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51. Analysis of the influence of the ghrelin receptor rs509035, rs512692 and rs2922126 polymorphisms in the risk of cardiovascular disease in patients with rheumatoid arthritis.

Author

Rodríguez-Rodríguez, Luis, García-Bermúdez, M., González-Juanatey, Carlos, Vázquez-Rodríguez, Tomás R., Miranda-Filloy, J. A., Fernández-Gutiérrez, B., Llorca, Javier, Martín, J., González-Gay, M. A., Rodríguez-Rodríguez, Luis, García-Bermúdez, M., González-Juanatey, Carlos, Vázquez-Rodríguez, Tomás R., Miranda-Filloy, J. A., Fernández-Gutiérrez, B., Llorca, Javier, Martín, J., and González-Gay, M. A.

Published
2011

52. Association of acid phosphatase locus 1*C allele with the risk of cardiovascular events in rheumatoid arthritis patients

Author

Teruel, María, Martín, J. E., González-Juanatey, Carlos, López-Mejías, Raquel, Miranda-Filloy, J. A., Blanco, Ricardo, Balsa, A., Pascual-Salcedo, Dora, Rodríguez-Rodríguez, Luis, Fernández-Gutiérrez, B., Ortiz, Ana María, González-Álvaro, Isidoro, Gómez-Vaquero, C., Bottini, N., Llorca, Javier, González-Gay, M. A., Martín, J., Teruel, María, Martín, J. E., González-Juanatey, Carlos, López-Mejías, Raquel, Miranda-Filloy, J. A., Blanco, Ricardo, Balsa, A., Pascual-Salcedo, Dora, Rodríguez-Rodríguez, Luis, Fernández-Gutiérrez, B., Ortiz, Ana María, González-Álvaro, Isidoro, Gómez-Vaquero, C., Bottini, N., Llorca, Javier, González-Gay, M. A., and Martín, J.

Abstract

Introduction Acid phosphatase locus 1 (ACP1) encodes a low molecular weight phosphotyrosine phosphatase implicated in a number of different biological functions in the cell. The aim of this study was to determine the contribution of ACP1 polymorphisms to susceptibility to rheumatoid arthritis (RA), as well as the potential contribution of these polymorphisms to the increased risk of cardiovascular disease (CV) observed in RA patients. Methods A set of 1,603 Spanish RA patients and 1,877 healthy controls were included in the study. Information related to the presence/absence of CV events was obtained from 1,284 of these participants. All individuals were genotyped for four ACP1 single-nucleotide polymorphisms (SNPs), rs10167992, rs11553742, rs7576247, and rs3828329, using a predesigned TaqMan SNP genotyping assay. Classical ACP1 alleles (*A, *B and *C) were imputed with SNP data. Results No association between ACP1 gene polymorphisms and susceptibility to RA was observed. However, when RA patients were stratified according to the presence or absence of CV events, an association between rs11553742*T and CV events was found (P = 0.012, odds ratio (OR) = 2.62 (1.24 to 5.53)). Likewise, the ACP1*C allele showed evidence of association with CV events in patients with RA (P = 0.024, OR = 2.43). Conclusions Our data show that the ACP1*C allele influences the risk of CV events in patients with RA.

Published
2011

53. A1298C polymorphism in the MTHFR gene predisposes to cardiovascular risk in rheumatoid arthritis

Author

Palomino-Morales, Rogelio, Vázquez-Rodríguez, Tomás R., Miranda-Filloy, J. A., Fernández-Gutiérrez, B., Martín, J., González-Gay, M. A., Palomino-Morales, Rogelio, Vázquez-Rodríguez, Tomás R., Miranda-Filloy, J. A., Fernández-Gutiérrez, B., Martín, J., and González-Gay, M. A.

Abstract

[Introduction]: We determined the contribution of the methylene tetrahydrofolate reductase (MTHFR) 677 C>T and 1298 A>C gene polymorphisms to the susceptibility to rheumatoid arthritis (RA). We also assessed whether these two MTHFR gene polymorphisms may be implicated in the development of cardiovascular (CV) events and subclinical atherosclerosis manifested by the presence of endothelial dysfunction, in a series of Spanish patients with RA. [Methods]: Six hundred and twelve patients fulfilling the 1987 American College of Rheumatology classification criteria for RA, seen at the rheumatology outpatient clinics of Hospital Xeral-Calde, Lugo and Hospital San Carlos, Madrid, were studied. Patients and controls (n = 865) were genotyped using predesigned TaqMan SNP genotyping assays. [Results]: No significant differences in allele or genotype frequencies for the MTHFR gene polymorphisms between RA patients and controls were found. Also, no association between the MTHFR 677 C>T polymorphism and CV events or endothelial dysfunction was observed. However, the MTHFR 1298 allele C frequency was increased in patients with CV events after 5 years (38.7% versus 30.3%; odds ratio = 1.45; 95% confidence interval = 1.00 to 2.10; P = 0.04) and 10 years (42.2% versus 31.0%; odds ratio = 1.62; 95% confidence interval = 1.08 to 2.43; P = 0.01) follow up. Moreover, patients carrying the MTHFR 1298 AC and CC genotypes had a significantly decreased flow-mediated endothelium-dependent vasodilatation (4.3 ± 3.9%) compared with those carrying the MTHFR 1298 AA genotype (6.5 ± 4.4%) (P = 0.005). [Conclusions]: Our results show that the MTHFR 1298 A>C gene polymorphism confers an increased risk for subclinical atherosclerosis and CV events in patients with RA.

Published
2010

54. Association between IL-18 gene polymorphisms and biopsy-proven giant cell arteritis

Author

Palomino-Morales, Rogelio, Vázquez-Rodríguez, Tomás R., Torres, Orlando, Morado, Inmaculada C., Castañeda, Santos, Miranda-Filloy, J. A., Callejas-Rubio, J. L., Fernández-Gutiérrez, B., González-Gay, M. A., Martín, J., Palomino-Morales, Rogelio, Vázquez-Rodríguez, Tomás R., Torres, Orlando, Morado, Inmaculada C., Castañeda, Santos, Miranda-Filloy, J. A., Callejas-Rubio, J. L., Fernández-Gutiérrez, B., González-Gay, M. A., and Martín, J.

Abstract

[Introduction] The objective was to investigate the potential implication of the IL18 gene promoter polymorphisms in the susceptibility to giant-cell arteritis (GCA)., [Methods] In total, 212 patients diagnosed with biopsy-proven GCA were included in this study. DNA from patients and matched controls was obtained from peripheral blood. Samples were genotyped for the IL18-137 G>C (rs187238), the IL18-607 C>A (rs1946518), and the IL18-1297 T>C (rs360719) gene polymorphisms with polymerase chain reaction, by using a predesigned TaqMan allele discrimination assay., [Results] No significant association between the IL18-137 G>C polymorphism and GCA was found. However, the IL18 -607 allele A was significantly increased in GCA patients compared with controls (47.8% versus 40.9% in patients and controls respectively; P = 0.02; OR, 1.32; 95% CI, 1.04 to 1.69). It was due to an increased frequency of homozygosity for the IL18 -607 A/A genotype in patients with GCA (20.4%) compared with controls (13.4%) (IL18 -607 A/A versus IL18 -607 A/C plus IL18 -607 C/C genotypes: P = 0.04; OR, 1.59; 95% CI, 1.02 to 2.46). Also, the IL18-1297 allele C was significantly increased in GCA patients (30.7%) compared with controls (23.0%) (P = 0.003; OR, 1.48; 95% CI, 1.13 to 1.95). In this regard, an increased susceptibility to GCA was observed in individuals carrying the IL18-1297 C/C or the IL18-1297 C/T genotypes compared with those carrying the IL18-1297 T/T genotype (IL18-1297 C/C plus IL18-1297 T/C versus IL18-1297 T/T genotype in GCA patients compared with controls: P = 0.005; OR, 1.61; 95% CI, 1.15 to 2.25). We also found an additive effect of the IL18 -1297 and -607 polymorphisms with TLR4 Asp299Gly polymorphism. The OR for GCA was 1.95 for combinations of genotypes with one or two risk alleles, whereas carriers of three or more risk alleles have an OR of 3.7., [Conclusions] Our results show for the first time an implication of IL18 gene-promoter polymorphisms in the susceptibility to biopsy-proven GCA. In addition, an additive effect between the associated IL18 and TLR4 genetic variants was observed.

Published
2010

55. Coefficient shifts in geographical ecology: an empirical evaluation of spatial and non-spatial regression

Author

Bini, L. M., Diniz-Filho, J. A. F., Rangel, T. F. L. V. B., Akre, T. S. B., Albaladejo, R. G., Albuquerque, F. S., Aparicio, A., Araújo, M. B., Baselga, A., Beck, J., Bellocq, M. I., Böhning-Gaese, K., Borges, P. A. V., Castro-Parga, I., Chey, V. K., Chown, S. L., Marco, P., Dobkin, D. S., Ferrer-Castán, D., Field, R., Filloy, J., Fleishman, E., Gómez, J. F., Hortal, J., Iverson, J. B., Kerr, J. T., Kissling, W. D., Kitching, I. J., León-Cortés, J. L., Lobo, J. M., Montoya, D., Morales-Castilla, I., Moreno, J. C., Oberdorff, T., Olalla-Tárraga, M. Á., Pausas, J. G., Qian, H., Rahbek, Carsten, Rodríguez, M. Á., Rueda, M., Ruggiero, A., Sackmann, P., Sanders, N. J., Terribile, L. C., Vetaas, O. R., Hawkins, B. A., Bini, L. M., Diniz-Filho, J. A. F., Rangel, T. F. L. V. B., Akre, T. S. B., Albaladejo, R. G., Albuquerque, F. S., Aparicio, A., Araújo, M. B., Baselga, A., Beck, J., Bellocq, M. I., Böhning-Gaese, K., Borges, P. A. V., Castro-Parga, I., Chey, V. K., Chown, S. L., Marco, P., Dobkin, D. S., Ferrer-Castán, D., Field, R., Filloy, J., Fleishman, E., Gómez, J. F., Hortal, J., Iverson, J. B., Kerr, J. T., Kissling, W. D., Kitching, I. J., León-Cortés, J. L., Lobo, J. M., Montoya, D., Morales-Castilla, I., Moreno, J. C., Oberdorff, T., Olalla-Tárraga, M. Á., Pausas, J. G., Qian, H., Rahbek, Carsten, Rodríguez, M. Á., Rueda, M., Ruggiero, A., Sackmann, P., Sanders, N. J., Terribile, L. C., Vetaas, O. R., and Hawkins, B. A.

Abstract

Udgivelsesdato: April 2009, A major focus of geographical ecology and macroecology is to understand the causes of spatially structured ecological patterns. However, achieving this understanding can be complicated when using multiple regression, because the relative importance of explanatory variables, as measured by regression coefficients, can shift depending on whether spatially explicit or non-spatial modeling is used. However, the extent to which coefficients may shift and why shifts occur are unclear. Here, we analyze the relationship between environmental predictors and the geographical distribution of species richness, body size, range size and abundance in 97 multi-factorial data sets. Our goal was to compare standardized partial regression coefficients of non-spatial ordinary least squares regressions (i.e. models fitted using ordinary least squares without taking autocorrelation into account; "OLS models" hereafter) and eight spatial methods to evaluate the frequency of coefficient shifts and identify characteristics of data that might predict when shifts are likely. We generated three metrics of coefficient shifts and eight characteristics of the data sets as predictors of shifts. Typical of ecological data, spatial autocorrelation in the residuals of OLS models was found in most data sets. The spatial models varied in the extent to which they minimized residual spatial autocorrelation. Patterns of coefficient shifts also varied among methods and datasets, although the magnitudes of shifts tended to be small in all cases. We were unable to identify strong predictors of shifts, including the levels of autocorrelation in either explanatory variables or model residuals. Thus, changes in coefficients between spatial and non-spatial methods depend on the method used and are largely idiosyncratic, making it difficult to predict when or why shifts occur. We conclude that the ecological importance of regression coefficients cannot be evaluated with confidence irrespective of whether spatial

Published
2009

56. No evidence of association between functional polymorphisms located withinIL6RandIL6STgenes and Henoch-Schönlein purpura

Author

López-Mejías, R., primary, Sevilla Pérez, B., additional, Genre, F., additional, Castañeda, S., additional, Ortego-Centeno, N., additional, Llorca, J., additional, Ubilla, B., additional, Ochoa, R., additional, Pina, T., additional, Marquez, A., additional, Sala-Icardo, L., additional, Miranda-Filloy, J. A., additional, Rueda-Gotor, J., additional, Martín, J., additional, Blanco, R., additional, and González-Gay, M. A., additional

Published
2013
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58. Lack of association between ADIPOQ rs266729 and ADIPOQ rs1501299 polymorphisms and cardiovascular disease in rheumatoid arthritis patients

Author

Rodríguez‐Rodríguez, L., primary, García‐Bermúdez, M., additional, González‐Juanatey, C., additional, Vazquez‐Rodriguez, T. R., additional, Miranda‐Filloy, J. A., additional, Fernandez‐Gutierrez, B., additional, Llorca, J., additional, Martin, J., additional, and González‐Gay, M. A., additional

Published
2010
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64. Analysis of two autoimmunity genes, IRAK1 and MECP2, in giant cell arteritis

Author

Márquez, A., Solans, R., Hernández-Rodríguez, J., Cid, M. C., Castañeda, S., Ramentol, M., Morado, I. C., Rodríguez-Rodríguez, L., Narváez, J., Gómez-Vaquero, C., Miranda-Filloy, J. A., Martínez-Taboada, V. M., Rios, R., Sopeña, B., Monfort, J., García-Villanueva, M. J., Martínez-Zapico, A., Marí-Alfonso, B., Sánchez-Martín, J., Unzurrunzaga, A., Raya, E., Miguel, E., Hidalgo-Conde, A., Ricardo Blanco, González-Gay, M. A., and Martín, J.

69. Interleukin 1 beta (IL1ß) rs16944 genetic variant as a genetic marker of severe renal manifestations and renal sequelae in Henoch-Schönlein purpura

Author

López-Mejías, R., Genre, F., Remuzgo-Martínez, S., Sevilla Pérez, B., Castañeda, S., Llorca, J., Ortego-Centeno, N., Ubilla, B., Mijares, V., Pina, T., Calvo-Río, V., Miranda-Filloy, J. A., Navas Parejo, A., Argila, D., Sánchez-Pérez, J., Rubio, E., Luque, M. L., Blanco-Madriga, J. M., Galíndez-Aguirregoikoa, E., Martín, J., Blanco, R., and González-Gay, M. A.

Subjects
Genetic Markers, Male, Adolescent, Genotype, IgA Vasculitis, Child, Preschool, Interleukin-1beta, Humans, Female, Kidney Diseases, Child, Polymorphism, Single Nucleotide
Abstract

Data from a small series suggested that the Interleukin 1 beta (IL1ß) rs16944 polymorphism may be associated with severe renal involvement and persistent renal damage (renal sequelae) in Henoch-Schönlein purpura (HSP). To confirm this association, we assessed the largest cohort of Caucasian HSP patients ever considered for genetic studies.338 Spanish HSP patients and 635 sex and ethnically matched controls were recruited in this study. All patients were required to have had at least 6 months' follow-up. Patients and controls were genotyped for IL1β rs16944 by TaqMan genotyping assay.No differences between IL1β rs16944 genotype or allele frequencies were found either in the case/control study or when HSP patients were stratified according to the age at disease onset, presence of nephritis or gastrointestinal manifestations. Nevertheless, 4 (25%) of the 16 HSP patients who developed severe renal manifestations carried the TT genotype versus 29 (9%) of 322 who did not develop this complication (p=0.01, OR=5.48, 95% CI: 1.01-28.10). Accordingly, patients carrying the mutant T allele had an increased risk of developing severe nephropathy (p=0.016, OR=2.35, 95% CI: 1.09-5.07). Additionally, a significant increase of the TT genotype was observed in patients with persistent renal damage when compared with those patients without this complication (25% versus 8.6%, respectively; p=0.0035, OR=4.90, 95% CI: 1.26- 18.51). Moreover, renal sequelae were more common in patients carrying the mutant T allele (p=0.0076, OR=2.20, 95% CI: 1.17-4.14).Our results support that the IL1ß rs16944 polymorphism may be a potential marker of severe renal manifestations and renal sequelae in HSP.

72. Influence of IL17A gene on the pathogenesis of immunoglobulin-A vasculitis

Author

López-Mejías, R., Genre, F., Remuzgo-Martínez, S., Pulito-Cueto, Verónica, Sevilla-Pérez, B., Llorca, J., Ortego-Centeno, N., Mijares, V., Lera-Gómez, L., Leonardo, M.T., Peñalba, A., Cabero, M.J., Martín-Penagos, L., Miranda-Filloy, J. A., Navas Parejo, A., Sánchez Pérez, J., de Argila, D., Rubio, E., León Luque, M., Blanco-Madrigal, J.M., Galíndez-Agirregoikoa, E., Martín, J., Blanco, R., Castañeda, S., and González-Gay, M. A.

Subjects
Vasculitis, Haplotypes, Case-Control Studies, Interleukin-17, Humans, Gene Regulatory Networks, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, Immunoglobulin A
Abstract

OBJECTIVES: Cytokines signaling pathway genes represent a key component of the genetic network implicated in the pathogenesis of immunoglobulin-A vasculitis (IgAV), an inflammatory vascular pathology. Interleukin (IL)17A is described as a genetic risk locus for some autoimmune diseases, such as giant cell arteritis and spondyloarthritis. Accordingly, we aimed to determine the potential influence of IL17A on the pathogenesis of IgAV. METHODS: Five IL17A tag polymorphisms (rs4711998, rs8193036, rs3819024, rs2275913 and rs7747909), which cover the major variability of this gene, were genotyped in 360 Caucasian patients with IgAV and 1,003 sex and ethnically matched healthy controls using TaqMan probes. RESULTS: No statistically significant differences between patients with IgAV and healthy controls were observed when each IL17A genetic variant was analysed independently. Similarly, no statistically significant differences between patients with IgAV and healthy controls were found when the five IL17A polymorphisms were evaluated combined conforming haplotypes. In addition, there were no statistically significant differences in genotype, allele and haplotype frequencies of IL17A when patients with IgAV were stratified according to the age at disease onset or to the presence/absence of gastrointestinal or renal manifestations. CONCLUSIONS: Our results do not support an influence of IL17A on the pathogenesis of IgAV.

74. Lack of association between LEP rs2167270 (19 G>A) polymorphism and disease susceptibility and cardiovascular disease in patients with rheumatoid arthritis

Author

Garcia-Bermudez, M., Gonzalez-Juanatey, C., Rodriguez-Rodriguez, L., Vazquez-Rodriguez, T. R., Miranda-Filloy, J. A., Fernandez-Gutierrez, B., Llorca, J., Javier Martin, and Gonzalez-Gay, M. A.

Subjects
Arthritis, Rheumatoid, Leptin, Male, Polymorphism, Genetic, Gene Frequency, Genotype, Cardiovascular Diseases, Risk Factors, Humans, Female, Genetic Predisposition to Disease, Middle Aged, Aged
Abstract

To assess the potential association between LEP rs2167270 (19 GA) gene polymorphism and disease susceptibility and cardiovascular disease (CV) in patients with rheumatoid arthritis (RA).773 patients fulfilling the 1987 American College of Rheumatology classification criteria for RA, seen at the rheumatology outpatient clinics of Hospital Xeral-Calde, Lugo, and Hospital San Carlos, Madrid, Spain, and 957 matched controls, were studied. Patients were genotyped for the LEP rs2167270 (19GA) polymorphism, located within the 5´UTR, using predesigned TaqMan single nucleotide polymorphism genotyping assay. Also, HLA-DRB1 genotyping was performed using molecular based methods. Subclinical atherosclerosis was assessed in a subgroup of patients with no history of CV events by brachial artery reactivity to determine flow-mediated endothelium-dependent and endothelium-independent vasodilatation (n=133) and by B-mode ultrasonography of the carotid artery intima-media thickness (n=113).No statistically significant differences in the genotype or allele frequencies of the LEP rs2167270 gene polymorphism between patients with RA and controls were seen. Likewise, LEP rs2167270 polymorphism did not influence the development of CV events. Also, no significant differences in LEP rs2167270 genotype or allele distribution were seen when results of surrogate markers of subclinical atherosclerosis were assessed.LEP rs2167270 polymorphism does not seem to be a genetic risk factor for disease susceptibility or clinically evident CV disease and subclinical atherosclerosis in patients with RA.

75. Association of apolipoprotein B/apolipoprotein A1 ratio and cardiovascular events in rheumatoid arthritis: Results of the CARMA study

Author

Zegarra-Mondragón, S., López-González, R., Martín-Martínez, M. A., García-Gómez, C., Sánchez-Alonso, F., González-Juanatey, C., Arija, S. M., Hernán, G. B., Pardo, S. M., Escribano, A. R., García, E. P., Frías, E. D., Redondo, J. R., Sánchez, M. D., Cambrón, A. B. R., Ramos, M. J. M., Montero, S. A. R., Marco, M. T. N., Valle, M. M., Gonzalez, J. G., Corral, J. B., Llorca, J., Castañeda, S., González-Gay, M. A., Rabago, E. G., Morales, E. A. B., Carlos Fernández Lopez, J., Villar, N. O., Sandoval, A. A., Blanco García, F. J., Miquel, C. A., González Fernández, M. J., Codina, R. H., Yoldi, B., Ramentol, M., Ávila, G., Barril, S. M., Quesada, E., Steiner, M., Muñoz, S., Cobo, T., Gamero, F., Torón, J. G., Espino, P., Ros, I., Ibáñez, M., Murillo, C., Molina, J. T., Raimon Sanmarti, Berman, H., Cabrera, S., Ruiz, V., Patón, O. F., Gutierrez, B. F., Abasolo, L., Pina, J. M., Canals, D. F., Nolla, J. M., Arias, M. G., Uriarte, M., García Vadillo, J. A., Vicuña, R. G., Nebro, A. F., López, M. A. B., Ureña, I., Irigoyen, M. V., Cagigal, V. C., Garrido, D. P., García Aparicio, A. M., Gómez, R. B., Bautista, P. G., Sanz, A. H., Manero, F. J., Zorzo, F. J., Ubeda, E. G., Gracía, J. M., Audera, C. B., Medrano, M., Pecondón, Á, Erausquin, C., Ojeda, S., Quevedo, J. C., Francisco, F., Lozano, C. R., López Longo, F. J., Gerona, D., Fernández, C. G., Monteagudo, I., Del Pino, J., González, M. D. S., Corrales, A., Peiró, M. E., Senabre, J. M., Rosas, J. C., Rotés, I., Moreno, E., Erra, A., Grado, D., Calvo, J., Rueda, A., Möller, I., Rodríguez, I., Barbadillo, C., Raya, E., Morales, P., Nieto, A., Jiménez, I., Magro, C., Expósito, S. R., Nievas, G. S., Navarro, E. J., Fernández, M. S., García Morales, M. A., Bastero, I. L., Consuegra, G. G., Palmou, N., Pujol, M., Alonso, E. R., Salvador, G., Alvarez, B. G., Cantabrana, A., Bustabad, S., Muñoz, A., Jimenez, L. M., Hernandez, T. G., González Polo, F. J., Almagro, R. M., Moreno, J. M., Serret, E. G., Barroso, C. L., Méndez, L. C., Carballido, C. F., Del Castillo, P. M., Naredo, E., Valenciano, A. C., Villa, C. M., Turrión, A., Sánchez, J., Galindo, M., Collantes, E., Ruiz, D., Font, P., Bonilla, G., Meseguer, A. L., Moreno Martínez, M. J., Beteta Fernández, M. D., Linares, L. F., González Gómez, M. L., Rivera, N. A., Berrizbeitia, O. F., García Vivar, M. L., Riera, M., León, Y. M., Maymó, J., Amirall, M., Escolano, S. I., Serrano, S. S., Lis Bona, M. P., Fiter, J., Melón, J. F., Espadaler, L., Maiz, O., Belzunegui, J., Díaz, C., Valls, R., Castellví, I., Bonet, M., Ruzafa, E. M., Alen, J. C., Sandoval, T. P., Evrard, E. R., Godo, J. R., Espartero, C. F., Navarro Blasco, F. J., Antonio González, J., and Miranda-Filloy, J. A.

76. Apelin serum levels in non-diabetic ankylosing spondylitis patients undergoing TNF-α antagonist therapy

Author

Genre, F., Miranda-Filloy, J. A., López-Mejias, R., Carnero-López, B., Ochoa, R., Rueda, J., González-Juanatey, C., Ricardo Blanco, Llorca, J., and González-Gay, M. A.

Abstract

To determine whether disease activity, systemic inflammation and metabolic syndrome are potential determinants of circulating apelin in ankylosing spondylitis (AS) patients undergoing TNF-a antagonist-infliximab therapy.

78. Correlation between insulin resistance and serum ghrelin in non-diabetic ankylosing spondylitis patients undergoing anti-TNF-α therapy

Author

Genre, F., López-Mejías, R., Miranda-Filloy, J. A., Carnero-López, B., Ines Gomez-Acebo, Blanco, R., Ochoa, R., Rueda, J., González-Juanatey, C., Llorca, J., and González-Gay, M.

Subjects
musculoskeletal diseases, digestive, oral, and skin physiology
Abstract

To evaluate whether anti-TNF-a therapy (infliximab) administration alters circulating levels of ghrelin, an anti-inflammatory gastric peptide. We also assessed possible associations of circulating ghrelin concentrations with CRP and ESR levels, metabolic syndrome, demographic characteristics and other adipokines in ankylosing spondylitis (AS) patients.

84. Lack of association of NAMPT rs9770242 and rs59744560 polymorphisms with disease susceptibility and cardiovascular risk in patients with rheumatoid arthritis

Author

Garcia-Bermudez, M., Gonzalez-Juanatey, C., Rodriguez-Rodriguez, L., Miranda-Filloy, J. A., Perez-Esteban, S., Vazquez-Rodriguez, T. R., Castaneda, S., Balsa, A., Fernandez-Gutierrez, B., Llorca, J., Gonzalez-Alvaro, I., Javier Martin, and Gonzalez-Gay, M. A.

Subjects
Adult, Male, Brachial Artery, Polymorphism, Single Nucleotide, Risk Assessment, Arthritis, Rheumatoid, Gene Frequency, Risk Factors, Odds Ratio, Humans, Genetic Predisposition to Disease, Nicotinamide Phosphoribosyltransferase, Promoter Regions, Genetic, Aged, Ultrasonography, Analysis of Variance, Chi-Square Distribution, HLA-DR Antigens, Middle Aged, Vasodilation, Carotid Arteries, Logistic Models, Phenotype, Cardiovascular Diseases, Spain, Case-Control Studies, Cytokines, Female, Tunica Intima, Tunica Media, HLA-DRB1 Chains
Abstract

Visfatin is an adipokine encoded by the NAMPT (PBEF1) gene. In this study we assessed the potential association of two NAMPT gene polymorphisms with disease susceptibility and cardiovascular (CV) risk in patients with rheumatoid arthritis (RA).A total of 1,395 patients fulfilling the 1987 ACR classification criteria for RA and 1,230 matched controls, were genotyped for the NAMPT rs9770242 and rs59744560 gene polymorphisms, located within the proximal promoter, using predesigned TaqMan single nucleotide polymorphism genotyping assay. Also, HLA-DRB1 genotyping was performed using molecular based methods. In a second step, 1,196 patients in whom full information was available were assessed to determine the influence of NAMPT rs9770242 and rs59744560 polymorphisms in the development of CV events. Also, the potential influence of these polymorphisms in the development of subclinical atherosclerosis was assessed in a subgroup of patients with no history of CV events by brachial artery reactivity to determine flow-mediated endothelium-dependent and endothelium-independent vasodilatation (n=125) and by B-mode ultrasonography to determine the carotid artery intima-media thickness (n=105).No statistically significant differences in the allele or genotype frequencies for the NAMPT gene polymorphisms between RA patients and controls were found. A modest non significant lower frequency of the minor allele G of rs9770242 polymorphism was observed among patients with CV disease (20.62%) compared to those without CV disease (22.83%) (p=0.39). Also, a slight nonsignificant lower frequency of the minor allele T of rs59744560 polymorphism in patients with CV events (9.81%) compared with those RA patients who did not experience CV disease (13.07%) (p=0.11) was observed. Likewise, no significant association between the NAMPT polymorphisms with surrogate markers of subclinical atherosclerosis was found in patients with RA.NAMPT rs9770242 and rs59744560 polymorphisms are not markers of disease susceptibility and CV disease in RA.

85. Influence of MHCIITA rs3087456 and rs4774 polymorphisms in the susceptibility to cardiovascular disease of patients with rheumatoid arthritis

Author

García-Bermúdez, M., González-Juanatey, C., Lopez-Mejias, R., Rodriguez-Rodriguez, L., Pérez-Esteban, S., Castañeda, S., Urcelay, E., Miranda-Filloy, J. A., Gómez-Vaquero, C., Fernández-Gutierrez, B., Balsa, A., González-Alvaro, I., Ricardo Blanco, Llorca, J., Martín, J., and González-Gay, M. A.

Subjects
Adult, Male, Genotype, Nuclear Proteins, Middle Aged, Polymorphism, Single Nucleotide, Arthritis, Rheumatoid, Gene Frequency, Cardiovascular Diseases, Trans-Activators, Humans, Female, Genetic Predisposition to Disease, Aged
Abstract

MHCIITA is a major regulator of MHC expression that has been reported to be involved in the susceptibility to rheumatoid arthritis (RA) and myocardial infarction. In this study we investigated the potential association of two MHCIITA gene polymorphisms with cardiovascular (CV) risk in patients with RA.1302 patients fulfilling the 1987 ACR classification criteria for RA were genotyped for the MHCIITA rs3087456 and rs4774 gene polymorphisms to determine the influence of MHCIITA variants in the development of CV events. The potential influence of these polymorphisms in the development of subclinical atherosclerosis was also analysed in a subgroup of patients with no history of CV events by the assessment of two surrogate markers of atherosclerosis; brachial and carotid ultrasonography to determine endothelial function and carotid artery intima-media thickness, respectively.No statistically significant differences in the allele or genotype frequencies for each individual MHCIITA gene polymorphism between RA patients who experienced CV events, or not, were found. This was also the case when each polymorphism was assessed according to results obtained from surrogate markers of atherosclerosis. Also, in assessing the combined influence of both MHCIITA gene polymorphisms in the risk of CV disease after adjustment for gender, age at time of disease diagnosis, follow-up time, traditional CV risk factors, and shared epitope status, patients with CV events only showed a marginally decreased frequency of the MHCIITA rs3087456-rs4774 G-G allele combination (p=0.08; odds ratio: 0.63 [95% confidence interval: 0.37-1.05]).Our data do not support an influence of MHCIITA rs3087456 and rs4774 polymorphisms in the increased risk of CV events of patients with RA.

100. Grassland Afforestation Drives Biotic Homogenisation of Soil Microbial Communities at a Regional Scale.

Author

Ribero MN, Schiaffino MR, and Filloy J

Abstract

Grassland afforestation poses a threat to biodiversity beyond land-use conversion. Diversity patterns are shaped by temporal dynamics, particularly, time since afforestation can decline beta diversity and lead to biotic homogenisation. Our study examines the effect of grassland afforestation on soil prokaryotic and fungal beta diversity. We evaluate the contributions of colonisation and extinction processes to beta diversity, as well as the replacement of endemic species by ubiquitous ones. Along a 200 km climatic gradient in Argentina's Pampas region, we analysed grasslands and mature eucalypt plantations at different times since afforestation. Soil samples were collected at each site and analysed using 16S (V3-V4) and ITS2 amplicon sequencing to identify prokaryotic and fungal communities, respectively. The analyses revealed biotic homogenisation at the transition from grassland to newly planted stands, evidenced by a decrease in intratreatment beta diversity. Increasing time since afforestation did not exacerbate this decline. However, our findings indicate that there are different responses between prokaryotes and fungi. The homogenisation of prokaryotes in young stands is due to the low heterogeneity in colonising communities. On the other hand, the decline in fungal beta diversity is likely caused by other mechanisms beyond extinction or replacement. The study highlights the impacts of the afforestation process on the beta diversity of soil microbial communities of grasslands, affecting taxonomic groups in different ways. Although microbial diversity may be partially restored in time in eucalypt plantations, it is important to investigate its underlying mechanisms and the ecological implications for microbial diversity and its spatial distribution., (© 2024 John Wiley & Sons Ltd.)

Published
2025
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