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Your search keyword '"Repessé, Yohann"' showing total 38 results
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38 results on '"Repessé, Yohann"'

1. Type 2N von Willebrand disease: genotype drives different bleeding phenotypes and treatment needs

Author

Daniel, Mélanie Y., Ternisien, Catherine, Castet, Sabine, Falaise, Céline, D’Oiron, Roseline, Volot, Fabienne, Itzhar, Nathalie, Pan-Petesch, Brigitte, Jeanpierre, Emmanuelle, Paris, Camille, Zawadzki, Christophe, Desvages, Maximilien, Dupont, Annabelle, Veyradier, Agnès, Repessé, Yohann, Babuty, Antoine, Trossaërt, Marc, Boisseau, Pierre, Denis, Cécile V., Lenting, Peter J., Goudemand, Jenny, Rauch, Antoine, and Susen, Sophie

Published
2024
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7. Gastrointestinal bleeding from angiodysplasia in von Willebrand disease: Improved diagnosis and outcome prediction using videocapsule on top of conventional endoscopy

Author

Rauch, Antoine, Paris, Camille, Repesse, Yohann, Branche, Julien, D’Oiron, Roseline, Harroche, Annie, Ternisien, Catherine, Castet, Sabine‐Marie, Lebreton, Aurélien, Pan‐Petesch, Brigitte, Volot, Fabienne, Claeyssens, Segolene, Chamouni, Pierre, Gay, Valérie, Berger, Claire, Desprez, Dominique, Falaise, Céline, Biron Andreani, Christine, Marichez, Catherine, Pradines, Benedicte, Zawadzki, Christophe, Itzhar Baikian, Nathalie, Borel‐Derlon, Annie, Goudemand, Jenny, Gerard, Romain, and Susen, Sophie

Published
2021
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13. Real Life Population Pharmacokinetics Modelling of Eight Factors VIII in Patients with Severe Haemophilia A: Is It Always Relevant to Switch to an Extended Half-Life?

Author

Allard, Quentin, primary, Djerada, Zoubir, additional, Pouplard, Claire, additional, Repessé, Yohann, additional, Desprez, Dominique, additional, Galinat, Hubert, additional, Frotscher, Birgit, additional, Berger, Claire, additional, Harroche, Annie, additional, Ryman, Anne, additional, Flaujac, Claire, additional, Chamouni, Pierre, additional, Guillet, Benoît, additional, Volot, Fabienne, additional, Szymezak, Jean, additional, Nguyen, Philippe, additional, and Cazaubon, Yoann, additional

Published
2020
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15. Risk stratification integrating genetic data for factor VIII inhibitor development in patients with severe hemophilia A

Author

Bachelet, Delphine, Albert, Thilo, Mbogning, Cyprien, Hässler, Signe, Zhang, Yuan, Schultze-Strasser, Stephan, Repessé, Yohann, Rayes, Julie, Pavlova, Anna, Pezeshkpoor, Behnaz, Liphardt, Kerstin, Davidson, Julie E., Hincelin-Méry, Agnès, Dönnes, Pierre, Lacroix-Desmazes, Sébastien, Königs, Christoph, Oldenburg, Johannes, Broët, Philippe, Bachelet, Delphine, Albert, Thilo, Mbogning, Cyprien, Hässler, Signe, Zhang, Yuan, Schultze-Strasser, Stephan, Repessé, Yohann, Rayes, Julie, Pavlova, Anna, Pezeshkpoor, Behnaz, Liphardt, Kerstin, Davidson, Julie E., Hincelin-Méry, Agnès, Dönnes, Pierre, Lacroix-Desmazes, Sébastien, Königs, Christoph, Oldenburg, Johannes, and Broët, Philippe

Abstract

Replacement therapy in severe hemophilia A leads to factor VIII (FVIII) inhibitors in 30% of patients. Factor VIII gene (F8) mutation type, a family history of inhibitors, ethnicity and intensity of treatment are established risk factors, and were included in two published prediction tools based on regression models. Recently investigated immune regulatory genes could also play a part in immunogenicity. Our objective is to identify bio-clinical and genetic markers for FVIII inhibitor development, taking into account potential genetic high order interactions. The study population consisted of 593 and 79 patients with hemophilia A from centers in Bonn and Frankfurt respectively. Data was collected in the European ABIRISK tranSMART database. A subset of 125 severely affected patients from Bonn with reliable information on first treatment was selected as eligible for risk stratification using a hybrid tree-based regression model (GPLTR). In the eligible subset, 58 (46%) patients developed FVIII inhibitors. Among them, 49 (84%) were "high risk" F8 mutation type. 19 (33%) had a family history of inhibitors. The GPLTR model, taking into account F8 mutation risk, family history of inhibitors and product type, distinguishes two groups of patients: a high-risk group for immunogenicity, including patients with positive HLA-DRB1*15 and genotype G/A and A/A for IL-10 rs1800896, and a low-risk group of patients with negative HLA-DRB1*15 / HLA-DQB1*02 and T/T or G/T for CD86 rs2681401. We show associations between genetic factors and the occurrence of FVIII inhibitor development in severe hemophilia A patients taking into account for high-order interactions using a generalized partially linear tree-based approach., ABIRISK consortium

Published
2019
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16. Risk stratification integrating genetic data for factor VIII inhibitor development in patients with severe hemophilia A

Author

de Frutos, Pablo Garcia, ABIRISK consortium, Bachelet, Delphine, Albert, Thilo, Mbogning, Cyprien, Hässler, Signe, Zhang, Yuan, Schultze-Straßer, Stephan, Repessé, Yohann, Rayes, Julie, Pavlova, Anna, Pezeshkpoor, Behnaz, Liphardt, Kerstin, Davidson, Julie E., Hincelin-Méry, Agnès, Dönnes, Pierre, Lacroix-Desmazes, Sébastien, Königs, Christoph, Oldenburg, Johannes, Broët, Philippe, de Frutos, Pablo Garcia, ABIRISK consortium, Bachelet, Delphine, Albert, Thilo, Mbogning, Cyprien, Hässler, Signe, Zhang, Yuan, Schultze-Straßer, Stephan, Repessé, Yohann, Rayes, Julie, Pavlova, Anna, Pezeshkpoor, Behnaz, Liphardt, Kerstin, Davidson, Julie E., Hincelin-Méry, Agnès, Dönnes, Pierre, Lacroix-Desmazes, Sébastien, Königs, Christoph, Oldenburg, Johannes, and Broët, Philippe

Abstract

Replacement therapy in severe hemophilia A leads to factor VIII (FVIII) inhibitors in 30% of patients. Factor VIII gene (F8) mutation type, a family history of inhibitors, ethnicity and intensity of treatment are established risk factors, and were included in two published prediction tools based on regression models. Recently investigated immune regulatory genes could also play a part in immunogenicity. Our objective is to identify bio-clinical and genetic markers for FVIII inhibitor development, taking into account potential genetic high order interactions. The study population consisted of 593 and 79 patients with hemophilia A from centers in Bonn and Frankfurt respectively. Data was collected in the European ABIRISK tranSMART database. A subset of 125 severely affected patients from Bonn with reliable information on first treatment was selected as eligible for risk stratification using a hybrid tree-based regression model (GPLTR). In the eligible subset, 58 (46%) patients developed FVIII inhibitors. Among them, 49 (84%) were “high risk” F8 mutation type. 19 (33%) had a family history of inhibitors. The GPLTR model, taking into account F8 mutation risk, family history of inhibitors and product type, distinguishes two groups of patients: a high-risk group for immunogenicity, including patients with positive HLA-DRB1*15 and genotype G/A and A/A for IL-10 rs1800896, and a low-risk group of patients with negative HLA-DRB1*15 / HLA-DQB1*02 and T/T or G/T for CD86 rs2681401. We show associations between genetic factors and the occurrence of FVIII inhibitor development in severe hemophilia A patients taking into account for high-order interactions using a generalized partially linear tree-based approach.

Published
2019

17. Role of factor VIII-binding capacity of endogenous von Willebrand factor in the development of factor VIII inhibitors in patients with severe hemophilia A

Author

Repessé, Yohann, primary, Costa, Catherine, additional, Palla, Roberta, additional, Moshai, Elika Farrokhi, additional, Borel-Derlon, Annie, additional, D’Oiron, Roseline, additional, Rothschild, Chantal, additional, El-Beshlawy, Amal, additional, Elalfy, Mohsen, additional, Ramanan, Vijay, additional, Eshghi, Peyman, additional, Oldenburg, Johannes, additional, Pavlova, Anna, additional, Rosendaal, Frits R, additional, Peyvandi, Flora, additional, Kaveri, Srinivas V., additional, and Lacroix-Desmazes, Sébastien, additional

Published
2019
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18. SAT237 - Prognosis of alcoholic or viral B/C cirrhosis according to ABO blood group: results of abocirralvir, from CIRRAL and ANRS CO12 CirVir cohorts

Author

Ollivier-Hourmand, Isabelle, Nahon, Pierre, Chaffaut, Cendrine, Dao, Thong, Nguyen, Nga, Patrick, Marcellin, Roulot, Dominique, de Lédinghen, Victor, Pol, Stanislas, Guyader, Dominique, Mabile-Archambeaud, Isabelle, Zoulim, Fabien, Oberti, Frédéric, Tran, Albert, Bronowicki, Jean-Pierre, Dalteroche, Louis, Ouzan, Denis, Peron, Jean Marie, Zarski, Jean-Pierre, Bourliere, Marc, Larrey, Dominique, Louvet, Alexandre, Cales, Paul, Abergel, Armand, Mathurin, Philippe, Mallat, Ariane, Blanc, Jean-Frédéric, Khac, Eric Nguyen, Riachi, Ghassan, Alric, Laurent, Serfaty, Lawrence, Antonini, Tereza, Moreno, Christophe, Attali, Pierre, Thabut, Dominique, Pilette, Christophe, Grange, Jean Didier, Silvain, Christine, Carbonell, Nicolas, Chabert, Brigitte Bernard, Goria, Odile, Wartelle-Bladou, Claire, Moirand, Romain, Christidis, Christos, Perlemuter, Gabriel, Ozenne, Violaine, Henrion, Jean, Hillaire, Sophie, Di Martino, Vincent, Amiot, Xavier, Sutton, Angela, Barget, Nathalie, Repesse, Yohann, Chevret, Sylvie, and Ganne-Carrié, Nathalie

Published
2020
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19. Potent Thrombolytic Effect of N -Acetylcysteine on Arterial Thrombi

Author

Martinez de Lizarrondo, Sara, primary, Gakuba, Clément, additional, Herbig, Bradley A., additional, Repessé, Yohann, additional, Ali, Carine, additional, Denis, Cécile V., additional, Lenting, Peter J., additional, Touzé, Emmanuel, additional, Diamond, Scott L., additional, Vivien, Denis, additional, and Gauberti, Maxime, additional

Published
2017
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28. VWF protects FVIII from endocytosis by dendritic cells and subsequent presentation to immune effectors

Author

Dasgupta, Suryasarathi, primary, Repessé, Yohann, additional, Bayry, Jagadeesh, additional, Navarrete, Ana-Maria, additional, Wootla, Bharath, additional, Delignat, Sandrine, additional, Irinopoulou, Theano, additional, Kamaté, Caroline, additional, Saint-Remy, Jean-Marie, additional, Jacquemin, Marc, additional, Lenting, Peter J., additional, Borel-Derlon, Annie, additional, Kaveri, Srinivas V., additional, and Lacroix-Desmazes, Sébastien, additional

Published
2006
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30. Development of Inhibitory Antibodies to Therapeutic Factor VIII in Severe Hemophilia A Is Associated with Microsatellite Polymorphism in the HMOX1 promoter

Author

Repesse, Yohann, Peyron, Ivan, Dimitrov, Jordan, Dasgupta, Suryasarathi, Moshai, Elika Farrokhi, Borel-Derlon, Annie, Costa, Catherine, Guillet, Benoist, d'Oiron, Roseline, Aouba, Achille, Rothschild, Chantal, Oldenburg, Johannes, Pavlova, Ana, Kaveri, Srinivas, and Lacroix-Desmazes, Sebastien

Published
2012
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33. Octreotide for recurrent intestinal bleeding due to ventricular assist device.

Author

Coutance, Guillaume, Saplacan, Vladimir, Belin, Annette, Repessé, Yohann, Buklas, Dimitrios, and Massetti, Massimo

Abstract

We report the case of a 64-year-old Jarvik 2000 recipient with a high risk of bleeding (anticoagulation treatment and acquired von Willebrand disease), who presented with intractable gastrointestinal hemorrhage due to severe gastric angiodysplasia. He was successfully treated with long-acting octreotide. [ABSTRACT FROM PUBLISHER]

Published
2014
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37. Development of inhibitory antibodies to therapeutic factor VIII in severe hemophilia A is associated with microsatellite polymorphisms in the HMOX1 promoter.

Author

Repessé Y, Peyron I, Dimitrov JD, Dasgupta S, Moshai EF, Costa C, Borel-Derlon A, Guillet B, D'Oiron R, Aouba A, Rothschild C, Oldenburg J, Pavlova A, Kaveri SV, and Lacroix-Desmazes S

Subjects
Antibodies blood, Case-Control Studies, Hemophilia A blood, Hemophilia A drug therapy, Humans, Severity of Illness Index, Factor VIII therapeutic use, Heme Oxygenase-1 genetics, Hemophilia A genetics, Microsatellite Repeats genetics, Polymorphism, Single Nucleotide genetics, Promoter Regions, Genetic genetics
Abstract

Induction of heme oxygenase-1, a stress-inducible enzyme with anti-inflammatory activity, reduces the immunogenicity of therapeutic factor VIII in experimental hemophilia A. In humans, heme oxygenase-1 expression is modulated by polymorphisms in the promoter of the heme oxygenase-1-encoding gene (HMOX1). We investigated the relationship between polymorphisms in the HMOX1 promoter and factor VIII inhibitor development in severe hemophilia A. We performed a case-control study on 99 inhibitor-positive patients and 263 patients who did not develop inhibitors within the first 150 cumulative days of exposure to therapeutic factor VIII. Direct sequencing and DNA fragment analysis were used to study (GT)n polymorphism and single nucleotide polymorphisms located at -1135 and -413 in the promoter of HMOX1. We assessed associations between the individual allele frequencies or genotypes, and inhibitor development. Our results demonstrate that inhibitor-positive patients had a higher frequency of alleles with large (GT)n repeats (L: n≥30), which are associated with lesser heme oxygenase-1 expression (odds ratio 2.31; 95% confidence interval 1.46-3.66; P<0.001]. Six genotypes (L/L, L/M, L/S, M/M, M/S and S/S) of (GT)n repeats were identified (S: n<21; M: 21≤n<30). The genotype group including L alleles (L/L, L/M and L/S) was statistically more frequent among inhibitor-positive than inhibitor-negative patients, as compared to the other genotypes (33.3% versus 17.1%) (odds ratio 2.21, 95% confidence interval 1.30-3.76; P<0.01). To our knowledge, this is the first association identified between HMOX1 promoter polymorphism and development of anti-drug antibodies. Our study paves the way towards modulation of the endogenous anti-inflammatory machinery of hemophilia patients to reduce the risk of inhibitor development.

Published
2013
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38. Factor VIII bypasses CD91/LRP for endocytosis by dendritic cells leading to T-cell activation.

Author

Dasgupta S, Navarrete AM, André S, Wootla B, Delignat S, Repessé Y, Bayry J, Nicoletti A, Saenko EL, d'Oiron R, Jacquemin M, Saint-Remy JM, Kaveri SV, and Lacroix-Desmazes S

Subjects
Animals, Cell Separation, Endocytosis, Factor VIII metabolism, Hemophilia A genetics, Humans, Leukocytes, Mononuclear cytology, Ligands, Low Density Lipoprotein Receptor-Related Protein-1, Lymphocyte Activation, Mice, Monocytes cytology, Monocytes metabolism, Antigens, CD biosynthesis, Dendritic Cells cytology, Factor VIII biosynthesis, T-Lymphocytes cytology
Abstract

Background: The development of factor VIII (FVIII) inhibitors remains the major hurdle in the clinical management of patients with hemophilia A. FVIII uptake by professional antigen-presenting cells (APC) is the first step involved in initiation of immune responses to FVIII. Studies on FVIII catabolism have highlighted the role played by CD91/LRP as a potential target for increasing FVIII half-life in patients and prolonging treatment efficiency. We investigated the involvement of CD91 in FVIII endocytosis by human dendritic cells (DC), a model of professional APC., Design and Methods: Immature DC were generated from circulating monocytes from healthy donors. Surface expression of CD91 was assessed by flow cytometry. Uptake of fluorescein isothiocyanate-conjugated ligands by immature DC was studied in the presence of various blocking agents., Results: CD91 was expressed on approximately 20% of DC and mediated the internalization of its model ligand, alpha2-macroglobulin. DC internalized FVIII and activated a human FVIII-specific T-cell clone in a dose-dependent manner. FVIII uptake by DC and subsequent T-cell activation were not inhibited by receptor-associated protein., Conclusions: Our results indicate that CD91 and other members of the LDL receptor family are not strongly implicated in FVIII internalization by monocyte-derived DC, and suggest the involvement of alternative divalent ion-dependent endocytic receptors.

Published
2008
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