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4. Capilaroscopia periungueal en el Grupo Español de Enfermedades Autoinmunes Sistémicas (GEAS). Resultados de una encuesta electrónica

Author

Luis Sáez-Comet, Patricia Fanlo-Mateo, Borja Gracia-Tello, José Antonio Todolí Parra, Mayka Freire-Dapena, Gerard Espinosa-Garriga, Begoña Marí Alfonso, Francisco García-Hernández, Alfredo Guillén del Castillo, Norberto Ortego Centeno, Juan José Ríos Blanco, Albert Selva-O’Callaghan, and Vicens Fonollosa Pla

Subjects
business.industry, Medicine, General Medicine, business, Humanities
Published
2020
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5. Nailfold capillaroscopy in the Spanish Group of Systemic Autoimmune Diseases (GEAS). Results of an electronic survey

Author

Luis Sáez-Comet, Patricia Fanlo-Mateo, Borja Gracia-Tello, José Antonio Todolí Parra, Mayka Freire-Dapena, Gerard Espinosa-Garriga, Begoña Marí Alfonso, Francisco García-Hernández, Alfredo Guillén del Castillo, Norberto Ortego Centeno, Juan José Ríos Blanco, Albert Selva-O’Callaghan, and Vicens Fonollosa Pla

Subjects
medicine.medical_specialty, business.industry, medicine, MEDLINE, business, Dermatology, Nailfold Capillaroscopy
Published
2020
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6. Delirium como síntoma de presentación atípico de lupus eritematoso sistémico

Author

Patricia Fanlo-Mateo, Vanesa Antoña-Sáenz, Amaia Redondo-Arriazu, Fernando Pérez-Nievas, and Laureano Menéndez-Ozcoidi

Abstract

El lupus eritematoso sistémico (LES) es una enfermedad autoinmune multisistémica que puede afectar al sistema nervioso central (SNC) y al sistema nervioso periférico (SNP) en forma de lupus neuropsiquiátrico (LES-NP). Hasta el 95% de los pacientes podrán desarrollar LES-NP en cualquier momento de la enfermedad. Múltiples factores (autoanticuerpos, microvasculopatía y citocinas proinflamatorias) se han asociado con su patogenia. El diagnóstico de LES-NP supone un reto para el clínico, ya que sólo se conseguirá el diagnóstico una vez que se hayan descartado otras causas. El manejo de esta patología se basa en el tratamiento sintomático asociado o no a inmunosupresores.

Published
2017
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7. Immunochip Analysis Identifies Multiple Susceptibility Loci for Systemic Sclerosis

Author

Maureen D. Mayes, Lara Bossini-Castillo, Olga Gorlova, José Ezequiel Martin, Xiaodong Zhou, Wei V. Chen, Shervin Assassi, Jun Ying, Filemon K. Tan, Frank C. Arnett, John D. Reveille, Sandra Guerra, María Teruel, Francisco David Carmona, Peter K. Gregersen, Annette T. Lee, Elena López-Isac, Eguzkine Ochoa, Patricia Carreira, Carmen Pilar Simeón, Iván Castellví, Miguel Ángel González-Gay, Alexandra Zhernakova, Leonid Padyukov, Marta Alarcón-Riquelme, Cisca Wijmenga, Matthew Brown, Lorenzo Beretta, Gabriela Riemekasten, Torsten Witte, Nicolas Hunzelmann, Alexander Kreuter, Jörg H.W. Distler, Alexandre E. Voskuyl, Annemie J. Schuerwegh, Roger Hesselstrand, Annika Nordin, Paolo Airó, Claudio Lunardi, Paul Shiels, Jacob M. van Laar, Ariane Herrick, Jane Worthington, Christopher Denton, Fredrick M. Wigley, Laura K. Hummers, John Varga, Monique E. Hinchcliff, Murray Baron, Marie Hudson, Janet E. Pope, Daniel E. Furst, Dinesh Khanna, Kristin Phillips, Elena Schiopu, Barbara M. Segal, Jerry A. Molitor, Richard M. Silver, Virginia D. Steen, Robert W. Simms, Robert A. Lafyatis, Barri J. Fessler, Tracy M. Frech, Firas AlKassab, Peter Docherty, Elzbieta Kaminska, Nader Khalidi, Henry Niall Jones, Janet Markland, David Robinson, Jasper Broen, Timothy R.D.J. Radstake, Carmen Fonseca, Bobby P. Koeleman, Javier Martin, Norberto Ortego-Centeno, Raquel Ríos, José Luis Callejas, Nuria Navarrete, Rosa García Portales, María Teresa Camps, Antonio Fernández-Nebro, María F. González-Escribano, Julio Sánchez-Román, Francisco José García-Hernández, María Jesús Castillo, María Ángeles Aguirre, Inmaculada Gómez-Gracia, Benjamín Fernández-Gutiérrez, Luis Rodríguez-Rodríguez, Esther Vicente, José Luis Andreu, Mónica Fernández de Castro, Paloma García de la Peña, Francisco Javier López-Longo, Lina Martínez, Vicente Fonollosa, Gerard Espinosa, Carlos Tolosa, Anna Pros, Mónica Rodríguez Carballeira, Francisco Javier Narváez, Manel Rubio Rivas, Vera Ortiz Santamaría, Bernardino Díaz, Luis Trapiella, María del Carmen Freire, Adrián Sousa, María Victoria Egurbide, Patricia Fanlo Mateo, Luis Sáez-Comet, Federico Díaz, Vanesa Hernández, Emma Beltrán, José Andrés Román-Ivorra, Elena Grau, Juan José Alegre Sancho, Francisco J. Blanco García, Natividad Oreiro, Luis Fernández Sueiro, Rheumatology, CCA - Disease profiling, Groningen Institute for Gastro Intestinal Genetics and Immunology (3GI), and Translational Immunology Groningen (TRIGR)

Subjects
Male, Linkage disequilibrium, systemic sclerosis, Genome-wide association study, immunochip array, DNASE-GAMMA, Linkage Disequilibrium, DISEASE, Autophagy-Related Protein 5, DEAD-box RNA Helicases, FUNCTIONAL POLYMORPHISM, 0302 clinical medicine, HLA Antigens, Risk Factors, Genetics(clinical), Genetics (clinical), Genetics, 0303 health sciences, HLA, Female, Chromosomes, Human, Pair 3, Microtubule-Associated Proteins, SNPs, GENETIC RISK-FACTOR, Genotype, Single-nucleotide polymorphism, Locus (genetics), Human leukocyte antigen, Biology, Polymorphism, Single Nucleotide, Article, Interleukin-12 Subunit p35, White People, 03 medical and health sciences, Proto-Oncogene Proteins, Microchip Analytical Procedures, LUPUS-ERYTHEMATOSUS, Humans, Genetic Predisposition to Disease, JAPANESE POPULATION, Allele, GENOME-WIDE ASSOCIATION, Alleles, 030304 developmental biology, Genetic association, 030203 arthritis & rheumatology, PRIMARY BILIARY-CIRRHOSIS, Endodeoxyribonucleases, Scleroderma, Systemic, Chromosomes, Human, Pair 11, Haplotype, DNASE1L3, RHEUMATOID-ARTHRITIS, Logistic Models, Genetic Loci, Case-Control Studies, Carrier Proteins, FOLLOW-UP, Genome-Wide Association Study
Abstract

In this study, 1,833 systemic sclerosis (SSc) cases and 3,466 controls were genotyped with the Immunochip array. Classical alleles, amino acid residues, and SNPs across the human leukocyte antigen (HLA) region were imputed and tested. These analyses resulted in a model composed of six polymorphic amino acid positions and seven SNPs that explained the observed significant associations in the region. In addition, a replication step comprising 4,017 SSc cases and 5,935 controls was carried out for several selected non-HLA variants, reaching a total of 5,850 cases and 9,401 controls of European ancestry. Following this strategy, we identified and validated three SSc risk loci, including DNASE1L3 at 3p14, the SCHIP1-IL12A locus at 3q25, and ATG5 at 6q21, as well as a suggested association of the TREH-DDX6 locus at 11q23. The associations of several previously reported SSc risk loci were validated and further refined, and the observed peak of association in PXK was related to DNASE1L3. Our study has increased the number of known genetic associations with SSc, provided further insight into the pleiotropic effects of shared autoimmune risk factors, and highlighted the power of dense mapping for detecting previously overlooked susceptibility loci.

Published
2014
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