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43 results on '"Egurbide, M. V."'

1. First clinical symptom as a prognostic factor in systemic sclerosis: results of a retrospective nationwide cohort study

Author

Rubio-Rivas, Manuel, Corbella, Xavier, Pestaña-Fernández, Melany, Tolosa-Vilella, Carles, Guillen-del Castillo, Alfredo, Colunga-Argüelles, Dolores, Trapiella-Martínez, Luis, Iniesta-Arandia, Nerea, Castillo-Palma, María Jesús, Sáez-Comet, Luis, Egurbide-Arberas, María Victoria, Ortego-Centeno, Norberto, Freire, Mayka, Vargas-Hitos, Jose Antonio, Ríos-Blanco, Juan José, Todolí-Parra, Jose Antonio, Rodríguez-Carballeira, Mónica, Marín-Ballvé, Adela, Segovia-Alonso, Pablo, Pla-Salas, Xavier, Madroñero-Vuelta, Ana Belén, Ruiz-Muñoz, Manuel, Fonollosa-Pla, Vicent, Simeón-Aznar, Carmen Pilar, on behalf of RESCLE investigators, Autoimmune Diseases Study Group (GEAS), Callejas Moraga, E, Calvo, E., Carbonell, C., Castillo, M. J., Chamorro, A. J., Colunga, D., Corbella, X., Egurbide, M. V., Espinosa, G., Fonollosa, V., Freire, M., García Hernández, F. J., González León, R., Guillén del Castillo, A., Iniesta, N., Lorenzo, R., Madroñero, A. B., Marí, B., Marín, A., Ortego-Centeno, N., Pérez Conesa, M., Pestaña, M., Pla, X., Ríos Blanco, J. J., Rodríguez Carballeira, M., Rubio Rivas, M., Ruiz Muñoz, M., Sáez Comet, L., Segovia, P., Simeón, C. P., Soto, A., Tarí, E., Todolí, J. A., Tolosa, C., Trapiella, L., Vargas Hitos, J. A., and Verdejo, G.

Published
2018
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2. A replication study confirms the association of TNFSF4 (OX40L) polymorphisms with Systemic Sclerosis in a large European cohort

Author

Airó P, Lie B A, Palm Ø, Nordin A, Padykov L, Claes K, Denton C, Fonseca C, Madhok R, Shiels P, Chee M M, Schuerwegh A J, Voskuyl A E, De Langhe E, Westhovens R, Smith V, De Keyser F, Houssiau F, Koeleman B P, Coenen MJH, Witte T, Riemekasten G, Hesselstrand R, González-Gay M A, Pros A, García de la Peña P, Follonosa V, Egurbide M V, Fernández-Nebro A, Gallego M, Castellví I, García-Hernández F J, Gómez-Gracia I, Román-Ivorra J A, Tolosa C, Rodríguez L, Vicente-Rabaneda E, González-Escribano M F, Navarrete N, Camps M T, Carreira P, Espinosa G, Ortego-Centeno N, Vonk M C, Beretta L, Simeon C P, Broen JCA, Bossini-Castillo L, Scorza R, van Laar J M, Hunzelmann N, Kreuter A, Herrick A, Worthington J, Radstake TRDJ, Martín J, and Rueda B

Subjects
Medicine
Published
2010
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3. No evidence of association between functional polymorphisms located within IL6R and IL6ST genes and systemic sclerosis

Author

Cénit, M. C., Simeón, C. P., Fonollosa, V., Espinosa, G., Beltrán, E., Sáez-Comet, L., Vicente-Rabaneda, E., García-Hernández, F. J., Martínez-Estupiñán, L., Rodríguez-Carballeira, M., Hernández, V., de la Peña, P. G., Fernández-Castro, M., Narváez, F. J., Pros, A., Gallego, M., Ríos-Fernández, R., Camps, M. T., Fernández-Nebro, A., Egurbide, M. V., Carreira, P., González-Gay, M. A., and Martín, J.

Published
2012
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4. S.12.1 Is H1N1 influenza vaccine safe and effective in patients with SSc?

Author

Carmona, F., Gutala, R., Simeón, C. P., Carreira, P., Ortego Centeno, N., Vicente Rabaneda, E., García Hernández, F. J., García De La Peña, P., Fernández Castro, M., Martínez Estupiñán, L., Egurbide, M. V., Tsao, B. P, Gourh, P., Agarwal, S. K., Assassi, S., Mayes, M. D., Arnett, F. C., Tan, F. K., and Martín, J.

Published
2012

7. GWAS for systemic sclerosis identifies multiple risk loci and highlights fibrotic and vasculopathy pathways

Author

Lopez-Isac, Elena, Acosta-Herrera, Marialbert, Kerick, Martin, Assassi, Shervin, Satpathy, Ansuman T., Granja, Jeffrey, Mumbach, Maxwell R., Beretta, Lorenzo, Simeon, Carmen P., Carreira, Patricia, Ortego-Centeno, Norberto, Castellvi, Ivan, Bossini-Castillo, Lara, David Carmona, F., Orozco, Gisela, Hunzelmann, Nicolas, Distler, Joerg H. W., Franke, Andre, Lunardi, Claudio, Moroncini, Gianluca, Gabrielli, Armando, de Vries-Bouwstra, Jeska, Wijmenga, Cisca, Koeleman, Bobby P. C., Nordin, Annika, Padyukov, Leonid, Hoffmann-Vold, Anna-Maria, Lie, Benedicte, Rios, R., Callejas, J. L., Vargas-Hitos, J. A., Garcia-Portales, R., Camps, M. T., Fernandez-Nebro, A., Gonzalez-Escribano, M. F., Garcia-Hernandez, F. J., Castillo, M. J., Aguirre, M. A., Gomez-Gracia, I., Fernandez-Gutierrez, B., Rodriguez-Rodriguez, L., Garcia de la Pena, P., Vicente, E., Andreu, J. L., Fernandez de Castro, M., Lopez-Longo, F. J., Martinez, L., Fonollosa, V, Guillen, A., Espinosa, G., Tolosa, C., Pros, A., Rodriguez-Carballeira, M., Narvaez, F. J., Rubio-Rivas, M., Ortiz-Santamaria, V, Madronero, A. B., Gonzalez-Gay, M. A., Diaz, B., Trapiella, L., Sousa, A., Egurbide, M. V., Fanlo-Mateo, P., Saez-Comet, L., Diaz, F., Hernandez, V, Beltran, E., Roman-Ivorra, J. A., Grau, E., Alegre-Sancho, J. J., Freire, M., Blanco-Garcia, F. J., Oreiro, N., Witte, T., Kreuter, A., Riemekasten, G., Airo, P., Magro, C., Voskuyl, A. E., Vonk, M. C., Hesselstrand, R., Proudman, Susanna, Stevens, Wendy, Nikpour, Mandana, Zochling, J., Sahhar, J., Roddy, J., Nash, P., Tymms, K., Rischmueller, M., Lester, S., Vyse, Timothy, Herrick, Ariane L., Worthington, Jane, Denton, Christopher P., Allanore, Yannick, Brown, Matthew A., Radstake, Timothy R. D. J., Fonseca, Carmen, Chang, Howard Y., Mayes, Maureen D., Martin, Javier, Lopez-Isac, Elena, Acosta-Herrera, Marialbert, Kerick, Martin, Assassi, Shervin, Satpathy, Ansuman T., Granja, Jeffrey, Mumbach, Maxwell R., Beretta, Lorenzo, Simeon, Carmen P., Carreira, Patricia, Ortego-Centeno, Norberto, Castellvi, Ivan, Bossini-Castillo, Lara, David Carmona, F., Orozco, Gisela, Hunzelmann, Nicolas, Distler, Joerg H. W., Franke, Andre, Lunardi, Claudio, Moroncini, Gianluca, Gabrielli, Armando, de Vries-Bouwstra, Jeska, Wijmenga, Cisca, Koeleman, Bobby P. C., Nordin, Annika, Padyukov, Leonid, Hoffmann-Vold, Anna-Maria, Lie, Benedicte, Rios, R., Callejas, J. L., Vargas-Hitos, J. A., Garcia-Portales, R., Camps, M. T., Fernandez-Nebro, A., Gonzalez-Escribano, M. F., Garcia-Hernandez, F. J., Castillo, M. J., Aguirre, M. A., Gomez-Gracia, I., Fernandez-Gutierrez, B., Rodriguez-Rodriguez, L., Garcia de la Pena, P., Vicente, E., Andreu, J. L., Fernandez de Castro, M., Lopez-Longo, F. J., Martinez, L., Fonollosa, V, Guillen, A., Espinosa, G., Tolosa, C., Pros, A., Rodriguez-Carballeira, M., Narvaez, F. J., Rubio-Rivas, M., Ortiz-Santamaria, V, Madronero, A. B., Gonzalez-Gay, M. A., Diaz, B., Trapiella, L., Sousa, A., Egurbide, M. V., Fanlo-Mateo, P., Saez-Comet, L., Diaz, F., Hernandez, V, Beltran, E., Roman-Ivorra, J. A., Grau, E., Alegre-Sancho, J. J., Freire, M., Blanco-Garcia, F. J., Oreiro, N., Witte, T., Kreuter, A., Riemekasten, G., Airo, P., Magro, C., Voskuyl, A. E., Vonk, M. C., Hesselstrand, R., Proudman, Susanna, Stevens, Wendy, Nikpour, Mandana, Zochling, J., Sahhar, J., Roddy, J., Nash, P., Tymms, K., Rischmueller, M., Lester, S., Vyse, Timothy, Herrick, Ariane L., Worthington, Jane, Denton, Christopher P., Allanore, Yannick, Brown, Matthew A., Radstake, Timothy R. D. J., Fonseca, Carmen, Chang, Howard Y., Mayes, Maureen D., and Martin, Javier

Abstract

Systemic sclerosis (SSc) is an autoimmune disease that shows one of the highest mortality rates among rheumatic diseases. We perform a large genome-wide association study (GWAS), and meta-analysis with previous GWASs, in 26,679 individuals and identify 27 independent genome-wide associated signals, including 13 new risk loci. The novel associations nearly double the number of genome-wide hits reported for SSc thus far. We define 95% credible sets of less than 5 likely causal variants in 12 loci. Additionally, we identify specific SSc subtype-associated signals. Functional analysis of high-priority variants shows the potential function of SSc signals, with the identification of 43 robust target genes through HiChIP. Our results point towards molecular pathways potentially involved in vasculopathy and fibrosis, two main hallmarks in SSc, and highlight the spectrum of critical cell types for the disease. This work supports a better understanding of the genetic basis of SSc and provides directions for future functional experiments.

Published
2019

9. The Systemic Lupus Erythematosus IRF5 Risk Haplotype Is Associated with Systemic Sclerosis

Author

Carmona, F.D., Martín, J. E., Beretta, L., Simeón, Carmen P., Carreira, P., Callejas-Rubio, J. L., Fernández-Castro, Monica, Sáez-Comet, L., Beltrán, E., Camps, M. T., Egurbide, M. V., Airó, Paolo, Scorza, R., Lunardi, C., Hunzelmann, Nicolas, Riemekasten, G., Witte, Torsten, Kreuter, A., Distler, J. H., Madhok, R., Shiels, Paul G., Laar, Jacob M. van, Fonseca, C., Denton, C., Herrick, A., Worthington, J., Schuerwegh, A. J., Vonk, Madelon C., Voskuyl, Alexandre E., Radstake, T. R., and Martín, J.

Abstract

Systemic sclerosis (SSc) is a fibrotic autoimmune disease in which the genetic component plays an important role. One of the strongest SSc association signals outside the human leukocyte antigen (HLA) region corresponds to interferon (IFN) regulatory factor 5 (IRF5), a major regulator of the type I IFN pathway. In this study we aimed to evaluate whether three different haplotypic blocks within this locus, which have been shown to alter the protein function influencing systemic lupus erythematosus (SLE) susceptibility, are involved in SSc susceptibility and clinical phenotypes. For that purpose, we genotyped one representative single-nucleotide polymorphism (SNP) of each block (rs10488631, rs2004640, and rs4728142) in a total of 3,361 SSc patients and 4,012 unaffected controls of Caucasian origin from Spain, Germany, The Netherlands, Italy and United Kingdom. A meta-analysis of the allele frequencies was performed to analyse the overall effect of these IRF5 genetic variants on SSc. Allelic combination and dependency tests were also carried out. The three SNPs showed strong associations with the global disease (rs4728142: P = 1.34×10-8, OR = 1.22, CI 95% = 1.14-1.30; rs2004640: P = 4.60×10-7, OR = 0.84, CI 95% = 0.78-0.90; rs10488631: P = 7.53×10-20, OR = 1.63, CI 95% = 1.47-1.81). However, the association of rs2004640 with SSc was not independent of rs4728142 (conditioned P = 0.598). The haplotype containing the risk alleles (rs4728142*A-rs2004640*T-rs10488631*C: P = 9.04×10-22, OR = 1.75, CI 95% = 1.56-1.97) better explained the observed association (likelihood P-value = 1.48×10-4), suggesting an additive effect of the three haplotypic blocks. No statistical significance was observed in the comparisons amongst SSc patients with and without the main clinical characteristics. Our data clearly indicate that the SLE risk haplotype also influences SSc predisposition, and that this association is not sub-phenotype-specific. © 2013 Carmona et al.

Published
2013

10. Confirmation of CCR6 as a risk factor for anti-topoisomerase I antibodies in systemic sclerosis

Author

Ochoa, E., Martin, J. -E., Assassi, S., Beretta, L., Carreira, P., Guillen, A., Simeon, C. P., Koumakis, E., Dieude, P., Allanore, Y., Garcia-Hernandez, F. J., Espinosa, G., Castellvi, I., Trapiella, J. L., Rodriguez, L., Gonzalez-Gay, M. A., Egurbide, M. V., Saez, L., Callejas-Rubio, J. L., Vargas-Hitos, J. A., Hunzelmann, N., Riemekasten, G., Witte, T., Distler, J. H. W., Kreuter, A., Lunardi, C., Santaniello, A., Tan, F. K., Shiels, P. G., Herrick, A., Worthington, J., Vonk, M. C., Koeleman, B. P., Radstake, T. R. D. J., Mayes, M. D., Martin, J., Ochoa, E., Martin, J. -E., Assassi, S., Beretta, L., Carreira, P., Guillen, A., Simeon, C. P., Koumakis, E., Dieude, P., Allanore, Y., Garcia-Hernandez, F. J., Espinosa, G., Castellvi, I., Trapiella, J. L., Rodriguez, L., Gonzalez-Gay, M. A., Egurbide, M. V., Saez, L., Callejas-Rubio, J. L., Vargas-Hitos, J. A., Hunzelmann, N., Riemekasten, G., Witte, T., Distler, J. H. W., Kreuter, A., Lunardi, C., Santaniello, A., Tan, F. K., Shiels, P. G., Herrick, A., Worthington, J., Vonk, M. C., Koeleman, B. P., Radstake, T. R. D. J., Mayes, M. D., and Martin, J.

Abstract

Objective. The current knowledge of the influence of systemic sclerosis (SSc) risk loci in the clinical sub-phenotypes is still limited. The main limitation lies in the low frequency of some sub-phenotypes which could be solved by replication studies in independent cohorts and meta-analysis between studies. In this regard, CCR6 gene variants have been recently associated with anti-topoisomerase I positive (ATA+) production in SSc patients in a candidate gene study. This gene has been proposed to have a critical role in IL-17-driven autoimmunity in human diseases. Methods. In order to confirm the association between CCR6 and ATA+ SSc patients, we performed an independent replication study in populations of European ancestry. We studied two CCR6 genetic variants (rs968334 and rs3093024) in a total of 901 ATA+ SSc cases, 3,258 ATA- SSc cases and 7,865 healthy controls and compared allelic frequencies for those SNPs in ATA+ SSc with healthy controls and also with ATA- SSc patients. Results. The comparison performed between ATA+ SSc patients and healthy controls showed significant association with SNP rs968334 (p=4.88 x 10(-2), OR= 1.11). When we compared ATA+ SSc cases with ATA- SSc, both SNPs, rs3093024 and rs968334, showed significant associations (p=2.89 x 10(-2), OR-1.13; p=1.69 x 10(-2), OR=1.15). Finally, in order to increase even more sample size and statistical power, we meta-analysed our study with the previous reported and found a significant association between SNP rs3093024 and ATA+ SSc patients (p= 1.00 x 10(-4), OR= 1.16) comparing with healthy controls. Conclusion. Our work confirms the association of CCR6 gene and ATA+ SSc patients.

Published
2015

11. KCNA5 gene is not confirmed as a systemic sclerosis-related pulmonary arterial hypertension genetic susceptibility factor

Author

Bossini-Castillo, L., Simeón, Carmen P., Beretta, L., Broen, Jasper C., Vonk, Madelon C., Callejas-Rubio, J. L., Carreira, P., Rodríguez-Rodríguez, Luis, García-Portales, Rosa, González-Gay, M. A., Castellví, I., Camps, M. T., Tolosa, Carlos, Vicente, Esther, Egurbide, M. V., Spanish Scleroderma Group, Schuerwegh, A. J., Hesselstrand, R., Lunardi, C., Laar, Jacob M. van, Shiels, Paul G., Herrick, A., Worthington, J., Denton, C., Radstake, T. R., Fonseca, C., Martín, J., Bossini-Castillo, L., Simeón, Carmen P., Beretta, L., Broen, Jasper C., Vonk, Madelon C., Callejas-Rubio, J. L., Carreira, P., Rodríguez-Rodríguez, Luis, García-Portales, Rosa, González-Gay, M. A., Castellví, I., Camps, M. T., Tolosa, Carlos, Vicente, Esther, Egurbide, M. V., Spanish Scleroderma Group, Schuerwegh, A. J., Hesselstrand, R., Lunardi, C., Laar, Jacob M. van, Shiels, Paul G., Herrick, A., Worthington, J., Denton, C., Radstake, T. R., Fonseca, C., and Martín, J.

Abstract

Introduction Potassium voltage-gated channel shaker-related subfamily member 5 (KCNA5) is implicated in vascular tone regulation, and its inhibition during hypoxia produces pulmonary vasoconstriction. Recently, a protective association of the KCNA5 locus with systemic sclerosis (SSc) patients with pulmonary arterial hypertension (PAH) was reported. Hence, the aim of this study was to replicate these findings in an independent multicenter Caucasian SSc cohort. Methods The 2,343 SSc cases (179 PAH positive, confirmed by right-heart catheterization) and 2,690 matched healthy controls from five European countries were included in this study. Rs10744676 single-nucleotide polymorphism (SNP) was genotyped by using a TaqMan SNP genotyping assay. Results Individual population analyses of the selected KCNA5 genetic variant did not show significant association with SSc or any of the defined subsets (for example, limited cutaneous SSc, diffuse cutaneous SSc, anti-centromere autoantibody positive and anti-topoisomerase autoantibody positive). Furthermore, pooled analyses revealed no significant evidence of association with the disease or any of the subsets, not even the PAH-positive group. The comparison of PAH-positive patients with PAH-negative patients showed no significant differences among patients. Conclusions Our data do not support an important role of KCNA5 as an SSc-susceptibility factor or as a PAH-development genetic marker for SSc patients.

Published
2012

12. A replication study confirms the association of TNFSF4 (OX40L) polymorphisms with systemic sclerosis in a large European cohort.

Author

Bossini-Castillo, L., Broen, Jasper C., Simeón, Carmen P., Beretta, L., Vonk, Madelon C., Ortego-Centeno, N., Espinosa, Gerard, Carreira, P., Camps, M. T., Navarrete, N., González-Escribano, María Francisca, Vicente, Esther, Rodríguez-Rodríguez, Luis, Tolosa, Carlos, Román-Ivorra, J. A., Gómez-Gracía, I., García-Hernández, Francisco José, Castellví, I., Gallego, María, Fernández-Nebro, Antonio, García-Portales, Rosa, Egurbide, M. V., Fonollosa, V., García de la Peña, P., Pros, A., González-Gay, M. A., Hesselstrand, R., Riemekasten, G., Witte, Torsten, Coenen, M. J., Koeleman, B. P., Houssiau, F., Smith, V., Keyser, F. de, Westhovens, R., Langhe, E. de, Voskuyl, Alexandre E., Schuerwegh, A. J., Chee, M. M., Madhok, R., Shiels, Paul G., Fonseca, C., Denton, C., Claes, K., Padyukov, Leonid, Nordin, A., Palm, Øyvind, Lie, B. A., Airó, Paolo, Scorza, R., Laar, Jacob M. van, Hunzelmann, Nicolas, Kreuter, A., Herrick, A., Worthington, J., Radstake, T. R., Martín, J., Rueda, B., Bossini-Castillo, L., Broen, Jasper C., Simeón, Carmen P., Beretta, L., Vonk, Madelon C., Ortego-Centeno, N., Espinosa, Gerard, Carreira, P., Camps, M. T., Navarrete, N., González-Escribano, María Francisca, Vicente, Esther, Rodríguez-Rodríguez, Luis, Tolosa, Carlos, Román-Ivorra, J. A., Gómez-Gracía, I., García-Hernández, Francisco José, Castellví, I., Gallego, María, Fernández-Nebro, Antonio, García-Portales, Rosa, Egurbide, M. V., Fonollosa, V., García de la Peña, P., Pros, A., González-Gay, M. A., Hesselstrand, R., Riemekasten, G., Witte, Torsten, Coenen, M. J., Koeleman, B. P., Houssiau, F., Smith, V., Keyser, F. de, Westhovens, R., Langhe, E. de, Voskuyl, Alexandre E., Schuerwegh, A. J., Chee, M. M., Madhok, R., Shiels, Paul G., Fonseca, C., Denton, C., Claes, K., Padyukov, Leonid, Nordin, A., Palm, Øyvind, Lie, B. A., Airó, Paolo, Scorza, R., Laar, Jacob M. van, Hunzelmann, Nicolas, Kreuter, A., Herrick, A., Worthington, J., Radstake, T. R., Martín, J., and Rueda, B.

Abstract

Objectives: The aim of this study was to confirm the influence of TNFSF4 polymorphisms on systemic sclerosis (SSc) susceptibility and phenotypic features. Methods: A total of 8 European populations of Caucasian ancestry were included, comprising 3014 patients with SSc and 3125 healthy controls. Four genetic variants of TNFSF4 gene promoter (rs1234314, rs844644, rs844648 and rs12039904) were selected as genetic markers. Results: A pooled analysis revealed the association of rs1234314 and rs12039904 polymorphisms with SSc (OR 1.15, 95% CI 1.02 to 1.31; OR 1.18, 95% CI 1.08 to 1.29, respectively). Significant association of the four tested variants with patients with limited cutaneous SSc (lcSSc) was revealed (rs1234314 OR 1.22, 95% CI 1.07 to 1.38; rs844644 OR 0.91, 95% CI 0.83 to 0.99; rs844648 OR 1.10, 95% CI 1.01 to 1.20 and rs12039904 OR 1.20, 95% CI 1.09 to 1.33). Association of rs1234314, rs844648 and rs12039904 minor alleles with patients positive for anti-centromere antibodies (ACA) remained significant (OR 1.23, 95% CI 1.10 to 1.37; OR 1.12, 95% CI 1.01 to 1.25; OR 1.22, 95% CI 1.07 to 1.38, respectively). Haplotype analysis confirmed a protective haplotype associated with SSc, lcSSc and ACA positive subgroups (OR 0.88, 95% CI 0.82 to 0.96; OR 0.88, 95% CI 0.80 to 0.96; OR 0.86, 95% CI 0.77 to 0.97, respectively) and revealed a new risk haplotype associated with the same groups of patients (OR 1.14, 95% CI 1.03 to 1.26; OR 1.20, 95% CI 1.08 to 1.35; OR 1.23, 95% CI 1.07 to 1.42, respectively). Conclusions: The data confirm the influence of TNFSF4 polymorphisms in SSc genetic susceptibility, especially in subsets of patients positive for lcSSc and ACA.

Published
2011

13. Confirmation of association of the macrophage migration inhibitory factor gene with systemic sclerosis in a large European population.

Author

Bossini-Castillo, L., Simeón, Carmen P., Beretta, L., Vo, M. C., Callejas-Rubio, J. L., Espinosa, Gerard, Carreira, P., Camps, M. T., Rodríguez-Rodríguez, Luis, Rodríguez-Carballeira, Mónica, García-Hernández, Francisco José, López-Longo, Francisco Javier, Hernández-Hernández, V., Sáez-Comet, L., Egurbide, M. V., Hesselstrand, R., Nordin, A., Hoffmann-Vold, A. M., Vanthuyne, M., Smith, V., Langhe, E. de, Kreuter, A., Riemekasten, G., Witte, Torsten, Hunzelmann, Nicolas, Voskuyl, Alexandre E., Schuerwegh, A. J., Lunardi, C., Airó, Paolo, Scorza, R., Shiels, Paul G., Laar, Jacob M. van, Fonseca, C., Denton, C., Herrick, A., Worthington, J., Koeleman, B. P., Rueda, B., Radstake, T. R., Martín, J., Bossini-Castillo, L., Simeón, Carmen P., Beretta, L., Vo, M. C., Callejas-Rubio, J. L., Espinosa, Gerard, Carreira, P., Camps, M. T., Rodríguez-Rodríguez, Luis, Rodríguez-Carballeira, Mónica, García-Hernández, Francisco José, López-Longo, Francisco Javier, Hernández-Hernández, V., Sáez-Comet, L., Egurbide, M. V., Hesselstrand, R., Nordin, A., Hoffmann-Vold, A. M., Vanthuyne, M., Smith, V., Langhe, E. de, Kreuter, A., Riemekasten, G., Witte, Torsten, Hunzelmann, Nicolas, Voskuyl, Alexandre E., Schuerwegh, A. J., Lunardi, C., Airó, Paolo, Scorza, R., Shiels, Paul G., Laar, Jacob M. van, Fonseca, C., Denton, C., Herrick, A., Worthington, J., Koeleman, B. P., Rueda, B., Radstake, T. R., and Martín, J.

Abstract

The aim of this study was to confirm the implication of macrophage migration inhibitory factor (MIF) gene in SSc susceptibility or clinical phenotypes in a large European population.

Published
2011

14. Low-dose aspirin vs low-dose aspirin plus low-intensity warfarin in thromboprophylaxis: a prospective, multicentre, randomized, open, controlled trial in patients positive for antiphospholipid antibodies (ALIWAPAS)

Author

Cuadrado, M. J., primary, Bertolaccini, M. L., additional, Seed, P. T., additional, Tektonidou, M. G., additional, Aguirre, A., additional, Mico, L., additional, Gordon, C., additional, Ruiz-Irastorza, G., additional, Egurbide, M. V., additional, Gil, A., additional, Espinosa, G., additional, Houssiau, F., additional, Rahman, A., additional, Martin, H., additional, McHugh, N., additional, Galindo, M., additional, Akil, M., additional, Amigo, M. C., additional, Murru, V., additional, and Khamashta, M. A., additional

Published
2013
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16. S.12.1 Is H1N1 influenza vaccine safe and effective in patients with SSc?

Author

Andrade, D., primary, Seguro, L., additional, Ribeiro, A., additional, Moraes, J., additional, Saad, C., additional, Aikawa, N., additional, Calich, A., additional, Viana, V., additional, Pasoto, S., additional, Levy-Neto, M., additional, Laurindo, I., additional, Timenestsky, M., additional, Precioso, A., additional, Bonfa, E., additional, Sampaio-Barros, P., additional, Wang, J. C., additional, Assassi, S., additional, Guo, G., additional, Tu, W. Z., additional, Tan, F. K., additional, Mayes, M. D., additional, Reveille, J. D., additional, Wu, W. Y., additional, Zou, H. J., additional, Zhao, Y. Q., additional, Chu, H. Y., additional, Liu, J., additional, Zhou, X. D., additional, Dieude, P., additional, Bouaziz, M., additional, Riemekasten, G., additional, Airo, P., additional, Muller, M., additional, Cusi, D., additional, Chiocchia, G., additional, Boileau, C., additional, Allanore, Y., additional, Carmona, F., additional, Gutala, R., additional, Simeon, C. P., additional, Carreira, P., additional, Ortego Centeno, N., additional, Vicente Rabaneda, E., additional, Garcia Hernandez, F. J., additional, Garcia De La Pena, P., additional, Fernandez Castro, M., additional, Martinez Estupinan, L., additional, Egurbide, M. V., additional, Tsao, B. P., additional, Gourh, P., additional, Agarwal, S. K., additional, Arnett, F. C., additional, and Martin, J., additional

Published
2012
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17. Association of a non-synonymous functional variant of the ITGAM gene with systemic sclerosis

Author

Carmona, F. D., primary, Simeon, C. P., additional, Beretta, L., additional, Carreira, P., additional, Vonk, M. C., additional, Rios-Fernandez, R., additional, Espinosa, G., additional, Navarrete, N., additional, Vicente-Rabaneda, E., additional, Rodriguez-Rodriguez, L., additional, Tolosa, C., additional, Garcia-Hernandez, F. J., additional, Castellvi, I., additional, Egurbide, M. V., additional, Fonollosa, V., additional, Gonzalez-Gay, M. A., additional, Rodriguez-Carballeira, M., additional, Diaz-Gonzalez, F., additional, Saez-Comet, L., additional, Hesselstrand, R., additional, Riemekasten, G., additional, Witte, T., additional, Voskuyl, A. E., additional, Schuerwegh, A. J., additional, Madhok, R., additional, Shiels, P., additional, Fonseca, C., additional, Denton, C., additional, Nordin, A., additional, Palm, O., additional, Hoffmann-Vold, A.-M., additional, Airo, P., additional, Scorza, R., additional, Lunardi, C., additional, van Laar, J. M., additional, Hunzelmann, N., additional, Kreuter, A., additional, Herrick, A., additional, Worthington, J., additional, Koeleman, B. P. C., additional, Radstake, T. R. D. J., additional, and Martin, J., additional

Published
2011
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18. A replication study confirms the association of TNFSF4 (OX40L) polymorphisms with Systemic Sclerosis in a large European cohort

Author

Bossini-Castillo, L, primary, Broen, JCA, additional, Simeon, C P, additional, Beretta, L, additional, Vonk, M C, additional, Ortego-Centeno, N, additional, Espinosa, G, additional, Carreira, P, additional, Camps, M T, additional, Navarrete, N, additional, González-Escribano, M F, additional, Vicente-Rabaneda, E, additional, Rodríguez, L, additional, Tolosa, C, additional, Román-Ivorra, J A, additional, Gómez-Gracia, I, additional, García-Hernández, F J, additional, Castellví, I, additional, Gallego, M, additional, Fernández-Nebro, A, additional, Egurbide, M V, additional, Follonosa, V, additional, García de la Peña, P, additional, Pros, A, additional, González-Gay, M A, additional, Hesselstrand, R, additional, Riemekasten, G, additional, Witte, T, additional, Coenen, MJH, additional, Koeleman, B P, additional, Houssiau, F, additional, Smith, V, additional, De Keyser, F, additional, Westhovens, R, additional, De Langhe, E, additional, Voskuyl, A E, additional, Schuerwegh, A J, additional, Chee, M M, additional, Madhok, R, additional, Shiels, P, additional, Fonseca, C, additional, Denton, C, additional, Claes, K, additional, Padykov, L, additional, Nordin, A, additional, Palm, Ø, additional, Lie, B A, additional, Airó, P, additional, Scorza, R, additional, van Laar, J M, additional, Hunzelmann, N, additional, Kreuter, A, additional, Herrick, A, additional, Worthington, J, additional, Radstake, TRDJ, additional, Martín, J, additional, and Rueda, B, additional

Published
2010
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28. Confirmation of CCR6 as a risk factor for anti-topoisomerase I antibodies in systemic sclerosis

Author

Ochoa, E., Martin, J. -E, Assassi, S., Beretta, L., Carreira, P., Guillén, A., Simeón, C. P., Koumakis, E., Dieude, P., Allanore, Y., García-Hernández, F. J., Gerard Espinosa, Castellví, I., Trapiella, J. L., Rodriguez, L., González-Gay, M., Egurbide, M. V., Sáez, L., Callejas-Rubio, J. L., Vargas-Hitos, J. A., Hunzelmann, N., Riemekasten, G., Witte, T., Distler, J. H. W., Kreuter, A., Lunardi, C., Santaniello, A., Tan, F. K., Shiels, P. G., Herrick, A., Worthington, J., Vonk, M. C., Koeleman, B. P., Radstake, T. R. D. J., Mayes, M. D., Martin, J., Ortego-Centeno, N., Ríos, R., Granada, C., Camps, M. T., Fernández-Nebro, A., Sánchez-Román, J., Castillo, M. J., Aguirre, M., Gómez-Gracia, I., Fernández-Gutiérrez, B., Vicente, E., Andreu, J. L., Castro, M. F., La Peña, P. G., López-Longo, F. J., Martínez, L., Fonollosa, V., Tolosa, C., Pros, A., Carballeira, M. R., Narváez, F. J., Rivas, M. R., Santamaría, V. O., Madroñero, A. B., Díaz, B., Freire, M., Sousa, A., Mateo, P. F., Díaz, F., Hernández, V., Beltrán, E., Grau, E., Román-Ivorra, J. A., Alegre Sancho, J. J., Blanco García, F. J., Oreiro, N., and Spanish Scleroderma Group

29. Clinical and epidemiological differences between men and women with systemic sclerosis: A study in a Spanish systemic sclerosis cohort and literature review

Author

Dapena, M. F., Rivera, A., Sopeña, B., Vilella, C. T., Guillén-Del Castillo, A., Argüelles, D. C., Rubio, J. L. C., Rivas, M. R., Martínez, L. T., Parra, J. A. T., Carballeira, M. R., Arandia, N. I., Hernández, F. J. G., Arberas, M. V. E., Comet, L. S., Hitos, J. A. V., Blanco, J. J. R., Ballvé, A. M., Salas, X. P., Vuelta, A. B. M., Muñoz, M. R., Pla, V. F., Aznar, C. P. S., Boldova, R., Callejas Moraga, E., Callejas Rubio, J. L., Castillo, M. J., Colunga, D., Egurbide, M. V., Escobedo, J., Espinosa, G., Fonollosa, V., Freire, M., García Hernández, F. J., Guillén Del Castillo, A., Iniesta, N., Madroñero, A. B., Marí, B., Marín, A., Moreno Higueras, M., Ortego-Centeno, N., Pérez Conesa, M., Pla, X., Ríos Blanco, J. J., Rodero, M. M., Rodríguez Carballeira, M., Rubio Rivas, M., Ruiz Muñoz, M., Luis Sáez Comet, Simeón, C. P., Todolí, J. A., Tolosa, C., Trapiella, L., and Vargas Hitos, J. A.

30. LILRA3 deficiency is not involved in the giant cell arteritis and systemic sclerosis predisposition

Author

Márquez, A., Fernández-Aranguren, T., Witte, T., González-Gay, M. A., Martín, J., Carreira, P. E., Espinosa, G., Castellví, I., Egurbide, M. V., Vicente, E., Pros, A., Centeno, N. O., Ríos, R., Callejas, J. L., Hitos, J. A. V., Portales, R. G., Camps, M. T., Fernández-Nebro, A., González-Escribano, M. F., Sánchez-Román, J., García-Hernández, F. J., Castillo, M. J., MA Aguirre, Gómez-Gracia, I., Fernández-Gutiérrez, B., Andreu, J. L., Castro, M. F., La Peña, P. G., López-Longo, F. J., Martínez, L., Simeón, C. P., Fonollosa, V., Guillén, A., Tolosa, C., Carballeira, M. R., Rivas, M. R., Santamaría, V. O., Madroñero, A. B., Díaz, B., Trapiella, L., Freire, M., Sousa, A., Mateo, P. F., Díaz, F., Hernández, V., Beltrán, E., Grau, E., Román-Ivorra, J. A., Alegre Sancho, J. J., Blanco García, F. J., Oreiro, N., and Sáez-Comet, L.

31. Confirmation of CCR6 as a risk factor for anti-topoisomerase I antibodies in systemic sclerosis

Author

Ochoa, E., Martin, J. E., Assassi, S., Beretta, L., Patricia E Carreira, Guillen, A., Simeon, C. P., Koumakis, E., Dieude, P., Allanore, Y., Garcia-Hernandez, F. J., Espinosa, G., Castellvi, I., Trapiella, J. L., Rodriguez, L., Gonzalez-Gay, M. A., Egurbide, M. V., Saez, L., Callejas-Rubio, J. L., Vargas-Hitos, J. A., Hunzelmann, N., Riemekasten, G., Witte, T., Distler, J. H. W., Kreuter, A., Lunardi, C., Santaniello, A., Tan, F. K., Shiels, P. G., Herrick, A., Worthington, J., Vonk, M. C., Koeleman, B. P., Radstake, T. R. D. J., Mayes, M. D., Martin, J., and Spanish Seleroderma, Grp

Subjects
Receptors, CCR6, European Continental Ancestry Group, Type I, Polymorphism, Single Nucleotide, White People, Scleroderma, Gene Frequency, Autoantibodies, Biological Markers, Case-Control Studies, Chi-Square Distribution, DNA Topoisomerases, Type I, Europe, Genetic Association Studies, Genetic Predisposition to Disease, Humans, Odds Ratio, Phenotype, Risk Factors, Scleroderma, Systemic, United States, Receptors, Polymorphism, skin and connective tissue diseases, integumentary system, Systemic, Single Nucleotide, Inflammatory diseases Radboud Institute for Health Sciences [Radboudumc 5], CCR6, DNA Topoisomerases, Biomarkers
Abstract

Item does not contain fulltext OBJECTIVES: The current knowledge of the influence of systemic sclerosis (SSc) risk loci in the clinical sub-phenotypes is still limited. The main limitation lies in the low frequency of some sub-phenotypes which could be solved by replication studies in independent cohorts and meta-analysis between studies. In this regard, CCR6 gene variants have been recently associated with anti-topoisomerase I positive (ATA+) production in SSc patients in a candidate gene study. This gene has been proposed to have a critical role in IL-17-driven autoimmunity in human diseases. METHODS: In order to confirm the association between CCR6 and ATA+ SSc patients, we performed an independent replication study in populations of European ancestry. We studied two CCR6 genetic variants (rs968334 and rs3093024) in a total of 901 ATA+ SSc cases, 3,258 ATA- SSc cases and 7,865 healthy controls and compared allelic frequencies for those SNPs in ATA+ SSc with healthy controls and also with ATA- SSc patients. RESULTS: The comparison performed between ATA+ SSc patients and healthy controls showed significant association with SNP rs968334 (p=4.88 x 10-2, OR=1.11). When we compared ATA+ SSc cases with ATA- SSc, both SNPs, rs3093024 and rs968334, showed significant associations (p=2.89 x 10-2, OR=1.13; p=1.69 x 10-2, OR=1.15). Finally, in order to increase even more sample size and statistical power, we meta-analysed our study with the previous reported and found a significant association between SNP rs3093024 and ATA+ SSc patients (p=1.00 x 10-4, OR=1.16) comparing with healthy controls. CONCLUSIONS: Our work confirms the association of CCR6 gene and ATA+ SSc patients.

32. Confirmation of association of the macrophage migration inhibitory factor gene with systemic sclerosis in a large European population

Author

Bossini-Castillo, L., Simeon, C. P., Beretta, L., Vonk, M. C., Callejas-Rubio, J. L., Espinosa, G., Carreira, P., Camps, M. T., Rodríguez-Rodríguez, L., Rodríguez-Carballeira, M., García-Hernández, F. J., López-Longo, F. J., Hernández-Hernández, V., Sáez-Comet, L., Egurbide, M. V., Hesselstrand, R., Nordin, A., Hoffmann-Vold, A. M., Vanthuyne, M., Smith, V., Langhe, E., Kreuter, A., Riemekasten, G., Witte, T., Hunzelmann, N., Voskuyl, A. E., Schuerwegh, A. J., Lunardi, C., Airó, P., Scorza, R., Shiels, P., Laar, J. M., Fonseca, C., Denton, C., Herrick, A., Jane Worthington, Koeleman, B. P., Rueda, B., Radstake, T. R., Martin, J., Spanish Scleroderma Group, Rheumatology, and CCA - Innovative therapy

Subjects
Genetic Markers, Genotype, Single-nucleotide polymorphism, Polymorphism, Single Nucleotide, Scleroderma, Rheumatology, Polymorphism (computer science), Odds Ratio, MIF gene, systemic sclerosis, Medicine, SNP, Humans, Pharmacology (medical), Genetic Predisposition to Disease, Allele, skin and connective tissue diseases, Macrophage Migration-Inhibitory Factors, Macrophage migration inhibitory factor, Scleroderma, Systemic, integumentary system, business.industry, Case-control study, Translational research Immune Regulation [ONCOL 3], Infection and autoimmunity Auto-immunity, transplantation and immunotherapy [NCMLS 1], Genetic marker, Case-Control Studies, Immunology, Systemic sclerosis, Evaluation of complex medical interventions Auto-immunity, transplantation and immunotherapy [NCEBP 2], business, Polymorphisms
Abstract

The aim of this study was to confirm the implication of macrophage migration inhibitory factor (MIF) gene in SSc susceptibility or clinical phenotypes in a large European population.

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33. No evidence for association between the CCR5/Delta32CCR5 polymorphism and systemic sclerosis

Author

Carmona, F. D., Serrano-Lopera, A., López-Isac, E., Simeón, C. P., Carreira, P., Ríos-Fernandez, R., Espinosa, G., Camps, M. T., Navarrete, N., González-Escribano, M. F., Vicente-Rabaneda, E., Rodríguez-Rodríguez, L., Tolosa, C., Beltrani, E., Gómez-Garcia, I., Monica Fernandez Castro, López-Longo, F. J., García-Hernández, F. J., Castellví, I., Trapiella, L., Fernández-Nebro, A., García-Portales, R., Egurbide, M. V., Fonollosa, V., García La Peña, P., Pros, A., Rodríguez-Carballeira, M., Díaz-Gónzalez, F., Sáez-Comet, L., González-Gay, M. A., and Martín, J.

Subjects
Polymorphism, Genetic, Scleroderma, Systemic, Receptors, CCR5, Humans, Genetic Predisposition to Disease

35. Influence of antibody profile in clinical features and prognosis in a cohort of Spanish patients with systemic sclerosis

Author

Arandia, N. I., Simeón-Aznar, C. P., Del Castillo, A. G., Argüelles, D. C., Rubio-Rivas, M., Martínez, L. T., Hernández, F. J. G., Comet, L. S., Arberas, M. V. E., Ortego-Centeno, N., Freire, M., Alfonso, B. M., Hitos, J. A. V., Blanco, J. J. R., Parra, J. A. T., Rodríguez-Carballeira, M., Ballvé, A. M., Fernández, A. J. C., Salas, X. P., Vuelta, A. B. M., Muñoz, M. R., Pla, V. F., Espinosa, G., Callejas Moraga, E., Carbonell, C., Castillo, M. J., Chamorro, A. J., Colunga, D., Egurbide, M. V., Esteve, C., Fonollosa, V., García Hernández, F. J., González León, R., Guillén Del Castillo, A., Iniesta, N., Madroñero, A. B., Marí, B., Marín, A., Moreno Higueras, M., Pestaña, M., Pla, X., Ríos Blanco, J. J., Rodríguez Carballeira, M., Rubio Rivas, M., Ruiz Muñoz, M., Luis Sáez Comet, Segovia, P., Simeón, C. P., Soto- Peleteiro, A., Todolí, J. A., Tolosa C., Trapiella L., Vargas Hitos, J. A., and Vázquez-Triñanes C.

38. [The antiphospholipid syndrome in the 21st century].

Author

Ruiz-Irastorza G, Martinez-Berriotxoa A, and Egurbide MV

Subjects
Adult, Antibodies, Anticardiolipin, Anticoagulants administration & dosage, Anticoagulants therapeutic use, Aspirin administration & dosage, Aspirin therapeutic use, Clinical Trials as Topic, Dalteparin administration & dosage, Dalteparin therapeutic use, Enoxaparin administration & dosage, Enoxaparin therapeutic use, Female, Fetal Death etiology, Humans, Lupus Coagulation Inhibitor, Platelet Aggregation Inhibitors administration & dosage, Platelet Aggregation Inhibitors therapeutic use, Pregnancy, Pregnancy Complications etiology, Primary Prevention, Retrospective Studies, Risk Factors, Thrombosis drug therapy, Thrombosis prevention & control, Time Factors, Antiphospholipid Syndrome diagnosis, Antiphospholipid Syndrome drug therapy, Antiphospholipid Syndrome etiology, Antiphospholipid Syndrome immunology, Antiphospholipid Syndrome mortality
Abstract

The antiphospholipid syndrome (APS) is characterised by a great clinical variability, with diverse clinical presentations such as venous thromboembolism, preeclampsia, arterial thrombosis and renal and cerebral small vessel thrombosis. Given this wide spectrum of manifestations, it is very important to make an early diagnosis in order to start adequate medical therapy before irreversible damage ensues. Persistent positivity of lupus anticoagulant (LA), anticardiolipin antibodies (aCL) at high levels or the combined triple positivity of LA, aCL and anti-ss(2)GPI make the diagnosis of APS likely in the adequate clinical setting. The treatment of APS is based on antiaggregant and anticoagulant drugs. The optimal approach is still debated; however, indefinite anticoagulation is warranted. We recommend high intensity anticoagulation in patients with arterial and/or recurrent events, as well as a strict control of vascular risk factors. Pregnant women with APS should be best attended in combined medical-obstetric clinics. Low dose aspirin should be given to every pregnant woman with antiphospholipid antibodies, with the addition of low molecular weight heparin in those with previous thrombosis, previous fetal death or failure of monotherapy with aspirin.

Published
2009
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39. Sustained response to rituximab of autoimmune hemolytic anemia associated with antiphospholipid syndrome.

Author

Erdozain JG, Ruiz-Irastorza G, Egurbide MV, and Aguirre C

Subjects
Anemia, Hemolytic, Autoimmune etiology, Antibodies, Monoclonal, Murine-Derived, Antiphospholipid Syndrome diagnosis, Contraindications, Female, Humans, Kidney Failure, Chronic etiology, Kidney Failure, Chronic surgery, Kidney Transplantation, Methylprednisolone therapeutic use, Middle Aged, Postoperative Complications etiology, Prednisone therapeutic use, Remission Induction, Rituximab, Splenectomy, Stroke etiology, Tacrolimus therapeutic use, Vasculitis complications, Anemia, Hemolytic, Autoimmune drug therapy, Antibodies, Monoclonal therapeutic use, Antiphospholipid Syndrome complications, Immunosuppressive Agents therapeutic use
Abstract

Standard treatment for autoimmune hemolytic anemia (AIHA) due to warm antibodies includes combinations of glucocorticoids, immunosuppressive drugs (mainly azathioprine) and splenectomy. Patients who are refractory or intolerant to these therapies constitute an important therapeutic challenge. Rituximab, an anti-CD20 chimeric monoclonal antibody, can effectively deplete B-cells and is commonly used in B-cell non-Hodgkin lymphoma. In addition, it is being increasingly used in autoimmune disorders, such as idiopathic thrombocytopenic purpura, AIHA, systemic lupus erythematosus or vasculitis. We report a case of warm AIHA associated to primary antiphospholipid syndrome (APS). The patient was refractory to high-dose corticosteroids. Splenectomy was discarded in view of the high risk of thrombotic and/or hemorrhagic perioperative complications, due to the presence of APS. After treatment with four weekly doses of rituximab the patients had a rapid and sustained response which allowed progressive tapering of prednisone dose to 5 mg/d. In addition, IgM anticardiolipin titres decreased from > 600 MPL to < 100 MPL. Thirteen further cases of warm AIHA in adults treated with rituximab have been reviewed, showing excellent tolerance and high response rates. Rituximab may be considered prior to splenectomy in patients with refractory AIHA and high risk of complications following splenectomy.

Published
2004

40. [Pulmonary manifestations in Sjögren's syndrome].

Author

Aguirre Errasti C, Egurbide MV, and Alvarez Blanco A

Subjects
Bronchitis diagnosis, Bronchitis etiology, Cryptogenic Organizing Pneumonia diagnosis, Cryptogenic Organizing Pneumonia etiology, Diagnosis, Differential, Female, Humans, Hypertension, Pulmonary diagnosis, Hypertension, Pulmonary etiology, Lung Diseases diagnosis, Lymphoma diagnosis, Lymphoma etiology, Male, Middle Aged, Pulmonary Fibrosis diagnosis, Pulmonary Fibrosis etiology, Sjogren's Syndrome complications, Lung Diseases etiology, Sjogren's Syndrome diagnosis
Published
1996

41. [Bacteremic pneumonia caused by Branhamella catarrhalis in an immunocompromised patient].

Author

Mendarte U, Collazos J, Egurbide MV, and de Miguel J

Subjects
Aged, Amoxicillin therapeutic use, Clavulanic Acid, Clavulanic Acids therapeutic use, Humans, Male, Pneumonia drug therapy, Sepsis drug therapy, Bacterial Infections drug therapy, Immune Tolerance, Lymphoma complications, Moraxella catarrhalis, Pneumonia etiology, Sepsis etiology
Published
1991

42. [Temporal arteritis and aortic arch syndrome].

Author

Ayensa C, Muñoz J, Agud JM, Egurbide MV, and Martín E

Subjects
Female, Humans, Middle Aged, Aortic Arch Syndromes etiology, Giant Cell Arteritis complications
Published
1983

43. [Giant cell arteritis: temporal arteritis, rheumatic polymyalgia].

Author

Ayensa C, Echebarría MI, Muñoz J, Egurbide MV, Martín-Mola E, and Gaona T

Subjects
Aged, Arteritis pathology, Female, Giant Cell Arteritis pathology, Humans, Male, Middle Aged, Arteritis diagnosis, Giant Cell Arteritis diagnosis, Polymyalgia Rheumatica etiology
Abstract

Fourteen patients have been diagnosed for Giant Cell Arteritis by temporal biopsy or clinical criteria in the last five years. Two of them started with atypical symptoms. Polymyalgia Rheumatica was the commonest symptom (71%). Two patients (14%) had an irreversible blindness in eye one. Histologic changes of arteritis were shown by temporal biopsy in 8 cases, one of which had no cranial manifestations. A raised ESR was a constant finding (100%) followed by a alpha-2 globulin increase (93%) and anaemia (57%). One patient had rare complication of this disease: an aortic arch syndrome. The whole group responded well to the treatment.

Published
1983

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