Treatment with methotrexate and risk of relapses in patients with giant cell arteritis in clinical practice.

Objectives: To assess the incidence and the risk of relapses in giant cell arteritis (GCA) patients treated with and without methotrexate (MTX) in clinical practice. Other associated factors were also investigated.

Methods: An inception cohort of GCA was assembled in the out-patient clinic at Hospital Clínico San Carlos, including patients from the date of diagnosis (Jan-1991 until Sept-2013), and followed-up until lost of follow up or Sept-2014.

Long-term continuation of methotrexate therapy in giant cell arteritis patients in clinical practice.

Objectives: To assess the long-term continuation of methotrexate (MTX) in a cohort of patients with giant cell arteritis (GCA) in daily clinical practice. Factors associated with its discontinuation rate were also investigated.

Methods: A longitudinal study from 1991-2014, was performed.

A Genome-wide Association Study Identifies Risk Alleles in Plasminogen and P4HA2 Associated with Giant Cell Arteritis.

Giant cell arteritis (GCA) is the most common form of vasculitis in individuals older than 50 years in Western countries. To shed light onto the genetic background influencing susceptibility for GCA, we performed a genome-wide association screening in a well-powered study cohort. After imputation, 1,844,133 genetic variants were analyzed in 2,134 case subjects and 9,125 unaffected individuals from ten independent populations of European ancestry.

A large-scale genetic analysis reveals a strong contribution of the HLA class II region to giant cell arteritis susceptibility.

We conducted a large-scale genetic analysis on giant cell arteritis (GCA), a polygenic immune-mediated vasculitis. A case-control cohort, comprising 1,651 case subjects with GCA and 15,306 unrelated control subjects from six different countries of European ancestry, was genotyped by the Immunochip array. We also imputed HLA data with a previously validated imputation method to perform a more comprehensive analysis of this genomic region.

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

Objectives: The Xq28 region, containing IRAK and MECP2, represent a common susceptibility locus for a high number of autoimmune diseases. Our aim in the present study was to evaluate the influence of the IRAK1 and MECP2 autoimmunity-associated genetic variants in the giant cell arteritis (GCA) susceptibility and its clinical subphenotypes.

Methods: We analysed a total of 627 female biopsy-proven GCA patients and 1,520 female healthy controls of Spanish Caucasian origin.

Autoimmune disease-associated CD226 gene variants are not involved in giant cell arteritis susceptibility in the Spanish population.

Objectives: CD226 genetic variants have been associated with a number of autoimmune diseases. The aim of this study was to investigate the potential implication of the CD226 loci in the susceptibility to and main clinical manifestations of giant cell arteritis (GCA).

Methods: A Spanish Caucasian cohort of 455 patients diagnosed with biopsy-proven GCA and 1414 healthy controls were included in the study.

A nonsynonymous functional variant of the ITGAM gene is not involved in biopsy-proven giant cell arteritis.

Objective: To investigate whether a functional integrin alpha M (ITGAM) variant is involved in susceptibility to and clinical manifestations of giant cell arteritis (GCA).

Methods: A Spanish cohort of 437 white patients with biopsy-proven GCA and 1388 healthy controls were genotyped using the TaqMan allele discrimination technology.

Results: No association was observed between ITGAM rs1143679 and GCA (p = 0.

Role of the CCR5/Δ32CCR5 polymorphism in biopsy-proven giant cell arteritis.

To further explore the potential role of chemokines in giant cell arteritis (GCA), we have studied whether the CCR5/Δ32CCR5 polymorphism is implicated in the susceptibility to the disease and its specific features. A total of 352 Spanish patients with biopsy-proven GCA and 479 matched controls were assessed. DNA was obtained from peripheral blood.

Role of rs1343151 IL23R and rs3790567 IL12RB2 polymorphisms in biopsy-proven giant cell arteritis.

Objective: To assess the potential association between the rs1343151 IL23R and the rs3790567 IL12RB2 polymorphisms and giant cell arteritis (GCA). We also studied whether these polymorphisms might influence the phenotypic expression of GCA.

Methods: In total, 357 Spanish patients with biopsy-proven GCA and 574 matched controls were assessed.

Role of the rs6822844 gene polymorphism at the IL2-IL21 region in biopsy-proven giant cell arteritis.

Objectives: To assess the influence of the interleukin (IL)2-IL21 rs6822844 G/T polymorphism in the susceptibility to biopsy-proven giant cell arteritis (GCA) and in the clinical spectrum of manifestations of this vasculitis.

Methods: Two hundred and seventy-two biopsy-proven GCA patients were included in this study. DNA from patients and matched controls (n=791) was obtained from peripheral blood.

Influence of IL2RA rs2104286 polymorphism in the risk of biopsy-proven giant cell arteritis.

Objective: To assess the influence of the IL2RA rs2104286 A>G polymorphism on susceptibility to and clinical spectrum of manifestations of biopsy-proven giant cell arteritis (GCA).

Methods: Our study included 318 patients with biopsy-proven GCA. DNA from patients and healthy controls was obtained from peripheral blood.

Influence of CD40 rs1883832 polymorphism in susceptibility to and clinical manifestations of biopsy-proven giant cell arteritis.

Objective: To assess the potential association between CD40 rs1883832 polymorphism and biopsy-proven giant cell arteritis (GCA). We also studied the influence of the polymorphism on phenotypic expression of this vasculitis, in particular the development of visual ischemic manifestations.

Methods: Three hundred five Spanish patients with biopsy-proven GCA and 788 matched controls were assessed.

Role of BANK1 gene polymorphisms in biopsy-proven giant cell arteritis.

Objective: Giant cell arteritis (GCA) is a complex polygenic disease in which more than 1 genetic locus is likely to contribute to disease susceptibility and clinical expression. BANK, an adaptor molecule, has been suggested to participate in the B cell antigen receptors-mediated calcium homeostasis. We assessed for the first time the implication of BANK1 functional variants in susceptibility to GCA.

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

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.

Lack of association between the rs6920220 (G/A) polymorphism of the 6q23 region and biopsy-proven giant cell arteritis.

Objective: Recently, 2 independent studies have identified an association between several single-nucleotide polymorphisms (SNP) located in the 6q23 chromosomal region and rheumatoid arthritis (RA). Like RA, giant cell arteritis (GCA) is also a complex polygenic disease in which more than 1 genetic locus is likely to contribute to disease susceptibility and clinical expression. We analyzed the involvement of the rs6920220 (G/A) polymorphism from the 6q23/TNFAIP3 gene region in susceptibility to GCA.

Role of the C8orf13-BLK region in biopsy-proven giant cell arteritis.

Giant cell arteritis (GCA) is a complex polygenic disease in which more than one genetic locus is likely to contribute to disease susceptibility and clinical expression. In the present study, we have analyzed for first time the implication of rs13277113 and rs2736340 variants from the C8orf13-BLK gene region in the susceptibility to GCA. A total of 220 biopsy-proven GCA patients and 486 matched controls were assessed.

Lack of association between TRAF1/C5 gene polymorphisms and biopsy-proven giant cell arteritis.

Objective: A novel association with a 100-kb region on chromosome 9 that contains the tumor necrosis factor receptor-associated factor 1 (TRAF1) and C5 genes has been observed in some autoimmune rheumatic diseases, in particular in rheumatoid arthritis. We analyzed the influence of 2 single-nucleotide polymorphisms (SNP) from the TRAF1/C5 region in susceptibility to giant cell arteritis (GCA).

Methods: We assessed 220 patients with biopsy-proven GCA and 410 matched controls.

Lack of association between IRF5 gene polymorphisms and biopsy-proven giant cell arteritis.

Objective: Interferon (IFN) regulatory factors (IRF) are transcriptional mediators of IFN-induced signaling pathways and are involved in immune response. We have analyzed for the first time the association of 2 IRF5 gene variants in the susceptibility to giant cell arteritis (GCA).

Methods: Two hundred twenty patients with biopsy-proven GCA and 520 matched controls were assessed.

Association between toll-like receptor 4 gene polymorphism and biopsy-proven giant cell arteritis.

Objective: Dendritic cells localized at the adventitia-media border of the normal medium-sized arteries play a pivotal role in the initiation of giant cell arteritis (GCA). These cells express a singular surface receptor profile, including a series of Toll-like receptors (TLR). Ligands of TLR-4 promote activation and differentiation of adventitial dendritic cells and are directly implicated in the pathogenesis of GCA.

Lack of association between STAT4 gene polymorphism and biopsy-proven giant cell arteritis.

Objective: To investigate the potential implication of the STAT4 gene polymorphism rs7574865 in the predisposition to or the clinical expression of giant cell arteritis (GCA).

Methods: A total of 212 patients diagnosed with biopsy-proven GCA were studied. DNA from patients and controls matched by age, sex, and ethnicity was obtained from peripheral blood.

[Reduction in time until first treatment with disease modifying treatment in patients with rheumatoid arthritis].

Objective: To analyze changes in the lag time to first disease modifying antirheumatic drug (DMARD) prescription since onset of symptoms of rheumatoid arthritis (RA) over the last 2 decades in Spain.

Patients And Method: Review of medical records of 865 patients diagnosed with RA living in Spain and attended in specialty care settings of the National Health System. The principal variable was the lag time between the onset of symptoms of RA and the date of first DMARD therapy prescription.