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4. Autoantibody screening in Guillain-Barré syndrome

Author

Lleixà, Cinta, Martín-Aguilar, Lorena, Pascual-Goñi, Elba, Franco-Leyva, Teresa, Caballero, Marta, de Luna Salva, Noemí, Gallardo, Eduard, Suarez-Calvet, Xavier, Martínez-Martínez, Laura, Diaz-Manera, Jordi, Rojas-Garcia, Ricard, Cortés-Vicente, Elena, Turón, Joana, Casasnovas, Carlos, Homedes, C., Gutiérrez-Gutiérrez, G., Jimeno-Montero, M. C., Berciano, José, Sedano-Tous, M. J., García-Sobrino, Tania, Pardo, Julio, Márquez-Infante, C., Rojas-Marcos, I., Jericó, Ivonne, Martínez-Hernández, E., Morís, Germán, Domínguez-González, C., Juarez, Candido, Illa, Isabel, Querol, Luis, Universitat Autònoma de Barcelona, and Universidad de Cantabria

Subjects
Male, Cohort Studies, Pathogenesis, Ganglia, Spinal, Mass Screening, Prospective Studies, Neurons, biology, Guillain-Barre syndrome, General Neuroscience, Middle Aged, Guillain-Barré syndrome, Prognosis, medicine.anatomical_structure, Neurology, Nervous system--Diseases, Immunohistochemistry, Female, Antibody, Immunology, Immunocytochemistry, Immunoglobulins, Guillain-Barre Syndrome, Malalties del sistema nerviós, Cellular and Molecular Neuroscience, Antigen, Cell Line, Tumor, medicine, Guillain–Barré syndrome (GBS), Animals, Humans, RC346-429, Aged, Autoantibodies, Anti-ganglioside, business.industry, Research, Autoantibody, Nervous system Diseases, Neuron, medicine.disease, Rats, Spain, biology.protein, Macaca, Neurology. Diseases of the nervous system, Immunoglobulines, business
Abstract

Background Guillain–Barré syndrome (GBS) is an acute inflammatory neuropathy with a heterogeneous presentation. Although some evidences support the role of autoantibodies in its pathogenesis, the target antigens remain unknown in a substantial proportion of GBS patients. The objective of this study is to screen for autoantibodies targeting peripheral nerve components in Guillain–Barré syndrome. Methods Autoantibody screening was performed in serum samples from all GBS patients included in the International GBS Outcome study by 11 different Spanish centres. The screening included testing for anti-ganglioside antibodies, anti-nodo/paranodal antibodies, immunocytochemistry on neuroblastoma-derived human motor neurons and murine dorsal root ganglia (DRG) neurons, and immunohistochemistry on monkey peripheral nerve sections. We analysed the staining patterns of patients and controls. The prognostic value of anti-ganglioside antibodies was also analysed. Results None of the GBS patients (n = 100) reacted against the nodo/paranodal proteins tested, and 61 (61%) were positive for, at least, one anti-ganglioside antibody. GBS sera reacted strongly against DRG neurons more frequently than controls both with IgG (6% vs 0%; p = 0.03) and IgM (11% vs 2.2%; p = 0.02) immunodetection. No differences were observed in the proportion of patients reacting against neuroblastoma-derived human motor neurons. Reactivity against monkey nerve tissue was frequently detected both in patients and controls, but specific patterns were only detected in GBS patients: IgG from 13 (13%) patients reacted strongly against Schwann cells. Finally, we confirmed that IgG anti-GM1 antibodies are associated with poorer outcomes independently of other known prognostic factors. Conclusion Our study confirms that (1) GBS patients display a heterogeneous repertoire of autoantibodies targeting nerve cells and structures; (2) gangliosides are the most frequent antigens in GBS patients and have a prognostic value; (3) further antigen-discovery experiments may elucidate other potential antigens in GBS.

Published
2021

5. Intravenous immunoglobulin treatment for mild Guillain-Barré syndrome. An international observational study

Author

Verboon, C., Harbo, T., Cornblath, D. R., Hughes, R. A. C., Van Doorn, P. A., Lunn, M. P., Gorson, K. C., Barroso, F., Kuwabara, S., Galassi, G., Lehmann, H. C., Kusunoki, S., Reisin, R. C., Binda, D., Cavaletti, G., Andersen, Jacobs B. C. H., PhD (Aarhus University Hospital, Aarhus, Denmark), Attarian, S., PhD (CHU Timone, Marseille, France), Badrising, U. A., PhD (Leiden University Medical Centre, Leiden, The, Netherlands), Bateman, K., PhD (Groote Schuur Hospital, Cape, Town, South-Africa), Benedetti, L., PhD (Ospedale Sant’ Andrea La Spezia, Spezia, La, Italy), van den Berg, B., MD (Franciscus Gasthuis, Rotterdam, Van den Bergh, P., Luc, PhD (University Clinic St., Leuven, Belgium), Bertorini, T. E., MD (The University of Tennessee Health Science Center (UTHSC), Memphis, USA), Bhavaraju-Sanka, R., MD (University Hospital/ University of Texas Health Science Center, San Antonio Texas, USA), Bianco (Milan University, M., Humanitas Clinicala and Research Institute Milan, Briani, C., MD (University of Padova, Padova, Italy), Bürmann, J., MD (Universitätsklinikum des Saarlandes, Homburg, Germany), Casasnovas, C., Ciberer, PhD (Bellvitge University Hospital - IDIBELL Neurometabolic Diseases Group., Barcelona, Spain), Chao, C. C., PhD (National Taiwan University Hospital, Taipei, Taiwan), Chavada, G., PhD (Glasgow University, Glasgow, UK), Claeys, K. G., University Hospitals Leuven, PhD (1., Leuven, Belgium, KU Leuven, 2., Cosgrove, J. S., MD (Leeds General Infirmary, Leeds, UK), Dalakas, M. C., Thomas Jefferson University, MD (1., Philadelphia, Usa, National and Kapodistrian University of Athens, 2., Athens, Greece), Davidson, A., MD (University of Glasgow, van Dijk, G. W., MD (Canisius Wilhelmina Hospital, Nijmegen, Dardiotis, E., MD (University of Thessaly, Hospital of Larissa, Larissa, Greece), Derejko, M., MD (Odense University Hospital, Odense, Denmark), Dimachkie, M. M., MD (University of Kansas Medical Center, Kansas, City, Dornonville de la Cour, C., MD (National Hospital Copenhagen, Copenhagen, Denmark), Echaniz-Laguna, A., MD (Bicêtre University Hospital, Paris, France), Eftimov, F., PhD (Amsterdam University Medical Centre, Amsterdam, Faber, C. G., PhD (Maastricht University Medical Centre, Maastricht, Fazio, R., MD (Scientific Institute San Raffaele, Milan, Italy), Fulgenzi, J. Fehmi (University of Oxford E. A., MD (Hospital Cesar Milstein Buenos Aires, Buenos, Aires, Argentina), García-Sobrino, T., MD (Hospital Clínico de Santiago, Santiago de Compostela (A Coruña), Spain), Gijsbers, C. J., MD (Vlietland Hospital, Schiedam, Granit, V., MD (Montefiore Medical, Center, New, York, Grisanti, S., MD (Ospedale Sant’ Andrea La Spezia, Gutiérrez-Gutiérrez, G., MD (Hospital Universitario Infanta Sofia, San, Sebastian, Holbech, J. V., PhD (Odense University Hospital, Holt, J. K. L., Phd, FRCP (The Walton Centre, Liverpool, UK), Homedes, C., Ciberer, MD (Bellvitge University Hospital - IDIBELL Neurometabolic Diseases Group., Islam, B., PhD (International Centre for Diarrhoeal Disease Research, Bangladesh, (icddr, Dhaka, b), Bangladesh), Islam, Z., Jahan, I., PhD candidate (International Centre for Diarrhoeal Disease Research, Jericó Pascual, I., PhD (Complejo Hospitalario de Navarra, Pamplona, Spain), Karafiath, S., MD (University of Utah School of Medicine, Salt Lake City, Kerkhoff, H., PhD (Albert Schweitzer Hospital, Dordrecht, Kimpinski, K., MD (University Hospital, Lhsc, London-Ontario, Canada), Kohler, A., MD (Instituto de Investigaciones Neurológicas Raúl Carrea, Fleni, Kolb, N., MD (University of Vermont, Burlington, Vt, Kuitwaard, K., Albert Schweitzer Hospital, PhD (1., Erasmus MC, 2., Kuwahara, M., PhD (Kindai University, Osaka, Japan), Ladha, S. S., MD (Barrow Neurology Clinics, Phoenix, Arizona, Lee Pan, E., MBChB (Groote Schuur Hospital, Marfia, G. A., MD (Neurological Clinic, Policlinico Tor Vergata, Rome, Italy), Magot, A., MD (Reference Centre for NMD, Nantes University Hospital, France), Márquez Infante, C., MD (Hospital Universitario Virgen del Rocio, Seville, Spain), Martín-Aguilar, L., MD (Hospital de la Santa Creu, i Sant Pau, Universitat Autònoma de Barcelona, Martinez Hernandez, E., MD (Institut d’Investigacions Biomèdiques August Pi, i Sunyer (IDIBAPS), Hospital, Clinic, Mataluni, G., PhD (Neurological Clinic, Meekins, G., MD (University of Minnesota, Miller, J. A. L., PhD (Royal Victoria Infirmary, Newcastle, UK), Monges, M. S., Garrahan, MD (Hospital de Pediatría J. P., Nobile Orazio, E., PhD (Milan University, Pardal, A., MD (Hospital Britanico, Pardo Fernandez (Hospital Clínico de Santiago, J., Péréon, Y., PhD (Reference Centre for NMD, Pulley, M., MD (University of Florida, Jacksonville, USA), Querol Gutierrez, L., PhD (Hospital de la Santa Creu, i Sant Pau, Reddel, S. W., PhD (Concord Repatriation General Hospital, Sydney, Australia), van der Ree, T., (Westfriesgasthuis, Md, Hoorn, Rinaldi, S., Mbchb, Samijn, PhD (University of Oxford J. P. A., MD (Maasstad Hospital, Samukawa, M., Santoro, L., PhD (University Federico II, Napels, Italy), Savransky, A., Garrahan, PhD (Hospital de Pediatría J. P., Schwindling, L., Sedano Tous, M. J., MD (Hospital Universitario Marques de Valdecilla, Santander, Cantabria, Sekiguchi, Y., PhD (Chiba University, Chiba, Japan), Shahrizaila, N., MD (Neurology Unit, Department of Medicine, Faculty of Medicine, University of Malaya, Malaya), Silvestri, N. J., Sindrup, MD (Buffalo Jacobs School of Medicine S., Sommer, C. L., MD (Universitätsklinikum Würzburg, Würzburg, Germany), Spyropoulos (Royal Victoria Infirmary, A., Stein, B., Joseph’s Regional Medical Center, MD (St., Paterson, USA), Tan, C. Y., MRCP (Neurology Unit, Tankisi, H., Vermeij, F., Vytopil, M. V., Wirtz, PhD (Tufts University School of Medicine Lahey Hospital P. W., Phd, (HagaZiekenhuis, The, Hague, Waheed, W., MD (University of Vermont Medical Center, Burlington, Addington, USA). Other collaborators were:J. M., MD (University of Virginia, Charlottesville, USA), Ajroud-Driss, S., MD (Northwestern University Feinberg, Chicago, USA), Antonini, G., MD (Mental Health and Sensory Organs (NESMOS), Sapienza, University, Sant’Andrea, Hospital, Bella, I. R., MD (University of Mass Medical School, Worcester, USA), Brannagan, T. H., MD (Columbia University, New York City, Bunschoten, C., PhD candidate (Erasmus University Medical Centre, Busby, M., Bradford, UK), Butterworth, S., MD (Pinderfields Hospital, Wakefield, UK), Conti, M. E., MD (University Hospital Clinicas, Chen, S., Phd, (Rutgers, Robert Wood Johnson University Hospital, New, Brunswick, Doets, A., Feasby, T. E., MD (University of Calgary, Calgary, Canada), Fokke, C., MD (Gelre Hospital, Zutphen and Apeldoorn, Fujioka, T., MD (Toho University Medical Center, Tokyo, Japan), Garssen, M. P. J., PhD (Jeroen Bosch Hospital, Hertogenbosch, ’S, Gilchrist, J. M., MD (Soulthern Illinois University School of Medicine, Springfield, USA), Gilhuis, J., PhD (Reinier de Graaf Gasthuis, Delft, Goldstein, J. M., MD (Yale University School of Medicine, New, Haven, Goyal, N. A., MD (University of California, Irvine, USA), Hadden, R. D. M., PhD (King’s College Hospital, London, UK), Hsieh, S. T., Htut, M., George’s Hospital, MD (St., Illa, I., Jellema, K., PhD (Haaglanden Medisch Centrum, Kaida, K., PhD (National Defense Medical College, Saitama, Japan), Katzberg, H. D., MD (University of Toronto, Toronto, Canada), Kiers, L., MD (University of Melbourne, Royal Melbourne Hospital, Parkville, Australia), Kokubun, N., MD (Dokkyo Medical University, Tochigi, Japan), van Koningsveld, R., PhD (Elkerliek Hospital, Helmond and Deurne, van der Kooi, A. J., Kwan, J. Y., MD (University of Maryland School of Medicine, Baltimore, USA), Landschoff Lassen, L., MD (Glostrup Hospital, Glostrup, Denmark), Lawson, V., MD (Wexner Medical Center at The Ohio State University, Columbus, USA), Leonhard, S. E., Mandarakas, M., PhD (Erasmus University Medical Centre, Manji, H., FRCP (Ipswich Hospital, Ipswich, UK), Mattiazzi, M. G., MD (Hospital Militar Central, Mcdermott, C. J., MD (Royal Hallamshire Hospital, Nihr, Clinical, Sheffield, UK), Mohammad, Q. D., PhD (National Institute of Neurosciences and Hospital, Dhaka, Bangladesh), Morís de la Tassa, G., MD (Hospital UniversitarioCentral de Asturias, Asturias, Spain), Nascimbene, C., PhD (Luigi Sacco Hospital, Niks, E. H., Nowak, R. J., Osei-Bonsu, M., PhD (James Cook University Hospital, Middlesbrough, UK), Pascuzzi, R. M., MD (University of Indiana School of Medicine, Indianapolis, USA), Roberts, R. C., MD (Addenbrooke’s Hospital Cambridge, Cambridge, UK), Rojas-Marcos, I., MD (Hospital Univesitario Reina Sofia, Cordoba, Spain), Roodbol, J., Rudnicki, S. A., MD (University of Arkansas, Fayetteville, USA), Sachs, G. M., MD (University of Rhode Island, Providence, USA), Schenone, A., Department of Neurosciences, PhD (1., Rehabilitation, Ophthalmology, Genetics and Maternal and Infantile Sciences (DINOGMI), University of Genova, Genova, IRCCS Policlinico San Martino, Italy 2., Genova, Italy), Sheikh, K., PhD (The University of Texas Health Science Center at Houston, Houston, USA), Twydell, P., DO (Spectrum Health System, Grand, Rapids, Van Damme, P., PhD (University Hospital Leuven, Varrato, J. D., DO (Lehigh Valley Health Network, Allentown, USA), Visser, L. H., PhD (Elisabeth-TweeSteden Hospital, Tilburg and Waalwijk, Willison, H. J., PhD (University of Glasgow, van Woerkom (Erasmus MC, M., Zhou, L., PhD (Icahn School, Verboon, C, Harbo, T, Cornblath, D, Hughes, R, Van Doorn, P, Lunn, M, Gorson, K, Barroso, F, Kuwabara, S, Galassi, G, Lehmann, H, Kusunoki, S, Reisin, R, Binda, D, Cavaletti, G, Jacobs, B, consortium, IGOS, consortium, GOS, Neurosurgery, Neurology, and Immunology

Subjects
Adult, Male, medicine.medical_specialty, intravenous immunoglobulins, DIAGNOSIS, Guillain-Barre Syndrome, Settore MED/26, DISEASE, Disease course, Disability Evaluation, 03 medical and health sciences, 0302 clinical medicine, SDG 3 - Good Health and Well-being, hemic and lymphatic diseases, Internal medicine, Clinical endpoint, medicine, Humans, In patient, guillain-barré syndrome, 030212 general & internal medicine, NEUROPATHIES, biology, Guillain-Barre syndrome, business.industry, Guillain-Barré syndrome (GBS), treatment, course, Confounding, Immunoglobulins, Intravenous, Middle Aged, medicine.disease, Confidence interval, Psychiatry and Mental health, Treatment Outcome, biology.protein, Female, Surgery, Observational study, Neurology (clinical), Antibody, business, 030217 neurology & neurosurgery
Abstract

ObjectiveTo compare the disease course in patients with mild Guillain-Barré syndrome (GBS) who were treated with intravenous immunoglobulin (IVIg) or supportive care only.MethodsWe selected patients from the prospective observational International GBS Outcome Study (IGOS) who were able to walk independently at study entry (mild GBS), treated with one IVIg course or supportive care. The primary endpoint was the GBS disability score four weeks after study entry, assessed by multivariable ordinal regression analysis.ResultsOf 188 eligible patients, 148 (79%) were treated with IVIg and 40 (21%) with supportive care. The IVIg group was more disabled at baseline. IVIg treatment was not associated with lower GBS disability scores at 4 weeks (adjusted OR (aOR) 1.62, 95% CI 0.63 to 4.13). Nearly all secondary endpoints showed no benefit from IVIg, although the time to regain full muscle strength was shorter (28 vs 56 days, p=0.03) and reported pain at 26 weeks was lower (n=26/121, 22% vs n=12/30, 40%, p=0.04) in the IVIg treated patients. In the subanalysis with persistent mild GBS in the first 2 weeks, the aOR for a lower GBS disability score at 4 weeks was 2.32 (95% CI 0.76 to 7.13). At 1 year, 40% of all patients had residual symptoms.ConclusionIn patients with mild GBS, one course of IVIg did not improve the overall disease course. The certainty of this conclusion is limited by confounding factors, selection bias and wide confidence limits. Residual symptoms were often present after one year, indicating the need for better treatments in mild GBS.

Published
2021

7. Predicting Outcome in Guillain-Barré Syndrome

Author

Doets, Alex Y., Lingsma, Hester F., Walgaard, Christa, Islam, Badrul, Papri, Nowshin, Davidson, Amy, Yamagishi, Yuko, Kusunoki, Susumu, Dimachkie, Mazen M., Waheed, Waqar, Kolb, Noah, Islam, Zhahirul, Mohammad, Quazi Deen, Harbo, Thomas, Sindrup, Soren H., Chavada, Govindsinh, Willison, Hugh J., Casasnovas, Carlos, Bateman, Kathleen, Miller, James A.L., van den Berg, Bianca, Verboon, Christine, Roodbol, Joyce, Leonhard, Sonja E., Benedetti, Luana, Kuwabara, Satoshi, Van den Bergh, Peter, Monges, Soledad, Marfia, Girolama A., Shahrizaila, Nortina, Galassi, Giuliana, Péréon, Yann, Bürmann, Jan, Kuitwaard, Krista, Kleyweg, Ruud P., Marchesoni, Cintia, Sedano Tous, María J., Querol, Luis, Illa, Isabel, Wang, Yuzhong, Nobile-Orazio, Eduardo, Rinaldi, Simon, Schenone, Angelo, Pardo, Julio, Vermeij, Frederique H., Lehmann, Helmar C., Granit, Volkan, Cavaletti, Guido, Gutiérrez-Gutiérrez, Gerardo, Barroso, Fabio A., Visser, Leo H., Katzberg, Hans D., Dardiotis, Efthimios, Attarian, Shahram, van der Kooi, Anneke J., Eftimov, Filip, Wirtz, Paul W., Samijn, Johnny P.A., Gilhuis, H. Jacobus, Hadden, Robert D.M., Holt, James K.L., Sheikh, Kazim A., Karafiath, Summer, Vytopil, Michal, Antonini, Giovanni, Feasby, Thomas E., Faber, Catharina G., Gijsbers, Cees J., Busby, Mark, Roberts, Rhys C., Silvestri, Nicholas J., Fazio, Raffaella, van Dijk, Gert W., Garssen, Marcel P.J., Straathof, Chiara S.M., Gorson, Kenneth C., Jacobs, Bart C., Hughes, R.A.C., Cornblath, D.R., Hartung, H.P., van Doorn, P.A., de Koning, L.C., van Woerkom, M., Mandarakas, M., MPhty, BHIthSci(Hons), Reisin, R.C., Reddel, S.W., Ripellino, P., Hsieh, S.T., Addington, J.M., Ajroud-Driss, S., Andersen, H., Badrising, U.A., Bella, I.R., Bertorini, T.E., Bhavaraju-Sanka, R., Bianco, M., Brannagan, T.H., Briani, Chiara, Butterworth, S., Chao, C.C., Chen, S., Claeys, K.G., Conti, M.E., Cosgrove, J.S., Dalakas, M.C., Dornonville de la Cour, C., Echaniz-Laguna, A., Fehmi, J., Fokke, C., Fujioka, T., Fulgenzi, E.A., García-Sobrino, T., Gilchrist, J.M., Goldstein, J.M., Goyal, N.A., Grisanti, S.G., Gutman, L., Holbech, J.V., Homedes, C., Htut, M., Jellema, K., Pascual, I. Jericó, JimenoMontero, M.C., Kaida, K., Khoshnoodi, M., Kiers, L., Kimpinski, K., Köhler, A.A., Kokubun, N., Kuwahara, M., Kwan, J.Y., Ladha, S.S., Lassen, L. Landschoff, Lawson, V., Pan, E.B. Lee, Cejas, L. Léon, Lunn, M.P.T., Magot, A., Manji, H., Infante, C. Márquez, Martín-Aguilar, L., Hernandez, E. Martinez, Mataluni, G., Mattiazzi, M.G., McDermott, C.J., Meekins, G.D., Morís de la Tassa, G., Nascimbene, C., Nowak, R.J., Osei-Bonsu, M., Pascuzzi, R.M., Prada, V., Rojas-Marcos, I., Rudnicki, S.A., Sachs, G.M., Samukawa, M., Santoro, L., Savransky, A.G., Schwindling, L., Sekiguchi, Y., Sommer, C.L., Spyropoulos, A., Stein, B., Stino, A.M., Tan, C.Y., Tankisi, H., Twydell, P.T., van Damme, P., van der Ree, T., van Koningsveld, R., Varrato, J.D., Xing, C., Zhou, L., and Zivkovic, S.

Published
2022
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10. Clinical profile and satisfaction with anticoagulated treatment in patients with non-valvular atrial fibrillation attended in internal medicine and neurology departments of Spain,Perfil clínico y satisfacción con el tratamiento anticoagulante en pacientes con fibrilación auricular no valvular atendidos en consultas de medicina interna y neurología de España

Author

Reig-Roselló, G., Contreras, M. M., Suárez-Fernández, C., González-Hernández, A., Cardona, P., Pons-Amate, J. M., Martí-Fábregas, J., Vivancos, J., Pose, A., Díaz, J. A., Rodríguez, M., Pena, M., Arias, S., Larrosa, D., González, A., Rodríguez, E., González, M., Fernández, D., Barbagelata, C., Raña, N., Freire, S., Cerqueiro, J. M., Guerrero, H., Ramos, L., Álvarez, L., Lis, J. M., Caro, C., Seijo, M., Mederer, S., Zarraga, M. A., Ferreiro, J., Terrero, J. M., Arias, M., Pérez, R., Sánchez, J., Maciñeiras, J., Fernández, J., Jaén, F., Esteva, D., Zamora, M., Navarrete, N., García, J., Mérida, L., Corrales, M. A., Quirós, R., Cantero, J., Barrero, F. J., Villegas, I., Castro, J., Foronda, J., Carrillo, D., Vega, J., Trujillo, J. A., Montero, M., Jurado, A., Sánchez, C., Agüera-Morales, E., Sánchez, M., Durán, P., La Puerta, R. F., La Blanca, M. P., Martínez, M. P., Fernández, O., Tamayo, J. A., Bustamante, R., Serrano, P. J., Arjona, A., Payán, M., Gómez, R., Peña, D., Cabrerizo, E., Salgado, F., Georgieva, R. I., Gil-Núñez, A., Bello, E., Díaz, F., Medina, A., Castellano, A., Miranda, Y., Fabre, O., García Polo, I., Ibáñez, P., Sainz, C., Sierra, F., Aragón, E., Díaz, J., Aguilar, F., Ortega, M. A., Egido, J. A., Pontes, J. C., García, M. A., Cabrera, F., Batalla, B., Culla, A., Molina, C., Flores, A., Seró, L., Muchada, M., Meler, P., Sandra Boned Riera, Cánovas, D., Estela, J., Font, J., Purroy, F., Benabdelhak, I., Sanahuja, J., Roquer, J., Rodríguez, A., Ois, A., Cuadrado, E., Jiménez, J., Nogués, X., Kuprinski, J., Germán, A., Irigoyen, D., Cara, J. J., Font, M. A., Huertas, S., Martínez-Domeño, A., Arroyo, J. A., Delgado-Mederos, R., Gómez-Choco, M. J., Mengual, J. J., García, S. M., Castellanos, M. M., Eedenburg, C., Cañas, I., Espinosa, J., Montull, S., Quesada, H., Ustrell, X., Homedes, C., Navalpotro, I., Casanova, J., Lago, A. P., Morata, C., Gorriz, D., Moreno, I., Tembl, J., Ponz, A., Fonseca, M. J., Chamarro, R., Gil, R., Oliver, V., Pampliega, A., Artero, A., Puchades, F., Landete, L., Vilar, C., Jiménez, C., Vives, B., Moragues, M. D., Díaz, R., Tur, S., Escribano, J. B., Lucas, C., Martínez, F., Pons, J. M., Romero, A., García, D., Pérez, J., Villaverde, R., Martínez, S., Tejero, C., Pérez, C., Mostacero, E., Fernández, C., Luna, A., Pérez, T., González, F., Arce, A., Martínez, M., Díez, N., Gállego, J., Zandio, B., Herrera, M., Aymerich, N., Muñoz, R., Marta, J., Artal, J., Errea, J. M., Timiraos, J. J., Moreno, M. P., Freijo, M., García, J. M., Gil, M. C., Revilla, M. A., Palacio, E., Vázquez, J. L., Bestué, M., Latorre, A., Calvo, E., Ballester, L., Serrano, M., Juega, J. M., López, M. A., Irimia, P., Imaz, L., Fuentes, B., Sanz, B. E., Beltrán, L., Ruiz, G., Martínez, P., Sánchez, D., Barroso, E., Molina, I., Budiño, M. A., Masjuán, J., Felipe, A., Matute, C., Tejada, J., Morán, A., Fernández, E., Riveira, M. C., Carnedo, J., Manquillo, A., González, R., Fernández, J. C., Guillán, M., Yebra, M., Trejo, J. M., Saiz, J., Martínez-Acitores, J. C., Bravo, Y., Arenillas, J. F., Calleja, A., Cortijo, E., Reyes, J., López, L., Muñoz, P. L., Fidalgo, M. A., Hernández, J., Gómez, J. C., Morán, J. C., Gonzalo, S., Marrero, J., Satué, J. A., Belinchón, J. C., Moniche, F., Calderón, E., Escudero, I., La Torre, J., Casado, I., Antón, J., Portilla, J. C., Luengo, J., Rosal, J., Calzado, E., Anglada, J. C., Girón, J., Ramírez, J. M., Pijierro, A., Roa, A., Romero, J., Aguayo, M., Borrachero, C., Sanz, G., Gómez, M. J., Rico, M. A., Cayón, A., Carmona, E., Cerro, R., López, R., Aguirre, A., Lozano, F., and Rivera, J. M.

11. Quality of Life in Myasthenia Gravis and Correlation of MG-QOL15 with Other Functional Scales.

Author

Diez Porras L, Homedes C, Alberti MA, Velez Santamaria V, and Casasnovas C

Abstract

Health-related quality of life (HRQOL) in myasthenia gravis (MG) is frequently decreased. Further, there are many validated clinical scales and questionnaires to evaluate the clinical status in MG. We aimed to determine if there was an improvement in HRQOL following an intensive treatment for MG, identify which demographic and clinical features influenced patients' HRQOL, and investigate if the questionnaire MG-QOL15 correlated with other evaluation scales. We recruited 45 patients with generalised MG who were starting immunomodulatory treatment with intravenous immunoglobulins and prednisone for the first time. At each visit, we administered several validated scales for MG. The mean MG-QOL15 score improved significantly at 4 and 6 weeks of the study. Additionally, the MG-QOL15 score correlated strong with the Myasthenia Gravis-Activities of Daily Living (MG-ADL) and the Neuro-QOL Fatigue and weakest with the Quantitative Myasthenia Gravis Scoring System (QMG). The QMG score prior to study enrolment was associated with HRQOL. We observed that HRQOL in MG improved after receiving an intensive immunomodulatory treatment and achieving better control of the symptoms. The questionnaire MG-QOL15 correlated positively with other clinical measures. As MG is a fluctuating condition, and some symptoms are difficult to examine, we direct physicians toward the use of scales and questionnaires composed of items perceived by the patient.

Published
2022
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12. Autoantibody screening in Guillain-Barré syndrome.

Author

Lleixà C, Martín-Aguilar L, Pascual-Goñi E, Franco T, Caballero M, de Luna N, Gallardo E, Suárez-Calvet X, Martínez-Martínez L, Diaz-Manera J, Rojas-García R, Cortés-Vicente E, Turón J, Casasnovas C, Homedes C, Gutiérrez-Gutiérrez G, Jimeno-Montero MC, Berciano J, Sedano-Tous MJ, García-Sobrino T, Pardo-Fernández J, Márquez-Infante C, Rojas-Marcos I, Jericó-Pascual I, Martínez-Hernández E, Morís de la Tassa G, Domínguez-González C, Juárez C, Illa I, and Querol L

Subjects
Aged, Animals, Cell Line, Tumor, Cohort Studies, Female, Ganglia, Spinal metabolism, Ganglia, Spinal pathology, Guillain-Barre Syndrome epidemiology, Humans, Macaca, Male, Mass Screening methods, Middle Aged, Prospective Studies, Rats, Spain epidemiology, Autoantibodies blood, Guillain-Barre Syndrome blood, Guillain-Barre Syndrome diagnosis
Abstract

Background: Guillain-Barré syndrome (GBS) is an acute inflammatory neuropathy with a heterogeneous presentation. Although some evidences support the role of autoantibodies in its pathogenesis, the target antigens remain unknown in a substantial proportion of GBS patients. The objective of this study is to screen for autoantibodies targeting peripheral nerve components in Guillain-Barré syndrome., Methods: Autoantibody screening was performed in serum samples from all GBS patients included in the International GBS Outcome study by 11 different Spanish centres. The screening included testing for anti-ganglioside antibodies, anti-nodo/paranodal antibodies, immunocytochemistry on neuroblastoma-derived human motor neurons and murine dorsal root ganglia (DRG) neurons, and immunohistochemistry on monkey peripheral nerve sections. We analysed the staining patterns of patients and controls. The prognostic value of anti-ganglioside antibodies was also analysed., Results: None of the GBS patients (n = 100) reacted against the nodo/paranodal proteins tested, and 61 (61%) were positive for, at least, one anti-ganglioside antibody. GBS sera reacted strongly against DRG neurons more frequently than controls both with IgG (6% vs 0%; p = 0.03) and IgM (11% vs 2.2%; p = 0.02) immunodetection. No differences were observed in the proportion of patients reacting against neuroblastoma-derived human motor neurons. Reactivity against monkey nerve tissue was frequently detected both in patients and controls, but specific patterns were only detected in GBS patients: IgG from 13 (13%) patients reacted strongly against Schwann cells. Finally, we confirmed that IgG anti-GM1 antibodies are associated with poorer outcomes independently of other known prognostic factors., Conclusion: Our study confirms that (1) GBS patients display a heterogeneous repertoire of autoantibodies targeting nerve cells and structures; (2) gangliosides are the most frequent antigens in GBS patients and have a prognostic value; (3) further antigen-discovery experiments may elucidate other potential antigens in GBS., (© 2021. The Author(s).)

Published
2021
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13. Ulcerative jejunitis. Serious and uncommon manifestation in the outbreak of coeliac disease.

Author

García Mateo S, Velamazán Sandalinas R, Hijos Mallada G, Abad Baroja D, Hernández Ainsa M, Saura Blasco N, Laredo de la Torre V, Alfaro Almajano E, Cañamares Orbis P, Domper Arnal MJ, Sostres Homedes C, and Lausín JMB

Subjects
Enteritis diagnostic imaging, Enteritis drug therapy, Fatal Outcome, Humans, Jejunal Diseases diagnostic imaging, Jejunal Diseases drug therapy, Male, Middle Aged, Pulmonary Aspergillosis diagnosis, Tuberculosis, Pulmonary diagnosis, Ulcer diagnostic imaging, Ulcer drug therapy, Ulcer etiology, Celiac Disease complications, Enteritis etiology, Jejunal Diseases etiology
Published
2021
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14. Enteritis secondary to nivolumab, a growing cause of diarrhoea.

Author

Velamazan Sandalinas R, Laredo de la Torre V, García Mateo S, Abad Baroja D, Hijos Mallada G, Alfaro Almajano E, Cañamares Orbis P, Sostres Homedes C, Saura Blasco N, Hernández Ainsa M, and Domper MJ

Subjects
Aged, Humans, Male, Diarrhea chemically induced, Enteritis chemically induced, Nivolumab adverse effects
Published
2020
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15. Serum neurofilament light chain predicts long-term prognosis in Guillain-Barré syndrome patients.

Author

Martín-Aguilar L, Camps-Renom P, Lleixà C, Pascual-Goñi E, Díaz-Manera J, Rojas-García R, De Luna N, Gallardo E, Cortés-Vicente E, Muñoz L, Alcolea D, Lleó A, Casasnovas C, Homedes C, Gutiérrez-Gutiérrez G, Jimeno-Montero MC, Berciano J, Sedano-Tous MJ, García-Sobrino T, Pardo-Fernández J, Márquez-Infante C, Rojas-Marcos I, Jericó-Pascual I, Martínez-Hernández E, Morís de la Tassa G, Domínguez-González C, Illa I, and Querol L

Abstract

Objective: To study baseline serum neurofilament light chain (sNfL) levels as a prognostic biomarker in Guillain-Barré syndrome (GBS)., Methods: We measured NfL in serum (98 samples) and cerebrospinal fluid (CSF) (24 samples) of patients with GBS prospectively included in the International GBS Outcome Study (IGOS) in Spain using single-molecule array (SiMoA) and compared them with 53 healthy controls (HCs). We performed multivariable regression to analyse the association between sNfL levels and functional outcome at 1 year., Results: Patients with GBS had higher NfL levels than HC in serum (55.49 pg/mL vs 9.83 pg/mL, p<0.0001) and CSF (1308.5 pg/mL vs 440.24 pg/mL, p=0.034). Patients with preceding diarrhoea had higher sNfL than patients with respiratory symptoms or no preceding infection (134.90 pg/mL vs 47.86 pg/mL vs 38.02 pg/mL, p=0.016). sNfL levels correlated with Guillain-Barré Syndrome Disability Score and Inflammatory Rasch-built Overall Disability Scale (I-RODS) at every timepoint. Patients with pure motor variant and Miller Fisher syndrome showed higher sNfL levels than patients with sensorimotor GBS (162.18 pg/mL vs 95.50 pg/mL vs 38.02 pg/mL, p=0.025). Patients with acute motor axonal neuropathy cute motor axonal neuropathy had higher sNfL levels than other variants (190.55 pg/mL vs 46.79 pg/mL, p=0.013). sNfL returned to normal levels at 1 year. High baseline sNfL levels were associated with inability to run (OR=1.65, 95% CI 1.14 to 2.40, p=0.009) and lower I-RODS (β -2.60, 95% CI -4.66 to -0.54, p=0.014) at 1 year. Cut-off points predicting clinically relevant outcomes at 1 year with high specificity were calculated: inability to walk independently (>319 pg/mL), inability to run (>248 pg/mL) and ability to run (<34 pg/mL)., Conclusion: Baseline sNfL levels are increased in patients with GBS, are associated with disease severity and axonal variants and have an independent prognostic value in patients with GBS., Competing Interests: Competing interests: LAQ has provided expert testimony for Grifols, Sanofi-Genzyme, Novartis, UCB, Roche and CSL Behring and received research funds from Novartis Spain, Sanofi-Genzyme and Grifols. LM-A has received speaking honoraria from Roche. EP-G has received speaking honoraria from Roche and Biogen. JD-M has provided expert testimony for PTC and Sanofi-Genzyme, has been external advisor for Sanofi, Sarepta and Audentes and received research funds from Sanofi-Genzyme and Boehringer. DA participated in advisory boards from Fujirebio-Europe and Roche Diagnostics and received speaker honoraria from Fujirebio-Europe, Nutricia and from Krka Farmacéutica S.L. GG-G has received speaking honoraria from Sanofi-Genzyme, Takeda and has provided expert testimony for Biogen and CSL Behring. The other authors report no disclosures., (© Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.)

Published
2020
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16. Intravenous immunoglobulins may prevent prednisone-exacerbation in myasthenia gravis.

Author

Díez-Porras L, Homedes C, Alberti MA, Vélez-Santamaría V, and Casasnovas C

Subjects
Adult, Aged, Aged, 80 and over, Female, Humans, Male, Middle Aged, Immunoglobulins, Intravenous pharmacology, Myasthenia Gravis chemically induced, Myasthenia Gravis prevention & control, Prednisone adverse effects
Abstract

Corticosteroids may produce a paradoxical worsening of myasthenia gravis (MG) symptoms within the first weeks of treatment. We therefore wanted to assess the hypothesis that a prior infusion of intravenous immunoglobulin (IVIG) may have a protective effect. Our primary objectives were to show that the coadministration of immunoglobulins and glucocorticoids is safe and effective for controlling myasthenic symptoms, and to compare the exacerbation rate with this approach and historical practice without IVIG. We recruited 45 patients with generalized MG who required corticosteroids for the first time and we gave all IVIG before starting the full doses of prednisone. Monitoring was performed with validated scales, questionnaires, and blood tests over a 6-week period. Only 4.4% had severe adverse effects related to IVIG and 86.7% improved clinically. Notably, only 2.2% had a paradoxical symptom exacerbation in the first weeks of starting prednisone, which was statistically lower than the 42% reported in a historical series. We conclude that adjuvant therapy with IVIG when starting prednisone for the first time in patients with generalized MG is safe and effective. Given that the rate of paradoxical worsening was lower than that previously reported, the addition of IVIG may have a protective effect against such exacerbations.

Published
2020
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17. Eculizumab as a promising treatment in thymoma-associated myasthenia gravis.

Author

Vélez-Santamaría V, Nedkova V, Díez L, Homedes C, Alberti MA, and Casasnovas C

Abstract

Myasthenia gravis is a chronic autoimmune disorder caused by antibodies directed against the neuromuscular junction. Some patients may have an associated thymoma, which confers a worse prognosis. Eculizumab, a monoclonal antibody that inhibits the activation of terminal complement, has recently been approved for the treatment of refractory generalized myasthenia gravis. This is an early case report of thymoma-associated refractory myasthenia gravis successfully treated with eculizumab in a real-world setting., Competing Interests: Conflict of interest statement: The authors declare that there is no conflict of interest., (© The Author(s), 2020.)

Published
2020
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18. A novel mutation in the GFAP gene expands the phenotype of Alexander disease.

Author

Casasnovas C, Verdura E, Vélez V, Schlüter A, Pons-Escoda A, Homedes C, Ruiz M, Fourcade S, Launay N, and Pujol A

Subjects
Adolescent, Adult, Aged, Alexander Disease diagnostic imaging, Alexander Disease pathology, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Mutation genetics, Pedigree, Phenotype, Exome Sequencing, Young Adult, Alexander Disease diagnosis, Alexander Disease genetics, Glial Fibrillary Acidic Protein genetics
Abstract

Background: Alexander disease, an autosomal dominant leukodystrophy, is caused by missense mutations in GFAP . Although mostly diagnosed in children, associated with severe leukoencephalopathy, milder adult forms also exist., Methods: A family affected by adult-onset spastic paraplegia underwent neurological examination and cerebral MRI. Two patients were sequenced by whole exome sequencing (WES). A candidate variant was functionally tested in an astrocytoma cell line., Results: The novel variant in GFAP (Glial Fibrillary Acidic Protein) N-terminal head domain (p.Gly18Val) cosegregated in multiple relatives (LOD score: 2.7). All patients, even those with the mildest forms, showed characteristic signal changes or atrophy in the brainstem and spinal cord MRIs, and abnormal MRS. In vitro, this variant did not cause significant protein aggregation, in contrast to most Alexander disease mutations characterised so far. However, cell area analysis showed larger size, a feature previously described in patients and mouse models., Conclusion: We suggest that this variant causes variable expressivity and an attenuated phenotype of Alexander disease type II, probably associated with alternative pathogenic mechanisms, that is, astrocyte enlargement. GFAP analysis should be considered in adult-onset neurological presentations with pyramidal and bulbar symptoms, in particular when characteristic findings, such as the tadpole sign, are present in MRI. WES is a powerful tool to diagnose atypical cases., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2019. No commercial re-use. See rights and permissions. Published by BMJ.)

Published
2019
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20. Observational study of patients in Spain with amyotrophic lateral sclerosis: correlations between clinical status, quality of life, and dignity.

Author

Martínez-Campo Y, Homedes C, Lazaro A, Alarcón R, Campo D, Riera M, Domínguez R, Povedano M, and Casasnovas C

Subjects
Adult, Aged, Female, Humans, Male, Middle Aged, Prospective Studies, Psychometrics instrumentation, Psychometrics methods, Spain, Surveys and Questionnaires, Amyotrophic Lateral Sclerosis psychology, Health Status, Quality of Life psychology
Abstract

Background: Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease that dramatically affects patients' quality of life (QoL) and dignity of life (DoL). We aimed to study the impact of ALS on QoL and DoL and how these evolve throughout the duration of the disease., Methods: First, we performed an observational, descriptive study of 43 patients with ALS recruited from the ALS unit at our center and compared them with 20 healthy age- and sex-matched controls. Second, we performed a prospective cohort study, following up 23 patients with ALS over 3 months. All participants completed questionnaires about their functional status, QoL, and DoL., Results: QoL and DoL were significantly worse in the ALS group than in controls (both p < 0.001). During the three-month follow-up in the ALS cohort, statistically significant declines were observed in clinical status and QoL. For clinical status, median scores on the ALS Functional Rating scale changed from 30.95 points at baseline to 27.24 points after 3 months (p = 0.0003). For QoL, median scores on the ALS Assessment Questionnaire changed from 124.19 points at baseline to 131.81 at 3 months (p = 0.0062). However, no significant differences were found between the DoL scores at baseline (48.14 points) and 3 months (45 points) (p-value = 0.12)., Conclusions: ALS is a neurodegenerative disease that affects QoL and DoL alike. We found that clinical status and QoL both deteriorated in patients with ALS as the disease progressed, but that DoL was preserved. However, our findings are limited by small sample sizes. The preservation of DoL may be due to multiple factors, including the therapies provided by the ALS unit. These findings suggest that alongside QoL, DoL may be an important target in the management and care of ALS patients.

Published
2017
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