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217 results on '"Ternisien C"'

1. Cross‐reactivity of human anti‐FVIII antibodies to porcine rFVIII: French field study to validate the modified Nijmegen method.

Author

Le Cam Duchez, V., Ternisien, C., Guery, E. A., Eschwège, V., Jeanpierre, E., Nougier, C., Proulle, V., Stepanian, A., Tuffigo, M., Marlu, R., and Pouplard, C.

Subjects
*CROSS reactions (Immunology), *HEALTH facilities, *IMMUNOGLOBULINS, *FIELD research, *BLOOD coagulation factor VIII antibodies
Abstract

This document is a letter to the editor discussing a French field study on the cross-reactivity of human anti-FVIII antibodies to porcine rFVIII. The study aimed to validate the modified Nijmegen method used in French laboratories for the titration of anti-porcine FVIII inhibitors. The study compared the stability of rpFVIII in different dilution media and assessed the cross-reactivity of plasma samples from patients with AHA and congenital hemophilia A with inhibitors. The results showed a decrease in rpFVIII activity after incubation, but no statistical difference between dilution media. The study provides valuable information for the laboratory assessment of rpFVIII in the treatment of AHA. Another study discussed in the letter found that cross-reactivity with rpFVIII was detected in 26% of AHA samples and 75% of PWA samples, but high cross-reactivity above 20 BU/mL was rare and not observed in the AHA population. The study confirmed the feasibility of using imidazole buffer to detect anti-rpFVIII antibodies. [Extracted from the article]

Published
2024
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2. OC 60.5 Response to Desmopressin in Type 2N Von Willebrand’s Disease: A Genotype-Phenotype Analysis on a Cohort of 121 Patients

Author

Daniel, M., primary, Rauch, A., additional, Volot, F., additional, Pouymayou, K., additional, Pan-Petesch, B., additional, Castet, S., additional, Itzhar, N., additional, Veyradier, A., additional, Repessé, Y., additional, Ternisien, C., additional, Trossaert, M., additional, Boisseau, P., additional, Jeanpierre, E., additional, Paris, C., additional, Zawadzki, C., additional, Desvages, M., additional, Dupont, A., additional, Goudemand, J., additional, and Susen, S., additional

Published
2023
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3. PB0818 Impact of ABO Blood Group Genotype on VWF Level in Carriers of Type 3 von Willebrand Disease from the French von Willebrand Disease Reference Center

Author

Kitel, C., primary, Jeanpierre, E., additional, Boisseau, P., additional, Ternisien, C., additional, Desvages, M., additional, Rauch, A., additional, Paris, C., additional, Daniel, M., additional, Geffroy, S., additional, Duployez, N., additional, Goudemand, J., additional, Morange, P., additional, Zawadzki, C., additional, and Susen, S., additional

Published
2023
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31. Agreement between factor XIII activity and antigen assays in measurement of factor XIII: A French multicenter study of 147 human plasma samples

Author

Caron, C., primary, Meley, R., additional, Le Cam Duchez, V., additional, Aillaud, M. F., additional, Lavenu‐Bombled, C., additional, Dutrillaux, F., additional, Flaujac, C., additional, Ryman, A., additional, Ternisien, C., additional, Lasne, D., additional, Galinat, H., additional, and Pouplard, C., additional

Published
2017
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35. [Acquired von Willebrand disease and lymphoproliferative syndromes]

Author

Hunault-Berger M, Rachieru P, Ternisien C, Jardel H, Zandecki M, Boasson M, and Norbert IFRAH

Subjects
Male, von Willebrand Diseases, von Willebrand Factor, Humans, Female, Middle Aged, Prognosis, Lymphoproliferative Disorders, Aged
Abstract

Acquired von Willebrand disease occurs in patients with or without cutaneous and mucosal bleeding who have no personal or family history of the disease. The clinical course of these patients is poorly known due to the rarity of acquired von Willebrand factor (vWF) deficit. We conducted this study to assess the clinical course of acquired vWF deficit secondary to lymphoproliferative syndromes.We report the clinical course of acquired von Willebrand disease in 6 patients with monoclonal gammapathy of undetermined significance, multiple myeloma, chronic lymphoid leukemia, Wadenstöm's macroglobulinemia, or lymphoma who were followed for 1 to 11 years.Acquired von Willebrand disease was suspected in non-thrombocytopenic patients with a lymphoproliferative syndrome who developed a hemorrhagic syndrome. The vWF anomaly was symptomatic in 4 of 6 patients at diagnosis. Patients were given symptomatic treatment with vWF replacement therapy as needed and specific treatment for their lymphoproliferative syndrome. Administration of DDAVP was sufficient in 3 out of 4 patients to allow invasive procedures but was unable to control digestive ulcer bleeding that required infusion of factor VIII-vWF concentrate. For 2 patients, chemotherapy was initiated due to threatening massive hemorrhage. The result was spectacular. The 4 other patients have been asymptomatic without treatment for 3, 5, 6 and 11 years during which time their lymphoproliferative syndrome has been quiescent.The clinical features and laboratory findings are similar in patients with congenital or acquired von Willebrand disease, but specific and etiologic chemotherapy is indicated for patients with acquired disease.

Published
2002

48. Effect of phosphopyridoxylation on thrombin interaction with platelet glycoprotein Ib

Author

Marie-Claude Guillin, Ternisien C, Martine Jandrot-Perrus, and Marie-Geneviève Huisse

Subjects
Platelet Aggregation, Hirudin, Peptide, Platelet Membrane Glycoproteins, Platelet membrane glycoprotein, Tritium, Thrombin, medicine, Humans, Platelet, Trypsin, Cyanogen Bromide, chemistry.chemical_classification, Binding Sites, Heparin, Lysine, Hematology, General Medicine, Hirudins, Molecular Weight, Cross-Linking Reagents, chemistry, Biochemistry, Pyridoxal Phosphate, medicine.drug, Binding domain, Protein Binding
Abstract

The purpose of this study was to determine the effect of chemical modification of lysyl residues on thrombin interaction with platelet membrane proteins. Modification of lysyl residues by pyridoxal-5'-phosphate affected two different sites on thrombin and resulted in a greatly decreased binding to platelets. Using a crosslinking bifunctional reagent [bis(sulphosuccinimidyl) suberate (BS3)], we show that modified thrombin retained the ability to form high molecular mass (greater than or equal to 400 kDa) complexes with yet unidentified platelet proteins and to bind to platelet protease nexin I, but had lost the ability to bind to platelet glycoprotein Ib (GPIb). As previously reported by others, heparin protected one of the two sites from phosphopyridoxylation. In contrast modified thrombin, heparin-protected modified thrombin retained the ability to bind to GPIb, indicating that the lysyl residue(s) protected by heparin from the modification are essential for GPIb binding. While unprotected modified thrombin failed to bind hirudin, heparin-protected modified thrombin retained its ability to bind the carboxy-terminal hirudin peptide H54-65. Tritium-labelling of the modified lysyl residues and degradation of modified thrombins by CNBr or trypsin confirmed that the lysyl residue(s) protected by heparin and essential for GPIb binding are located in the thrombin binding domain for the carboxyl-terminal tail of hirudin, within the sequence 18-73 of the thrombin B chain.

Published
1991

50. Use of a thrombopoietin receptor agonist in von Willebrand disease type 2B (p.V1316M) with severe thrombocytopenia and intracranial hemorrhage.

Author

Espitia, O., Ternisien, C., Agard, C., Boisseau, P., Denis, C. V., and Fouassier, M.

Subjects
*HEMATOPOIETIC growth factors, *GRAY platelet syndrome, *BLOOD platelet disorders, *THROMBOPOIETIN receptor agonists, *CYTOKINE receptors
Abstract

We present here a 63-year old woman with a long history of immune thrombocytopenia. She was hospitalized for a traumatic intracranial hemorrhage with thrombocytopenia. Following inefficient treatment of four platelet transfusions, immunoglobulins, and corticosteroids, we initiated treatment with a thrombopoietin (TPO) receptor agonist (eltrombopag 25 mg/d) with a good efficacy. Her mother and sister also had chronic thrombocytopenia. Clinical history, hemostasis results, and gene analysis revealed von Willebrand disease (VWD) type 2B with the mutation (c.3946G>A; p.V1316M), which combines a von Willebrand factor defect with severe thrombocytopenia, as well as a thrombocytopathy. The efficacy of TPO receptor agonists appears to counterbalance, at least to some extent, the thrombocytopathy associated with this mutation. As such, the use of TPO receptor agonists could represent an alternative therapeutic approach in cases of VWD type 2B with severe thrombocytopenia. [ABSTRACT FROM PUBLISHER]

Published
2017
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