lupus when there are associated haematological abnormalities. It is probably directly related to the presence of circulating anticoagulant which inhibits the production and/or secretion of prostacyclin by the endothelial cells.

Abortion, Habitual↗
PubMed1984

[Biology of recurrent venous thrombosis].

Important recent advances in the field of the biology of recurrent venous thrombosis include greater understanding of congenital deficiency states involving antithrombin III (AT III) and protein C. Other disturbances demonstrated were related to fibrinolysis frequently, and rarely platelet function and coagulation factors. Possible existence of these anomalies requires investigation during biologic tests in cases of recurrent venous thrombosis, particularly in the presence of a family history or onset of the initial affection before 40 years of age. Confirmation of the importance of screening for such anomalies is supplied by results of a study of 11 families with antithrombin III deficiency and 9 families deficients in protein C, and a literature review of cases. However, currently available biologic tests provide data enabling only partial explanation of the mechanism underlying recurrent venous thrombosis accidents.

Antithrombin III Deficiency↗
PubMed1983

[Congenital dysfibrinogenemia. Apropos of 13 cases].

Approximately 100 families with congenital dysfibrinogenemia have already been reported in the literature. We have had the opportunity to study 13 affected families in France. The study of these dysfibrinogenemias has two purposes: 1) analysis of the relationships between the structural and functional abnormalities of the fibrinogen defect, since it appears that, in a significant percentage of dysfibrinogenemias, recurrent thrombosis has been observed. The diagnosis of dysfibrinogenemia is easily presumed in hemostasis laboratories since it rests upon prolonged thrombin and/or reptilase clotting times and the discrepancy between the fibrinogen levels obtained by an immunological method and a coagulation method. Many studies have been carried out during the last few years, and in at least seven cases the fibrinogen molecular defect has been elucidated.

Adolescent↗