135 results on '"Clanet, Michel"'
Search Results
102. Genetic interaction of CTLA‐4with HLA‐DR15 in multiple sclerosis patients
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Alizadeh, Mehdi, Babron, Marie‐Claude, Birebent, Brigitte, Matsuda, Fumihiko, Quelvennec, Erwann, Liblau, Roland, Cournu‐Rebeix, Isabelle, Momigliano‐Richiardi, Patricia, Sequeiros, Jorge, Yaouanq, Jacqueline, Genin, Emmanuelle, Vasilescu, Alexandre, Bougerie, Héloise, Trojano, Maria, Martins Silva, Berta, Maciel, Patricia, Clerget‐Darpoux, Françoise, Clanet, Michel, Edan, Gilles, Fontaine, Bertrand, and Semana, Gilbert
- Abstract
Multiple sclerosis is a chronic inflammatory disease of the central nervous system with a genetic component. Until now, the more consistent association with the disease is found with the major histocompatibility complex, especially HLA‐DRB1*1501‐DQB1*0602 haplotype. In this report, we demonstrate the interaction of Cytotoxic T Lymphocyte‐associated antigen 4 (CTLA‐4[CD152]) gene with DRB1*15 haplotype in multiple sclerosis genetic susceptibility. Our data were obtained from two European independent family‐based studies including 610 multiple sclerosis family trios. Ann Neurol 2003;54:119–122
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- 2003
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103. Evaluation of O-(2-[18F]-Fluoroethyl)-L-Tyrosine in the Diagnosis of Glioblastoma.
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Benouaich-Amiel, Alexandra, Lubrano, Vincent, Tafani, Mathieu, Uro-coste, Emmanuelle, Gantet, Pierre, Sol, Jean Christophe, Roux, Franck, Bousquet, Philippe, Julian, Anne, Sabatier, Jean, Tremoulet, Michel, Cances-Lauwers, Valerie, Delisle, Marie Bernadette, Clanet, Michel, Esquerré, Jean Philippe, and Payoux, Pierre
- Abstract
Objective: To assess the feasibility of synthesis of O-(2-[
18 F]-fluoroethyl)-L-tyrosine (FET), a new positron emission tomographic (PET) tracer described in several studies but not yet considered standard in management of glioma, in routine practice and to determine FET uptake in a homogeneous group of patients with suspected high-grade glioma. Design: Prospective nonrandomized trial. Patients: Twelve patients with suspicion of high-grade glioma. Results: The mean (SD) FET uptake ratio was 3.15 (0.72) for the 12 patients and 3.16(0.75) for the 11 patients with glioblastoma. Conclusion: The initial results are promising and indicate that FET PET is a valuable and applicable tool for the imaging of high-grade glioma. [ABSTRACT FROM AUTHOR]- Published
- 2010
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104. Involvement of de novoceramide biosynthesis in lymphotoxininduced oligodendrocyte death
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Plo, Isabelle, Ghandour, Saïd, Feutz, Anne-Catherine, Clanet, Michel, Laurent, Guy, and Bettaieb, Ali
- Abstract
BOTH experimental and clinical studies suggest that lymphotoxin (LT) plays an important role in multiple sclerosis (MS) by inducing oligodendrocyte (OL) depletion. However, the mechanism of LT cytotoxicity is unknown. Because of the role of ceramide as a cell death mediator for a large variety of cytotoxic molecules, we have investigated the possible role of this second messenger in LT-induced cytotoxicity on SV40 immortalized new-born mice OL. Human recombinant LT exposure (50 ng/ml) resulted in intracellular ceramide accumulation which peaked at 48 h (∼170 increase) and paralleled LT-induced cytotoxicity. Moreover, fumonisin B1, a potent and specific ceramide synthase inhibitor, not only inhibited ceramide accumulation but also protected OL from LT cytotoxicity. These results suggest that LT-induced ceramide synthase stimulation and subsequent increased intracellular ceramide concentration are implicated in oligodendrocyte death.
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- 1999
105. Ocrelizumab versus Placebo in Primary Progressive Multiple Sclerosis
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Montalban, Xavier, Hauser, Stephen L., Kappos, Ludwig, Arnold, Douglas L., Bar-Or, Amit, Comi, Giancarlo, Seze, Jérôme, Giovannoni, Gavin, Hartung, Hans-Peter, Hemmer, Bernhard, Lublin, Fred, Rammohan, Kottil W., Selmaj, Krzysztof, Traboulsee, Anthony, Sauter, Annette, Masterman, Donna, Fontoura, Paulo, Belachew, Shibeshih, Garren, Hideki, Mairon, Nicole, Chin, Peter, Wolinsky, Jerry S., Oratorio, Clinical Investigators, Reingold, Stephen C., Sandberg-Wollheim, Magnhild, Barkhof, Frederik, Dörner, Thomas, Evans, Scott, Mcfarland, Henry F., Steiner, Israel, Yaldizli, Özgür, D Souza, Marcus, Andelova, Michaela, Rust, Heiko, Sedal, Leslie, Taylor, Bruce, Assar, Hamid, Auff, Eduard, Berger, Thomas, Guger, Michael, Pilz, Georg, Wipfler, Peter, Bartholomé, Emmanuel, Decoo, Danny, Becker, Jefferson, Da Silva Filho, Irenio, Diniz, Denise, Gomes Neto, Antônio, Leon, Soniza, Haralanov, Lyubomir, Milanov, Ivan, Bar-Or, Amir, Freedman, Mark, Grand Maison, François, Marriott, James, O Connor, Paul, Selchen, Daniel, Yeung, Michael, Benesova, Yvonne, Krasulova, Eva, Vachova, Marta, Airas, Laura, Elovaara, Irina, Färkkilä, Markus, Korpela, Jaana, Sumelahti, Marja-Liisa, Brassat, David, Brochet, Bruno, Camu, William, Castelnovo, Giovanni, Clanet, Michel, Clavelou, Pierre, Debouverie, Marc, Defer, Giles, Gout, Olivier, Heinzlef, Olivier, Laplaud, David, Lebrun-Frenay, Christine, Papeix, Caroline, Pelletier, Jean, Tourbah, Ayman, Vermersch, Patrick, Vukusic, Sandra, Angstwurm, Klemens, Berghoff, Martin, Förch, Christian, Goebels, Norbert, Haas, Judith, Harms, Lutz, Kleiter, Ingo, Koehler, Jürgen, Lensch, Eckard, Limmroth, Volker, Meuth, Sven, Oschmann, Patrick, Platten, Michael, Then Bergh, Florian, Tumani, Hayrettin, Ziemann, Ulf, Ziemssen, Tjalf, Afradou, Theodora, Fakas, Nikolaos, Tsounis, Stefanos, Vlaikidis, Nikolaos, Jakab, Gábor, Komoly, Sámuel, Rózsa, Csilla, Sátori, Mária, Szabó, Gyöngyi, Vécsei, László, Achiron, Anat, Hellmann, Mark, Karni, Arnon, Karussis, Dimitrios, Milo, Ron, Shahien, Radi, Bertolotto, Antonio, Marrosu, Maria Giovanna, Uccelli, Antonio, Malciene, Lina, Rastenyte, Daiva, Sceponaviciute, Sigla, Castro Farfan, Freddy, Duriez Sotelo, Eduardo, Flores-Rivera, Jose, Reyes Morales, Sarug, Hintzen, Rogier, Hupperts, Raymond, Lynch, Christopher, Mossman, Stuart, Gulowsen Celius, Elisabeth, Gavidia Chucan, Jorge, Perez Villegas, Julio, Pretell Alva, Edwin, Bielecki, Dariusz, Brola, Waldemar, Kochanowicz, Jan, Maciejowski, Maciej, Stelmasiak, Zbigniew, Zbrojkiewicz, Janusz, Cunha, Luis, Gonçalves, José, Mendes, Irene, Sá, João, Salgado, Vasco, Silva, Ana, Balasa, Rodica, Manescu, Silviu, Panea, Cristina Aura, Simu, Mihaela Adriana, Yakupov, Eduard, Álvarez Cermeño, José, Álvarez Cermeño, Carlos, Arroyo, Rafael, Escartín Siquier, Antonio, Fernández, Oscar, Izquierdo Ayuso, Guillermo, Martinez Rodríguez, José Enrique, Fernandez Sanchez, Victoria, Olascoaga Urtaza, Francisco Javier, Meca, Virginia, Olascoaga, Javier, Oreja-Guevara, Celia, Perez Sempere, Angel, Prieto González, José María, Ramió Torrentá, Lluis, Rodríguez-Antigüeda, Alfredo, Saiz, Albert, Gobbi, Claudio, Kuhle, Jens, Galusha, Anatoliy, Goloborodko, Alla, Litovchenko, Tetyana, Moroz, Olena, Sergii Moskovko, Nehrych, Tetyana, Pashkovskyy, Valeriy, Shkolnyk, Valerii, Shulga, Olga, Sokolova, Larysa, Voloshyna, Nataliya, Brex, Peter, Constantinescu, Cris, Duddy, Martin, Schmierer, Klaus, Young, Carolyn, Agius, Mark, Ash, Paul, Bandari, Daniel, Belkin, Martin, Bernitsas, Evanthia, Bowen, James, Cahill, Jonathan, Carpenter, Adam, Carter, Jonathan, Cerghet, Mirela, Conway, Jill, Cooper, Joanna, Coyle, Patricia, Cross, Anne, Ford, Corey, Fox, Edward, Freedman, S. Mitchell, Frohman, Elliot, Gitt, Jeffrey, Gottesman, Malcolm, Gudesblatt, Mark, Hendin, Barry, Hutton, George, Klineova, Sylvia, Krupp, Lauren, Lynch, Sharon, Markowitz, Clyde, Mattson, David, Miller, Aaron, Miravalle, Augusto, Muley, Suraj, Nealon, Nancy, Pardo, Gabriel, Picone, Mary Ann, Racke, Michael, Rizvi, Syed, Rossman, Howard, Rowe, Vernon, Schulman, Alan, Shafer, Stuart, William, Sheremata, Stein, Lee, and Waubant, Emmanuelle
106. Early Clinical Remission as a Prognostic Factor for Medium Term Disability Progression in Multiple Sclerosis?
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Moreau, Thibault, Debouverie, Marc, Jerome de Seze, Ongagna, Jean-Claude, Clanet, Michel, Brassat, David, Lebrun-Frenay, Christine, Clavelou, Pierre, Laplaud, David, Papeix, Caroline, Vermersch, Patrick, Gout, Olivier, Stankoff, Bruno, Rollot, Fabien, Bonithon-Kopp, Claire, and Binquet, Christine
107. Diagnosis of Adult Onset Leukodystrophy in a Consecutive Study of 156 Patients
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Labauge, Pierre, Carra-Dalliere, Clarisse, Ayrignac, Xavier, Champfleur, Nicolas Menjot, Aubourg, Patrick, Bellesme, Celine, Pelletier, Jean, Audoin, Bertrand, Seze, Jerome, nicolas collongues, Magnin, Eloi, Rumbach, Lucien, Confavreux, Christian, Vukusic, Sandra, Camdessanche, Jean-Philippe, Cohen, Mikael, Frenay, Christine Lebrun, Brassat, David, Clanet, Michel, Vermersch, Patrick, Zephir, Helene, Outteryck, Olivier, Wiertlevski, Sandrine, Ouallet, Jean-Christophe, Brochet, Bruno, Goizet, Cyril, Denier, Christian, Debouverie, Marc, Pittion, Sophie, Edan, Gilles, Deburghgraeve, Veronique, Verny, Christophe, Amati-Bonneau, Patrizia, Bonneau, Dominique, Hannequin, Didier, Guyant-Marchal, Lucie, Derache, Nathalie, Moreau, Thibault, Giroud, Maurice, Guennoc, Anne Marie, Clavelou, Pierre, Taithe, Frederic, Mathis, Stephane, Magy, Laurent, Devoize, Jean Louis, Bataillard, Marc, Tanguy, Odile Boespflug, Tournier-Lasserve, Elisabeth, and Levade, Thierry
108. Fingolimod treatment after natalizumab-related progressive multifocal leukoencephalopathy: Three new cases.
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Peaureaux, Delphine, Pignolet, Beatrice, Biotti, Damien, Bucciarelli, Florence, Gaina, Jana, Bucur, Cristina, Clanet, Michel, Martin-Blondel, Guillaume, and Brassat, David
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FINGOLIMOD ,NATALIZUMAB ,MULTIPLE sclerosis diagnosis ,MULTIPLE sclerosis treatment ,MULTIPLE sclerosis ,ETIOLOGY of diseases ,PATIENTS - Abstract
The article presents case studies of multiple sclerosis (MS) patients treated with fingolimod from natalizumab. Topics discussed the diagnosis of the MS patients, the identification of the MS causes and symptoms, their treatment options using fingolimod and its effects on them, and their treatment processes.
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- 2015
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109. Molecular analysis of ANT1, TWINKLE and POLG in patients with multiple deletions or depletion of mitochondrial DNA by a dHPLC-based assay.
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Naïmi, Mourad, Bannwarth, Sylvie, Procaccio, Vincent, Pouget, Jean, Desnuelle, Claude, Pellissier, Jean-François, Rötig, Agnes, Munnich, Arnold, Calvas, Patrick, Richelme, Christian, Jonveaux, Philippe, Castelnovo, Giovanni, Simon, Mariella, Clanet, Michel, Wallace, Douglas, and Paquis-Flucklinger, Véronique
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MITOCHONDRIAL DNA - Abstract
A correction to the article "Molecular analysis of ANT1, TWINKLE and POLG in patients with multiple deletions or depletion of mitochondrial DNA by a dHPLC-based assay" that was published in a previous issue of the periodical is presented.
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- 2007
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110. Safety Profile of Mitoxantrone in a French Cohort of 802 Multiple Sclerosis Patients.
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Le Page, Emmanuelle, Leray, Emmanuelle, Brochet, Bruno, Clanet, Michel, Clermont-Ferrand, Pierre Clavelou, Confavreux, Christian, Debouverie, Marc, Lebrun, Christine, Lubetzki, Catherine, Madigand, Michel, Pelletier, Jean, Roullet, Etienne, Rumbach, Lucien, and Edan, Gilles
- Published
- 2006
111. Myelin oligodendrocyte glycoprotein (MOG) gene polymorphisms and multiple sclerosis: no evidence of disease association with MOG
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Roth, Marie-paule, Dolbois, Laurence, Borot, Nicolas, Pontarotti, Pierre, Clanet, Michel, and Coppin, Hélène
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- 1995
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112. A Role for VAV1in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis
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Jagodic, Maja, Colacios, Celine, Nohra, Rita, Dejean, Anne S., Beyeen, Amennai Daniel, Khademi, Mohsen, Casemayou, Audrey, Lamouroux, Lucille, Duthoit, Christine, Papapietro, Olivier, Sjöholm, Louise, Bernard, Isabelle, Lagrange, Dominique, Dahlman, Ingrid, Lundmark, Frida, Oturai, Annette B., Soendergaard, Helle B., Kemppinen, Anu, Saarela, Janna, Tienari, Pentti J., Harbo, Hanne F., Spurkland, Anne, Ramagopalan, Sreeram V., Sadovnick, Dessa A., Ebers, George C., Seddighzadeh, Maria, Klareskog, Lars, Alfredsson, Lars, Padyukov, Leonid, Hillert, Jan, Clanet, Michel, Edan, Gilles, Fontaine, Bertrand, Fournié, Gilbert J., Kockum, Ingrid, Saoudi, Abdelhadi, and Olsson, Tomas
- Abstract
VAV1plays a role in regulating proinflammatory cytokines, which underlie the susceptibility for developing experimental autoimmune encephalomyelitis and multiple sclerosis.
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- 2009
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113. Propos introductifs.
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Clanet M
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- 2023
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114. Safety, tolerability, and activity of mesenchymal stem cells versus placebo in multiple sclerosis (MESEMS): a phase 2, randomised, double-blind crossover trial.
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Uccelli A, Laroni A, Ali R, Battaglia MA, Blinkenberg M, Brundin L, Clanet M, Fernandez O, Marriot J, Muraro P, Nabavi SM, Oliveri RS, Radue E, Ramo Tello C, Schiavetti I, Sellner J, Sorensen PS, Sormani MP, Wuerfel JT, and Freedman MS
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- Adolescent, Adult, Humans, Middle Aged, Young Adult, Brain, Cross-Over Studies, Double-Blind Method, Malformations of Cortical Development, Mesenchymal Stem Cells, Multiple Sclerosis drug therapy
- Abstract
Background: Mesenchymal stem cells (MSCs), also known as mesenchymal stromal cells, have been proposed as a promising therapeutic option for people with multiple sclerosis on the basis of their immunomodulatory and neuroprotective properties. The MEsenchymal StEm cells for Multiple Sclerosis (MESEMS) study was devised to evaluate the safety, tolerability, and activity of autologous MSCs derived from bone marrow and infused intravenously in patients with active multiple sclerosis., Methods: MESEMS is a randomised phase 2 trial done at 15 sites in nine countries. Patients (aged 18-50 years) with active relapsing-remitting or progressive multiple sclerosis were included if they had a disease duration of 2-15 years since onset of multiple sclerosis and an Expanded Disability Status Scale score of 2·5-6·5. Patients were randomly assigned (1:1), according to a crossover design, to receive a single intravenous dose of autologous bone marrow-derived MSCs followed by placebo at week 24, or to receive placebo followed by autologous MSCs at week 24, with a follow-up visit at week 48. Primary objectives were to test safety and activity of MSC treatment. The primary safety endpoint was to assess the number and severity of adverse events within each treatment arm. The primary efficacy endpoint was the number of gadolinium-enhancing lesions (GELs) counted over week 4, 12, and 24 compared between treatment groups. The primary efficacy endpoint was assessed in the full analyis set, after all participants completed the week 24 visit. Efficacy endpoints were evaluated using a predefined statistical testing procedure. Safety was monitored throughout the study by recording vital signs and adverse events at each visit., Findings: From July 16, 2012, until July 31, 2019, 144 patients were randomly assigned to first receive early intravenous infusion of autologous bone marrow-derived MSCs (n=69) or placebo (n=75). MSC treatment did not meet the primary endpoint of efficacy on the total number of GELs accumulated from baseline to week 24 (rate ratio [RR] 0·94, 95% CI 0·58-1·50; p=0·78). 213 adverse events were recorded, similarly distributed between groups (93 cases recorded in 35 [51%] of 69 patients treated first with MSCs vs 120 cases in 42 [56%] of 75 patients infused first with placebo). The most frequent adverse events reported were infection and infestations, with a total of 54 (25%) of 213 adverse events (18 [19%] of 93 in the early-MSC group and 36 [30%] of 120 in the delayed-MSC group). Nine serious adverse events were reported in seven patients treated with placebo versus none in the MSC group. All serious adverse events were considered to be unrelated to the treatment infusion. No deaths were reported during the study., Interpretation: Bone marrow-derived MSC treatment was safe and well tolerated but did not show an effect on GELs, an MRI surrogate marker of acute inflammation, in patients with active forms of multiple sclerosis, at week 24. Thus, this study does not support the use of bone marrow-derived MSCs to treat active multiple sclerosis. Further studies should address the effect of MSCs on parameters related to tissue repair., Funding: Fondazione Italiana Sclerosi Multipla (FISM), the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS), and the Multiple Sclerosis International Federation (MSIF) for centralised activities. Individual trials participating in the MESEMS network are funded by the following agencies: FISM and Compagnia di San Paolo (Italy); The Danish Multiple Sclerosis Society, The Toyota Foundation, and Danish Blood Donors' Research Foundation (Denmark); the Spanish Health Research Institute Carlos 3 and the Andalusian Public Foundation Progreso y Salud (Spain); the Royan Institute for Stem Cell Biology and Technology (Iran); the Spinal Cord Injury and Tissue Regeneration Centre Salzburg, Paracelsus Medical University, and Salzburg (Austria); the Fondation pour l'aide à la recherche sur la sclérose en plaques (ARSEP), French Muscular Dystrophy Association (AFM)-Telethon (France); the UK Multiple Sclerosis Society and the UK Stem Cell Foundation (UK); and the Multiple Sclerosis Society of Canada and The Multiple Sclerosis Scientific Research Foundation and Research Manitoba (Canada)., Competing Interests: Declaration of interests AU received funding for research by Fondazione Italiana Sclerosi Multipla and Compagnia di San Paolo. AL has received personal compensation from Novartis, Sanofi Genzyme, Biogen, Merck, and Roche for public speaking and advisory boards. AL received funding for research by Fondazione Italiana Sclerosi Multipla, the Italian Ministry of Health, and the Italian Ministry of University. MAB reports personal fees from Sanofi Genzyme, Biogen, Merck, Novartis, Bristol-Myers Squibb, Roche and non-financial support from Biogen, Roche and Genzyme. LB has received travel grants from Sanofi Genzyme, and Biogen and has received personal compensation for public speaking and advisory boards for Genzyme, Sanofi, Biogen, Novartis, and Merck. LB has grants from Swedish medical research foundation, the Brain foundation, Novonordisk Foundation, the Stockholm Council, and Karolinska Institutet. JM has received grant funding from Research Manitoba, The Multiple Sclerosis Society of Canada, The Multiple Sclerosis Scientific Research Foundation, and Roche Canada. SMN has received speaker honoraria from Biogen, Bayer, Genzyme, Merck Serono, Novartis, Sanofi, Abidipharma, Zist Daru Danesh, and Actoverco. RSO is now a full-time employee at Genmab but worked at the Copenhagen University Hospital Rigshospitalet and declared no conflict of interest while the trial was ongoing. JS has received personal compensation for serving on scientific advisory boards or receiving speaker honoraria for Alexion, Celgene, Biogen, Merck, Novartis, and Roche. PSS has received personal compensation for serving on scientific advisory boards, steering committees, and independent data-monitoring committees or has received speaker honoraria for Biogen, Merck, Novartis, TEVA, and Celgene. MPS has received consultancy fees from Teva Pharmaceuticals, Biogen, Novartis, Roche, Merck, Sanofi, Celgene, GeNeuro, Meddey, and Immunic. JTW has received personal compensation for advisory boards of Actelion, Bayer, Biogen, Celgene, Genzyme-Sanofi, Idorsia, InmuneBio, Novartis, and Roche. MSF reported receiving honoraria or consulting fees from Actelion, Bayer, Biogen, Chugai, EMD Canada, Merck Serono, Novartis, Roche, Sanofi, and Teva Canada Innovation, he also served as a member of an advisory board, board of directors, or other similar group for Actelion, Bayer, Biogen, Merck Serono, Novartis, Opexa, Roche, and Sanofi, and participated in the speakers bureau for Sanofi. All other authors declare no competing interests., (Copyright © 2021 Elsevier Ltd. All rights reserved.)
- Published
- 2021
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115. Basket clinical trial design for targeted therapies for cancer: a French National Authority for Health statement for health technology assessment.
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Lengliné E, Peron J, Vanier A, Gueyffier F, Kouzan S, Dufour P, Guillot B, Blondon H, Clanet M, Cochat P, Degos F, Chevret S, Grande M, and Putzolu J
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- Antineoplastic Agents adverse effects, France, Government Agencies, Humans, Molecular Targeted Therapy, Neoplasms genetics, Neoplasms pathology, Treatment Outcome, Antineoplastic Agents therapeutic use, Clinical Trials as Topic, Neoplasms drug therapy, Research Design, Technology Assessment, Biomedical
- Abstract
During the past decade, health technology assessment bodies have faced new challenges in establishing the benefits of new drugs for individuals and health-care systems. A topic of increasing importance to the field of oncology is the so-called agnostic regulatory approval of targeted therapies for cancer (independent of tumour location and histology) granted on the basis of basket trials. Basket trials in oncology offer the advantage of simultaneously evaluating treatments for multiple tumours, even rare cancers, in a single clinical trial. To address the novel challenges introduced by these trials, an interdisciplinary panel was convened on behalf of the Transparency Committee of the French National Authority for Health to clarify an approach designed to guarantee a transparent, reproducible, and fair assessment of histology-agnostic treatments for reimbursement by the French National Health Insurance Fund. The requirements of this approach include the need for randomisation, clinically relevant endpoints, appropriate correction for multiple significance testing, characterisation of subgroup heterogeneity, and validation of underlying biomarker assays. A prospectively designated external control is encouraged when the implementation of a direct comparison is deemed infeasible. We also underline the importance of recording outcomes from basket trials in a registry for use as future external controls., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2021 Elsevier Ltd. All rights reserved.)
- Published
- 2021
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116. Observatoire Français de la Sclérose en Plaques (OFSEP): A unique multimodal nationwide MS registry in France.
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Vukusic S, Casey R, Rollot F, Brochet B, Pelletier J, Laplaud DA, De Sèze J, Cotton F, Moreau T, Stankoff B, Fontaine B, Guillemin F, Debouverie M, and Clanet M
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- Adult, Female, France epidemiology, Humans, Male, Middle Aged, Young Adult, Databases, Factual statistics & numerical data, Multiple Sclerosis epidemiology, Registries statistics & numerical data
- Abstract
The care of multiple sclerosis (MS) in France is based on two complementary interlinked networks: MS expert centers in university hospitals and regional networks of neurologists. The routine use of European database for multiple sclerosis (EDMUS) in all those centers has paved the way for the constitution of a national registry, designated as Observatoire Français de la Sclérose En Plaques (OFSEP). It promotes a prospective, standardized, high-quality, and multimodal collection of data. On June 2018, there were 68.097 files, with 71.1% females, representing 761,185 person-years. This huge database is open to the scientific community and might contribute exploring unresolved issues and unmet needs in MS.
- Published
- 2020
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117. Biallelic MYORG mutation carriers exhibit primary brain calcification with a distinct phenotype.
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Grangeon L, Wallon D, Charbonnier C, Quenez O, Richard AC, Rousseau S, Budowski C, Lebouvier T, Corbille AG, Vidailhet M, Méneret A, Roze E, Anheim M, Tranchant C, Favrole P, Antoine JC, Defebvre L, Ayrignac X, Labauge P, Pariente J, Clanet M, Maltête D, Rovelet-Lecrux A, Boland A, Deleuze JF, Frebourg T, Hannequin D, Campion D, and Nicolas G
- Subjects
- Adult, Brain metabolism, Calcinosis genetics, Female, Heterozygote, Humans, Male, Middle Aged, Mutation genetics, Pedigree, Phenotype, Xenotropic and Polytropic Retrovirus Receptor, Young Adult, Brain pathology, Brain Diseases genetics, Glycoside Hydrolases genetics, Nervous System Malformations genetics
- Abstract
Primary familial brain calcification (PFBC) is a rare neurogenetic disorder with diverse neuropsychiatric expression. Mutations in four genes cause autosomal dominant PFBC: SLC20A2, XPR1, PDGFB and PDGFRB. Recently, biallelic mutations in the MYORG gene have been reported to cause PFBC with an autosomal recessive pattern of inheritance. We screened MYORG in 29 unrelated probands negatively screened for the autosomal dominant PFBC genes and identified 11 families with a biallelic rare or novel predicted damaging variant. We studied the clinical and radiological features of 16 patients of these 11 families and compared them to that of 102 autosomal dominant PFBC patients carrying a mutation in one of the four known autosomal dominant PFBC genes. We found that MYORG patients exhibited a high clinical penetrance with a median age of onset of 52 years (range: 21-62) with motor impairment at the forefront. In particular, dysarthria was the presenting sign in 11/16 patients. In contrast to patients with autosomal dominant PFBC, 12/15 (80%) symptomatic patients eventually presented at least four of the following five symptoms: dysarthria, cerebellar syndrome, gait disorder of any origin, akinetic-hypertonic syndrome and pyramidal signs. In addition to the most severe clinical pattern, MYORG patients exhibited the most severe pattern of calcifications as compared to the patients from the four autosomal dominant PFBC gene categories. Strikingly, 12/15 presented with brainstem calcifications in addition to extensive calcifications in other brain areas (lenticular nuclei, thalamus, cerebellar hemispheres, vermis, ±cortex). Among them, eight patients exhibited pontine calcifications, which were observed in none of the autosomal dominant PFBC patients and hence appeared to be highly specific. Finally, all patients exhibited cerebellar atrophy with diverse degrees of severity on CT scans. We confirmed the existence of cerebellar atrophy by performing MRI voxel-based morphometry analyses of MYORG patients with autosomal dominant PFBC mutation carriers as a comparison group. Of note, in three families, the father carried small pallido-dentate calcifications while carrying the mutation at the heterozygous state, suggesting a putative phenotypic expression in some heterozygous carriers. In conclusion, we confirm that MYORG is a novel major PFBC causative gene and that the phenotype associated with such mutations may be recognized based on pedigree, clinical and radiological features., (© The Author(s) (2019). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)
- Published
- 2019
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118. MEsenchymal StEm cells for Multiple Sclerosis (MESEMS): a randomized, double blind, cross-over phase I/II clinical trial with autologous mesenchymal stem cells for the therapy of multiple sclerosis.
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Uccelli A, Laroni A, Brundin L, Clanet M, Fernandez O, Nabavi SM, Muraro PA, Oliveri RS, Radue EW, Sellner J, Soelberg Sorensen P, Sormani MP, Wuerfel JT, Battaglia MA, and Freedman MS
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- Adolescent, Adult, Clinical Trials, Phase I as Topic, Clinical Trials, Phase II as Topic, Cross-Over Studies, Disability Evaluation, Double-Blind Method, Europe, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Multicenter Studies as Topic, Multiple Sclerosis diagnostic imaging, Multiple Sclerosis physiopathology, Randomized Controlled Trials as Topic, Recovery of Function, Time Factors, Transplantation, Autologous, Treatment Outcome, Young Adult, Mesenchymal Stem Cell Transplantation adverse effects, Multiple Sclerosis surgery
- Abstract
Background: Multiple sclerosis (MS) is an inflammatory disease of the central nervous system with a degenerative component, leading to irreversible disability. Mesenchymal stem cells (MSC) have been shown to prevent inflammation and neurodegeneration in animal models of MS, but no large phase II clinical trials have yet assessed the exploratory efficacy of MSC for MS., Methods/design: This is an academic, investigator-initiated, randomized, double-blind, placebo-compared phase I/II clinical trial with autologous, bone-marrow derived MSC in MS. Enrolled subjects will receive autologous MSC at either baseline or at week 24, through a cross-over design. Primary co-objectives are to test safety and efficacy of MSC treatment compared to placebo at 6 months. Secondary objectives will evaluate the efficacy of MSC at clinical and MRI levels. In order to overcome funding constraints, the MEsenchymal StEm cells for Multiple Sclerosis (MESEMS) study has been designed to merge partially independent clinical trials, following harmonized protocols and sharing some key centralized procedures, including data collection and analyses., Discussion: Results will provide patients and the scientific community with data on the safety and efficacy of MSC for MS. The innovative approach utilized to obtain funds to support the MESEMS trial could represent a new model to circumvent limitation of funds encountered by academic trials., Trial Registration: Andalusia: NCT01745783 , registered on Dec 10, 2012. Badalona: NCT02035514 EudraCT, 2010-024081-21. Registered on 2012. Canada: ClinicalTrials.gov, NCT02239393 . Registered on September 12, 2014. Copenhagen: EudraCT, 2012-000518-13 . Registered on June 21, 2012. Italy: EudraCT, 2011-001295-19, and ClinicalTrials.gov, NCT01854957 . Retrospectively registered on May 16, 2013. London: Eudra CT 2012-002357-35, and ClinicalTrials.gov, NCT01606215 . Registered on May 25, 2012. Salzburg: EudraCT, 2015-000137-78 . Registered on September 15, 2015. Stockholm: ClinicalTrials.gov, NCT01730547 . Registered on November 21, 2012. Toulouse: ClinicalTrials.gov, NCT02403947 . Registered on March 31, 2015.
- Published
- 2019
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119. Late-onset neutropenia and neurological relapse, during long-term rituximab therapy in myelin oligodendrocyte glycoprotein-antibody spectrum disorder.
- Author
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Biotti D, Lerebours F, Bonneville F, Ciron J, Clanet M, and Brassat D
- Subjects
- Adult, Autoantibodies immunology, Autoantigens immunology, Female, Humans, Male, Middle Aged, Myelin-Oligodendrocyte Glycoprotein immunology, Neuromyelitis Optica immunology, Neuromyelitis Optica pathology, Recurrence, Immunologic Factors adverse effects, Neuromyelitis Optica drug therapy, Neutropenia chemically induced, Rituximab adverse effects
- Abstract
Late-onset neutropenia after rituximab therapy (LONART) is defined as a fall in the absolute neutrophil count below 500/mm
3 at least 3 weeks after rituximab infusion, in the absence of any other explanation. LONART is rare during dysimmune conditions but can be life-threatening. We report on two patients with LONART and associated neurological relapse occurring in myelin oligodendrocyte glycoprotein (MOG)-antibody spectrum disorders. Rituximab was reintroduced in one patient, while the second patient was switched to tocilizumab. LONART can occur during anti-MOG spectrum disorders. Neurologists should be aware of this rare and treatable complication. Regular monitoring of blood cell counts is needed, and patients should be informed of the need to consult their physician if symptoms of infection appear.- Published
- 2018
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120. ECTRIMS/EAN Guideline on the pharmacological treatment of people with multiple sclerosis.
- Author
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Montalban X, Gold R, Thompson AJ, Otero-Romero S, Amato MP, Chandraratna D, Clanet M, Comi G, Derfuss T, Fazekas F, Hartung HP, Havrdova E, Hemmer B, Kappos L, Liblau R, Lubetzki C, Marcus E, Miller DH, Olsson T, Pilling S, Selmaj K, Siva A, Sorensen PS, Sormani MP, Thalheim C, Wiendl H, and Zipp F
- Subjects
- Humans, Consensus, Evidence-Based Medicine standards, Immunologic Factors administration & dosage, Immunomodulation, Multiple Sclerosis drug therapy, Practice Guidelines as Topic standards
- Abstract
Background: Multiple sclerosis (MS) is a complex disease with new drugs becoming available in the past years. There is a need for a reference tool compiling current data to aid professionals in treatment decisions., Objectives: To develop an evidence-based clinical practice guideline for the pharmacological treatment of people with MS., Methods: This guideline has been developed using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) methodology and following the updated EAN recommendations. Clinical questions were formulated in Patients-Intervention-Comparator-Outcome (PICO) format and outcomes were prioritized. The quality of evidence was rated into four categories according to the risk of bias. The recommendations with assigned strength (strong and weak) were formulated based on the quality of evidence and the risk-benefit balance. Consensus between the panelists was reached by use of the modified nominal group technique., Results: A total of 10 questions were agreed, encompassing treatment efficacy, response criteria, strategies to address suboptimal response and safety concerns and treatment strategies in MS and pregnancy. The guideline takes into account all disease-modifying drugs approved by the European Medicine Agency (EMA) at the time of publication. A total of 21 recommendations were agreed by the guideline working group after three rounds of consensus., Conclusion: The present guideline will enable homogeneity of treatment decisions across Europe.
- Published
- 2018
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121. [Towards a national strategy on the diagnosis of neurocognitive disorders. A shared approach among the French National College of General Practitioners and specialists of neurocognitive disorders].
- Author
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Krolak-Salmon P, Letrilliart L, Ceccaldi M, Andrieu S, Guérin O, Dubois B, Brochet B, Vandel P, Jeandel C, Leperre-Desplanques A, Clanet M, and Druais PL
- Subjects
- Activities of Daily Living, Aged, 80 and over, Algorithms, Biomarkers cerebrospinal fluid, Dementia cerebrospinal fluid, Dementia diagnosis, Dementia epidemiology, Diagnosis, Differential, France epidemiology, General Practice, Humans, Interdisciplinary Communication, Mental Disorders diagnosis, Mental Status and Dementia Tests, Neurocognitive Disorders epidemiology, Neurocognitive Disorders prevention & control, Neurocognitive Disorders therapy, Neuroimaging, Neurologic Examination, Health Policy, Medicine, Neurocognitive Disorders diagnosis, Societies, Medical
- Abstract
Neurocognitive disorders leading to progressive cognitive, functional and behavioural impairment are often undiagnosed or diagnosed lately. But tailored care and therapeutics help in implementing secondary and tertiary prevention dynamics aiming at preserving quality of life and delaying, anticipating or preventing behavioural crisis and severe stages of dementia. Moreover, the diagnosis of numerous diseases induces specific care and therapeutics, as well access to research and clinical trials. For the first time, the representatives of the National College of General Practitioners, the French Federation of Memory Centres, the French Federation of Gerontology and Geriatrics, the French Federation of Neurology, the French Society of Psychogeriatrics and the national plan on neurodegenerative diseases propose a graduated and tailored diagnosis strategy involving primary care and specialists of neurocognitive disorders. This strategy has been built in the context of the national plan on neurodegenerative diseases, the European Joint Action "Act on dementia", and has been consensually agreed after a seminar animated by the National College of General Practitioners in March 2017., (Copyright © 2017 Elsevier Masson SAS. All rights reserved.)
- Published
- 2018
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122. MD1003 (high-dose biotin) for the treatment of progressive multiple sclerosis: A randomised, double-blind, placebo-controlled study.
- Author
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Tourbah A, Lebrun-Frenay C, Edan G, Clanet M, Papeix C, Vukusic S, De Sèze J, Debouverie M, Gout O, Clavelou P, Defer G, Laplaud DA, Moreau T, Labauge P, Brochet B, Sedel F, and Pelletier J
- Subjects
- Adult, Biotin administration & dosage, Biotin adverse effects, Double-Blind Method, Female, Humans, Male, Middle Aged, Vitamin B Complex administration & dosage, Vitamin B Complex adverse effects, Biotin pharmacology, Disease Progression, Multiple Sclerosis, Chronic Progressive drug therapy, Outcome Assessment, Health Care, Vitamin B Complex pharmacology
- Abstract
Background: Treatment with MD1003 (high-dose biotin) showed promising results in progressive multiple sclerosis (MS) in a pilot open-label study., Objective: To confirm the efficacy and safety of MD1003 in progressive MS in a double-blind, placebo-controlled study., Methods: Patients (n = 154) with a baseline Expanded Disability Status Scale (EDSS) score of 4.5-7 and evidence of disease worsening within the previous 2 years were randomised to 12-month MD1003 (100 mg biotin) or placebo thrice daily, followed by 12-month MD1003 for all patients. The primary endpoint was the proportion of patients with disability reversal at month 9, confirmed at month 12, defined as an EDSS decrease of ⩾1 point (⩾0.5 for EDSS 6-7) or a ⩾20% decrease in timed 25-foot walk time compared with the best baseline among screening or randomisation visits., Results: A total of 13 (12.6%) MD1003-treated patients achieved the primary endpoint versus none of the placebo-treated patients (p = 0.005). MD1003 treatment also reduced EDSS progression and improved clinical impression of change compared with placebo. Efficacy was maintained over follow-up, and the safety profile of MD1003 was similar to that of placebo., Conclusion: MD1003 achieves sustained reversal of MS-related disability in a subset of patients with progressive MS and is well tolerated., Competing Interests: Declaration of Conflicting Interests: The author(s) declared the following potential conflicts of interest with respect to the research, authorship and/or publication of this article: Prof. Ayman Tourbah has received consulting fees, travel grants and reports institutional financial compensation for patient visits during the trial from MedDay Pharmaceuticals and consulting and lecturing fees, travel grants and research support from Biogen Idec, Sanofi-Genzyme, Novartis, Merck Serono, Teva Pharmaceuticals and Roche. Prof. Gilles Edan reports personal fees from Biogen Idec and Novartis and grants and personal fees from Merck Serono, Teva, Sanofi and Bayer, outside the submitted work. Prof. Sandra Vukusic reports clinical trial support from MedDay Pharmaceuticals, Biogen Idec, Merck Serono, Novartis, Roche, Sanofi-Aventis, Teva Pharmaceuticals and Genzyme; advisory or consultancy fees from Biogen Idec, Genzyme, Merck Serono, Novartis, Roche, Sanofi-Aventis and Teva Pharmaceuticals; and invited congress support from Biogen Idec, Merck Serono, Novartis and Genzyme. Prof. Jérôme De Sèze reports clinical trial support from MedDay Pharmaceuticals, Biogen Idec, Merck Serono, Bayer, LFB, UCB, AB Sciences, Sanofi-Aventis, Teva Pharmaceuticals and Genzyme; advisory or consultancy fees from Biogen Idec, Merck Serono, Bayer, LFB, Sanofi-Aventis, Teva Pharmaceuticals, Almirall and Allergan; and invited congress support from Biogen Idec, Merck Serono, Bayer, LFB, Sanofi-Aventis, Teva Pharmaceuticals, Genzyme and Allergan. Dr Olivier Gout reports personal fees and non-financial support from Biogen Idec, Teva Pharmaceuticals, Genzyme and Novartis and personal fees from Merck, outside the submitted work. Prof. Gilles Defer reports personal fees from Biogen Idec, Novartis, Sanofi-Aventis, Genzyme and Teva Pharmaceuticals; grants from Novartis, Merck Serono and Teva Pharmaceuticals; and funding for travel from Merck Serono, Biogen Idec, Guerbet, Sanofi-Aventis, Novartis, Genzyme and Teva Pharmaceuticals, outside the submitted work. Prof. David-Axel Laplaud reports personal fees from Biogen and Teva Pharmaceuticals and grants and personal fees from Novartis and Genzyme, outside the submitted work. Prof. Thibault Moreau reports personal fees and non-financial support from Biogen, Novartis, Sanofi-Genzyme, Bayer, Merck, Teva Pharmaceuticals and Almirall, outside the submitted work. Prof. Bruno Brochet received grants from MedDay Pharmaceuticals during the conduct of the study; personal fees and non-financial support from Biogen Idec, Novartis and Genzyme; grants from Merck Serono; grants, personal fees and non-financial support from Teva Pharmaceuticals; and grants and non-financial support from Bayer, outside the submitted work. Dr Frédéric Sedel is CEO and a shareholder at MedDay Pharmaceuticals (the study sponsor). Prof. Jean Pelletier has received consulting and lecturing fees, travel grants and unconditional research support from Biogen Idec, Sanofi-Genzyme, Novartis, Merck Serono and Teva Pharmaceuticals. Dr Christine Lebrun-Frenay, Prof. Michel Clanet, Dr Caroline Papeix, Prof. Marc Debouverie, Prof. Pierre Clavelou and Prof. Pierre Labauge have nothing to disclose., (© The Author(s), 2016.)
- Published
- 2016
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123. Risk of relapse after natalizumab withdrawal: Results from the French TYSEDMUS cohort.
- Author
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Papeix C, Vukusic S, Casey R, Debard N, Stankoff B, Mrejen S, Uhry Z, Van Ganse E, Castot A, Clanet M, Lubetzki C, and Confavreux C
- Abstract
Objective: To assess disease activity within 12 months after natalizumab (NZ) discontinuation in a large French postmarketing cohort., Methods: In France, patients exposed at least once to NZ were included in the TYSEDMUS observational and multicenter cohort, part of the French NZ Risk Management Plan. Clinical disease activity during the year following NZ discontinuation was assessed in this cohort. Time to first relapse after NZ stop was analyzed using Kaplan-Meier method and potentially associated factors were studied using a multivariate Cox model., Results: Out of the 4,055 patients with multiple sclerosis (MS) included in TYSEDMUS, 1,253 discontinued NZ and 715 of them had relevant data for our study. The probability of relapse within the year after NZ stop was estimated at 45% (95% confidence interval 0.41-0.49)., Conclusions: This large and systematic survey of patients with MS after NZ withdrawal allows quantifying the risk of increased disease activity following treatment discontinuation. This study provides large-scale, multicenter, systematic data after NZ cessation in real-life settings.
- Published
- 2016
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124. Fingolimod treatment after natalizumab-related progressive multifocal leukoencephalopathy: three new cases.
- Author
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Peaureaux D, Pignolet B, Biotti D, Bucciarelli F, Gaina J, Bucur C, Clanet M, Martin-Blondel G, and Brassat D
- Subjects
- Adult, Female, Humans, Immunologic Factors therapeutic use, JC Virus, Male, Multiple Sclerosis, Relapsing-Remitting drug therapy, Natalizumab therapeutic use, Fingolimod Hydrochloride therapeutic use, Immunologic Factors adverse effects, Immunosuppressive Agents therapeutic use, Leukoencephalopathy, Progressive Multifocal chemically induced, Leukoencephalopathy, Progressive Multifocal drug therapy, Multiple Sclerosis, Relapsing-Remitting complications, Natalizumab adverse effects
- Published
- 2015
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125. Adult-onset genetic leukoencephalopathies: a MRI pattern-based approach in a comprehensive study of 154 patients.
- Author
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Ayrignac X, Carra-Dalliere C, Menjot de Champfleur N, Denier C, Aubourg P, Bellesme C, Castelnovo G, Pelletier J, Audoin B, Kaphan E, de Seze J, Collongues N, Blanc F, Chanson JB, Magnin E, Berger E, Vukusic S, Durand-Dubief F, Camdessanche JP, Cohen M, Lebrun-Frenay C, Brassat D, Clanet M, Vermersch P, Zephir H, Outteryck O, Wiertlewski S, Laplaud DA, Ouallet JC, Brochet B, Goizet C, Debouverie M, Pittion S, Edan G, Deburghgraeve V, Le Page E, Verny C, Amati-Bonneau P, Bonneau D, Hannequin D, Guyant-Maréchal L, Derache N, Defer GL, Moreau T, Giroud M, Guennoc AM, Clavelou P, Taithe F, Mathis S, Neau JP, Magy L, Devoize JL, Bataillard M, Masliah-Planchon J, Dorboz I, Tournier-Lasserve E, Levade T, Boespflug Tanguy O, and Labauge P
- Subjects
- Adolescent, Adult, Age of Onset, Aged, Cerebrovascular Disorders genetics, Cerebrovascular Disorders pathology, Female, France, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Retrospective Studies, White Matter pathology, Young Adult, Leukoencephalopathies genetics, Leukoencephalopathies pathology
- Abstract
Inherited white matter diseases are rare and heterogeneous disorders usually encountered in infancy. Adult-onset forms are increasingly recognized. Our objectives were to determine relative frequencies of genetic leukoencephalopathies in a cohort of adult-onset patients and to evaluate the effectiveness of a systematic diagnostic approach. Inclusion criteria of this retrospective study were: (i) symmetrical involvement of white matter on the first available brain MRI; (ii) age of onset above 16 years. Patients with acquired diseases were excluded. Magnetic resonance imaging analysis identified three groups (vascular, cavitary and non-vascular/non-cavitary) in which distinct genetic and/or biochemical testing were realized. One hundred and fifty-four patients (male/female = 60/94) with adult-onset leukoencephalopathies were identified. Mean age of onset was 38.6 years. In the vascular group, 41/55 patients (75%) finally had a diagnosis [including CADASIL (cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy, n = 32) and COL4A1 mutation, n = 7]. In the cavitary group, 13/17 (76%) patients had a diagnosis of EIF2B-related disorder. In the third group (n = 82), a systematic biological screening allowed a diagnosis in 23 patients (28%) and oriented direct genetic screening identified 21 additional diseases (25.6%). Adult-onset genetic leukoencephalopathies are a rare but probably underestimated entity. Our study confirms the use of a magnetic resonance imaging-based classification with a final diagnosis rate of 64% (98/154) cases., (© The Author (2014). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)
- Published
- 2015
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126. Christian Confavreux (1949 - 2013).
- Author
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Weinshenker BG, Vukusic S, and Clanet MG
- Subjects
- France, History, 20th Century, History, 21st Century, Humans, Biomedical Research history, Multiple Sclerosis history, Neurology history
- Published
- 2013
- Full Text
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127. Prospective evaluation of laparoscopic assisted cystectomy and ileal conduit in advanced multiple sclerosis.
- Author
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Guillotreau J, Panicker JN, Castel-Lacanal E, Viala F, Roumiguié M, Malavaud B, Marque P, Clanet M, Rischmann P, and Gamé X
- Subjects
- Adult, Constriction, Pathologic etiology, Disability Evaluation, Female, Humans, Kidney physiology, Laparoscopy adverse effects, Lower Urinary Tract Symptoms etiology, Male, Middle Aged, Multiple Sclerosis physiopathology, Neurologic Examination, Pyelonephritis etiology, Surveys and Questionnaires, Ureter pathology, Cystectomy adverse effects, Lower Urinary Tract Symptoms surgery, Multiple Sclerosis complications, Quality of Life, Urinary Diversion adverse effects
- Abstract
Objective: To assess the morbidity, mortality, and impact on quality of life and renal function after laparoscopic cystectomy and ileal conduit in patients with multiple sclerosis with lower urinary tract symptom refractory to conservative management., Materials and Methods: A prospective study was conducted between February 2004 and December 2010 on 44 consecutive patients with multiple sclerosis who underwent laparoscopic cystectomy and ileal conduit for lower urinary tract symptom. Median Expanded Disability Status Scale score was 8 (6.5-8.5). Mean duration of multiple sclerosis was 19.3 ± 7.9 years. The quality of life was determined using the validated Qualiveen questionnaire preoperatively and at minimum 6 months after the surgery., Results: No conversion to open surgery was required. Postoperative morbidity rate was 18.2%; minor (Clavien ≤ 2) and major (Clavien ≥ 3) complications occurred in 13.6% and 6.8%, respectively. Mean follow-up was 44.5 ± 20.6 months. Complications noted were asymptomatic ureteroileal stenosis (n = 6) and pyelonephritis (n = 3). Neurological status and Expanded Disability Status Scale score remained stable throughout. Renal function remained unchanged. Limitations, constraints, and specific urinary impact index subscores of the Qualiveen were significantly improved at 6 months time., Conclusion: Laparoscopic cystectomy and ileal conduit for lower urinary tract symptom in advanced multiple sclerosis is a safe procedure with low complications. Neurological status and renal function remain stable and quality of life improves and continues to remain improved during long-term follow-up, suggesting this to be an attractive option in patients with advanced multiple sclerosis with lower urinary tract symptom refractory to conservative treatment., (Copyright © 2012 Elsevier Inc. All rights reserved.)
- Published
- 2012
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128. Natalizumab treatment for multiple sclerosis: updated recommendations for patient selection and monitoring.
- Author
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Kappos L, Bates D, Edan G, Eraksoy M, Garcia-Merino A, Grigoriadis N, Hartung HP, Havrdová E, Hillert J, Hohlfeld R, Kremenchutzky M, Lyon-Caen O, Miller A, Pozzilli C, Ravnborg M, Saida T, Sindic C, Vass K, Clifford DB, Hauser S, Major EO, O'Connor PW, Weiner HL, Clanet M, Gold R, Hirsch HH, Radü EW, Sørensen PS, and King J
- Subjects
- Animals, Antibodies, Monoclonal adverse effects, Antibodies, Monoclonal, Humanized, Drug Monitoring methods, Humans, Integrin alpha4beta1 antagonists & inhibitors, Leukoencephalopathy, Progressive Multifocal chemically induced, Leukoencephalopathy, Progressive Multifocal diagnosis, Natalizumab, Treatment Outcome, Antibodies, Monoclonal therapeutic use, Drug Monitoring standards, Multiple Sclerosis, Relapsing-Remitting drug therapy, Patient Selection, Practice Guidelines as Topic standards
- Abstract
Natalizumab, a highly specific α4-integrin antagonist, is approved for treatment of patients with active relapsing-remitting multiple sclerosis (RRMS). It is generally recommended for individuals who have not responded to a currently available first-line disease-modifying therapy or who have very active disease. The expected benefits of natalizumab treatment have to be weighed against risks, especially the rare but serious adverse event of progressive multifocal leukoencephalopathy. In this Review, we revisit and update previous recommendations on natalizumab for treatment of patients with RRMS, based on additional long-term follow-up of clinical studies and post-marketing observations, including appropriate patient selection and management recommendations., (Copyright © 2011 Elsevier Ltd. All rights reserved.)
- Published
- 2011
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129. Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria.
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Polman CH, Reingold SC, Banwell B, Clanet M, Cohen JA, Filippi M, Fujihara K, Havrdova E, Hutchinson M, Kappos L, Lublin FD, Montalban X, O'Connor P, Sandberg-Wollheim M, Thompson AJ, Waubant E, Weinshenker B, and Wolinsky JS
- Subjects
- Early Diagnosis, Humans, Magnetic Resonance Imaging, Sensitivity and Specificity, Multiple Sclerosis diagnosis
- Abstract
New evidence and consensus has led to further revision of the McDonald Criteria for diagnosis of multiple sclerosis. The use of imaging for demonstration of dissemination of central nervous system lesions in space and time has been simplified, and in some circumstances dissemination in space and time can be established by a single scan. These revisions simplify the Criteria, preserve their diagnostic sensitivity and specificity, address their applicability across populations, and may allow earlier diagnosis and more uniform and widespread use., (Copyright © 2011 American Neurological Association.)
- Published
- 2011
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130. Relevance of the skewness index in DTI exploration of multiple sclerosis.
- Author
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Graulières E, Lotterie JA, Cassol E, Gerdelat A, Clanet M, and Berry I
- Subjects
- Adult, Female, Humans, Image Enhancement methods, Male, Reproducibility of Results, Sensitivity and Specificity, Algorithms, Diffusion Magnetic Resonance Imaging methods, Image Interpretation, Computer-Assisted methods, Multiple Sclerosis pathology, Nerve Fibers, Myelinated pathology, Subtraction Technique
- Abstract
Object: To this day, no parameter can really monitor the progression of multiple sclerosis (MS). In this study, an index the skewness (S) derived from parameters calculated in diffusion tensor imaging (DTI) has been tested on MS patients for its ability to monitor the disease course., Materials and Methods: Eighteen patients underwent two examinations within 3 months consisting of a clinical evaluation (EDSS) and DTI acquisitions on a 1.5 T imager. Tensor was calculated thanks to"home-made" software. Mean diffusivity (MD) and fractional anisotropy (FA) histograms were described for normal-appearing white matter (NAWM) and gray matter (GM) of patients with S and also with usually indices peak position (pp) and peak height (ph) for the whole group of patients and for two separate groups according to their clinical status (EDSS < or = 3 and EDSS > 3 at month 0)., Results: Although no significant clinical evolution is observed over 3 months, S in GM showed a significant shift for both MD/FA histograms towards abnormal values for the whole group of patients (p = 0.02/p = 0.04) and for the group with EDSS = 3 (p = 0.04/p = 0.007), while ph and pp do not., Conclusion: S in GM could be an alternative marker to monitor the disease course before the repercussion on the clinical score.
- Published
- 2009
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131. MS treatment optimization: report from the 21st ETRIMS/10th ACTRIMS Congress, 28 September-1 October 2005, Thessaloniki, Greece.
- Author
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Clanet M and Hohlfeld R
- Subjects
- Humans, Immunologic Factors therapeutic use, Multiple Sclerosis pathology, Multiple Sclerosis physiopathology, Multiple Sclerosis therapy
- Abstract
Around 3500 international delegates were presented with a broad scientific programme at the joint meeting of the 21st ECTRIMS and 10th ACTRIMS congress held last September. The meeting focused on the heterogeneity of MS and optimizing MS treatment--from the earliest stages to the long-term management of this chronic disease--with the goal of improving patient outcome.
- Published
- 2006
132. Motivating MS patients: the Annual Convention 2005 of the MS Forum, 22 May 2005, St Julians, Malta.
- Author
-
Clanet M
- Subjects
- Humans, Motivation, Multiple Sclerosis drug therapy, Patient Compliance, Patient Education as Topic
- Abstract
Motivation is a key issue for everyone caring for people with MS. One needs to consider how best to motivate healthcare professionals so that optimum patient management is maintained over the long term. In addition, there is the aspect of patient motivation, so that people continue the treatments available to them. This report focuses on three plenary presentations given when the extended MS Forum group discussed patient motivation, during the Annual Convention 2005.
- Published
- 2005
133. Therapeutic developments in MS: report from the 57th Annual Meeting of the American Academy of Neurology (AAN), 9-15 April 2004, Miami, Florida, USA.
- Author
-
Clanet M
- Subjects
- Humans, Health Education, Multiple Sclerosis therapy, Neurology methods
- Abstract
Over 6000 neurologists and neuroscientists from around the world gathered in April at the 57th Annual Meeting of the American Academy of Neurology (AAN). There were several scientific platform sessions devoted to MS at the meeting, concentrating on recent clinical trials (including new natalizumab data), outcomes assessment, imaging, surrogate markers and mechanism of action of current therapeutics. During the meeting, the 2005 John Dystel Prize for MS Research was awarded to Jack Antel of McGill University, Montreal, Canada. Professor Antel was honoured for his major contributions to research into interactions between the immune system and the brain, and its application to MS, and for his role as a leading MS clinician and investigator. Additional activities devoted to MS were posters, educational courses and seminars covering a wide variety of topics. This report focuses on some of the key studies presented in the field of therapeutic developments in MS.
- Published
- 2005
134. Diffusion tensor imaging in multiple sclerosis: a tool for monitoring changes in normal-appearing white matter.
- Author
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Cassol E, Ranjeva JP, Ibarrola D, Mékies C, Manelfe C, Clanet M, and Berry I
- Subjects
- Adult, Anisotropy, Diffusion, Disease Progression, Female, Humans, Male, Middle Aged, Models, Biological, Nerve Fibers pathology, Brain pathology, Diffusion Magnetic Resonance Imaging methods, Multiple Sclerosis, Chronic Progressive pathology, Multiple Sclerosis, Relapsing-Remitting pathology
- Abstract
Our objectives were to determine the reproducibility of diffusion tensor imaging (DTI) in volunteers and to evaluate the ability of the method to monitor longitudinal changes occurring in the normal-appearing white matter (NAWM) of patients with multiple sclerosis (MS). DTI was performed three-monthly for one year in seven MS patients: three relapsing-remitting (RRMS), three secondary progressive (SPMS) and one relapsing SP. They were selected with a limited cerebral lesion load. Seven age- and sex-matched controls also underwent monthly examinations for three months. Diffusivity and anisotropy were quantified over the segmented whole supratentorial white matter, with the indices of trace (Tr) and fractional anisotropy (FA). Results obtained in volunteers show the reproducibility of the method. Patients had higher trace and lower anisotropy than matched controls (P < 0.0001). Over the follow-up, both Tr and FA indicated a recovery after the acute phase in RRMS and a progressive shift towards abnormal values in SPMS. Although this result is not statistically significant, it suggests that DTI is sensitive to microscopic changes occurring in tissue of normal appearance in conventional images and could be useful for monitoring the course of the disease, even though it was unable to clearly distinguish between the various physiopathological processes involved.
- Published
- 2004
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135. Genetic interaction of CTLA-4 with HLA-DR15 in multiple sclerosis patients.
- Author
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Alizadeh M, Babron MC, Birebent B, Matsuda F, Quelvennec E, Liblau R, Cournu-Rebeix I, Momigliano-Richiardi P, Sequeiros J, Yaouanq J, Genin E, Vasilescu A, Bougerie H, Trojano M, Martins Silva B, Maciel P, Clerget-Darpoux F, Clanet M, Edan G, Fontaine B, and Semana G
- Subjects
- Abatacept, Antigens, CD, CTLA-4 Antigen, Cohort Studies, DNA Primers genetics, Genetic Predisposition to Disease, HLA-DR Serological Subtypes, Humans, Immunoblotting, Polymerase Chain Reaction, Polymorphism, Genetic genetics, Promoter Regions, Genetic genetics, Antigens, Differentiation genetics, HLA-DR Antigens genetics, Immunoconjugates, Multiple Sclerosis genetics
- Abstract
Multiple sclerosis is a chronic inflammatory disease of the central nervous system with a genetic component. Until now, the more consistent association with the disease is found with the major histocompatibility complex, especially HLA-DRB1*1501-DQB1*0602 haplotype. In this report, we demonstrate the interaction of Cytotoxic T Lymphocyte-associated antigen 4 (CTLA-4 [CD152]) gene with DRB1*15 haplotype in multiple sclerosis genetic susceptibility. Our data were obtained from two European independent family-based studies including 610 multiple sclerosis family trios. Ann Neurol 2003;54:119-122
- Published
- 2003
- Full Text
- View/download PDF
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