Abstract
Objective
Juvenile idiopathic arthritis (JIA) is a heterogeneous condition with very few clinical and laboratory signs that can help predict the course and severity of the disease in the individual patient. The cell-surface antigen HLA-B27 is well known to be associated with spondyloarthropathies, reactive arthritis, and enthesitis. HLA-B27 plays an important role in the classification of JIA, since evidence of sacroiliitis most often evolves after years of arthritis in other joints. We investigated the associations of HLA-B27 and the clinical manifestations of JIA using a method as close to a population-based study as possible.
Methods
We studied an incidence-based cohort of 305 patients collected prospectively in 3 Nordic countries (Sweden, Norway, Denmark). Clinical and serological data of the first 3 years of the disease were collected.
Results
HLA-B27 was found to be positive in 25.5% of the patients, and we found a higher proportion of HLA-B27-positive boys with older age at disease onset (p = 0.034). Regression analysis showed a correlation of 0.7 in the HLA-B27-positive boys, pointing to a higher risk of more joint involvement with older age at disease onset. By Fisher’s exact test, involvement of small joints in the lower extremities was associated with HLA-B27 in boys (p = 0.011), but not in girls (p = 0.687). HLA-B27 was associated with inflammatory back pain in both sexes (p = 0.041 in boys, p = 0.042 in girls), but with enthesitis only in boys (p < 0.001 in boys, p = 0.708 in girls).
Conclusion
HLA-B27 is of increasing importance with older age at disease onset in boys with JIA, predicting more active joints within the first 3 years of disease, and also involving small joints in the lower extremity to a greater degree than in HLA-B27-negative boys. During the first 3 years of disease the occurrence of HLA-B27 is associated with inflammatory back pain in both sexes, but with enthesitis only in boys. Our data present new challenges for the ILAR classification of JIA.
Key Indexing Terms:Footnotes
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L. Berntson, MD, PhD, Department of Women’s and Children’s Health, Uppsala University Children’s Hospital; M. Damgård, MD, Department of Pediatrics, Falun Hospital; B. Andersson Gäre, MD, PhD, Department of Pediatrics, Ryhov County Hospital; T. Herlin, MD, PhD, Århus University Hospital; S. Nielsen, MD, University Clinic of Pediatrics II, Rigshospitalet; E. Nordal, MD, Institute of Clinical Medicine/Institute of Community Medicine, University of Tromsø, and Department of Pediatrics, University Hospital of North Norway; M. Rygg, MD, PhD, Department of Laboratory Medicine, Children’s and Women’s Health, Faculty of Medicine, Norwegian University of Science and Technology, and Department of Pediatrics, St. Olavs Hospital; M. Zak, MD, University Clinic of Pediatrics II, Rigshospitalet; A. Fasth, MD, PhD, Professor of Pediatric Immunology, Department of Pediatrics, Göteborg University.
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Supported by grants from the Department of Women’s and Children’s Health, Uppsala University Children’s Hospital, Uppsala, The Queen Silvia Children’s Hospital, Göteborg, and the Dalarna Clinical Research Institute, Falun, Sweden; and the Swedish Rheumatism Association and King Gustaf V 80th Jubilee Fund.
- Accepted for publication May 26, 2008.
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