Suchergebnisse

To assess the baseline condition of the SI joints (SIJs) in healthy individuals without symptoms of back pain and to study the effect of mechanical stress caused by intense physical training on MRI of the SIJs. Twenty-two military recruits underwent an MRI of the SIJs before and after 6 weeks of intense standardized physical training. Bone marrow oedema and structural lesions were scored based on the Spondyloarthritis Research Consortium of Canada (SPARCC) method, by three trained readers blinded for time sequence and clinical findings. Additionally, fulfilment of the Assessment of SpondyloArthritis international Society (ASAS) definition of a positive MRI was evaluated. At baseline, 9/22 recruits (40.9%) already presented a SPARCC score a (c) 3/41; this number increased to 11/22 (50.0%) at week 6 (P = 0.625). In these patients, the mean (SD) SPARCC score was 2.4 (0.4) at baseline, compared to 3.7 (1.3) at week 6. Overall, the mean (SD) change in SPARCC score over time in all 22 patients was 0.9 (0.6) (P = 0.109). A positive MRI according to the ASAS definition was present in 5/22 recruits (22.7%) at baseline, which increased to 8/22 (36.4%) at follow-up (P = 0.375). Structural lesions were present in 6/22 subjects (27.3%), both at baseline and after 6 weeks of training. A substantial proportion of healthy active individuals without any symptoms of back pain displayed bone marrow oedema lesions on MRI at baseline. However, MRI lesions did not increase significantly after 6 weeks of intensive physical training. Our study underscores the necessity to interpret MRI findings of the SIJs in the appropriate clinical context, even in a young active population. ; Ghent University Hospital; Het Fonds voor Wetenschappelijk Reuma Onderzoek

Ankylosing spondylitis (AS) is a common, highly heritable, inflammatory arthritis for which HLA-B*27 is the major genetic risk factor, although its role in the aetiology of AS remains elusive. To better understand the genetic basis of the MHC susceptibility loci, we genotyped 7,264 MHC SNPs in 22,647 AS cases and controls of European descent. We impute SNPs, classical HLA alleles and amino-acid residues within HLA proteins, and tested these for association to AS status. Here we show that in addition to effects due to HLA-B*27 alleles, several other HLA-B alleles also affect susceptibility. After controlling for the associated haplotypes in HLA-B, we observe independent associations with variants in the HLA-A, HLA-DPB1 and HLA-DRB1 loci. We also demonstrate that the ERAP1 SNP rs30187 association is not restricted only to carriers of HLA-B*27 but also found in HLA-B*40:01 carriers independently of HLA-B*27 genotype. ; We thank all participating subjects with AS and healthy individuals who provided the DNA and clinical information necessary for this study. This work was in part funded by grants from Arthritis Research UK (19536 and 18797), the NIHR Oxford comprehensive Biomedical Research Centre (immunity and inflammation theme A93081) and NIHR Thames Valley collaborative research network and National Ankylosing Spondylitis Society (UK). SPARCC was established through the support of the Arthritis Society of Canada. Support was received from National Institutes of Health/National Institute of Allergy and Infectious Diseases grant 1U01AI09090-01. This work was supported in part by grant PI12/02587 (Inst. Carlos III, Spain) and by European Union 'Fondos FEDER'. Support was received from Agence Nationale de la Recherche (grant ANR 2010 GEMISA and Investissements d'Avenir programme ANR-11-IDEX-0005-02), the Société Française de Rhumatologie (SFR) and the Arthritis Foundation. M.W. is funded by the Intramural Research Program, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health. M.A.B. is funded by a National Health and Medical Research Council (Australia) Senior Principal Research Fellowship. D.M.E. is funded by an Australian Research Council Future Fellowship (FT130101709). P.I.W.d.B. is funded in part by the Netherlands Organization for Scientific Research (VIDI Vernieuwingsimpuls project 016.126.354) and by the National Institutes of Health (1R01AR062886-1). ; Peer reviewed