Vibeke Videm1,2, Ranjeny Thomas3,4, Matthew A Brown3,4, Mari Hoff3,4. 1. From the Department of Laboratory Medicine, Children's and Women's Health, and the Department of Public Health and General Practice and Department of Neuroscience, NTNU - Norwegian University of Science and Technology; Department of Immunology and Transfusion Medicine, and Department of Rheumatology, St. Olavs Hospital, Trondheim, Norway; University of Queensland, Translational Research Institute; Queensland University of Technology, Institute of Health and Biomedical Research, Princess Alexandra Hospital, Brisbane, Australia. vibeke.videm@ntnu.no. 2. V. Videm, MD, PhD, Professor, Department of Laboratory Medicine, Children's and Women's Health, NTNU, and Senior Consultant, Department of Immunology and Transfusion Medicine, St. Olavs Hospital; R. Thomas, MBBS, FRACP, MD, Professor, Translational Research Institute, University of Queensland; M.A. Brown, MBBS, MD, Director of Genomics, Queensland University of Technology, Institute of Health and Biomedical Research, Princess Alexandra Hospital; M. Hoff, MD, PhD, Associate Professor, Department of Public Health and General Practice and Department of Neuroscience, NTNU, and Senior Consultant, Department of Rheumatology, St. Olavs Hospital. vibeke.videm@ntnu.no. 3. From the Department of Laboratory Medicine, Children's and Women's Health, and the Department of Public Health and General Practice and Department of Neuroscience, NTNU - Norwegian University of Science and Technology; Department of Immunology and Transfusion Medicine, and Department of Rheumatology, St. Olavs Hospital, Trondheim, Norway; University of Queensland, Translational Research Institute; Queensland University of Technology, Institute of Health and Biomedical Research, Princess Alexandra Hospital, Brisbane, Australia. 4. V. Videm, MD, PhD, Professor, Department of Laboratory Medicine, Children's and Women's Health, NTNU, and Senior Consultant, Department of Immunology and Transfusion Medicine, St. Olavs Hospital; R. Thomas, MBBS, FRACP, MD, Professor, Translational Research Institute, University of Queensland; M.A. Brown, MBBS, MD, Director of Genomics, Queensland University of Technology, Institute of Health and Biomedical Research, Princess Alexandra Hospital; M. Hoff, MD, PhD, Associate Professor, Department of Public Health and General Practice and Department of Neuroscience, NTNU, and Senior Consultant, Department of Rheumatology, St. Olavs Hospital.
Abstract
OBJECTIVE: Self-reported diagnoses of inflammatory arthritis are not accurate. The primary study aim was to ascertain self-reported diagnoses of rheumatoid arthritis (RA) and ankylosing spondylitis (AS) in the Norwegian population-based Nord-Trøndelag Health Study (HUNT) using hospital case files. The secondary aim was to provide updated estimates of the prevalence and incidence of RA and AS. METHODS: All inhabitants ≥ 20 years old from the county of Nord-Trøndelag were invited. Data from 70,805 unique participants from HUNT2 (1995-1997) and HUNT3 (2006-2008) were included. For participants who self-reported RA or AS, case files from all 3 hospitals in the catchment area were evaluated using standardized diagnostic criteria. RESULTS: Of 2703 self-reported cases of RA, 19.1% were verified in hospital files. Of 1064 self-reported cases of AS, 15.8% were verified. Of 259 cases self-reporting both RA and AS, 8.1% had RA and 5.4% had AS. Overall, a self-report of 1 or both diagnoses could not be verified in 82.1%, including 22.8% with insufficient information or no case file. The prevalence of RA was 768 (95% CI 705-835) per 100,000. The incidence of RA from HUNT2 to HUNT3 was 0.48 (0.41-0.56) per 1000 per year. The prevalence of AS was 264 (228-305) per 100,000. The incidence of AS from HUNT2 to HUNT3 was 0.19 (0.15-0.24) per 1000 per year. CONCLUSION: Self-reported diagnoses of RA and AS are often false-positive. The prevalence and incidence of RA were comparable to reports from similar populations. The incidence of AS was higher than previously reported in a mixed population from Norway.
OBJECTIVE: Self-reported diagnoses of inflammatory arthritis are not accurate. The primary study aim was to ascertain self-reported diagnoses of rheumatoid arthritis (RA) and ankylosing spondylitis (AS) in the Norwegian population-based Nord-Trøndelag Health Study (HUNT) using hospital case files. The secondary aim was to provide updated estimates of the prevalence and incidence of RA and AS. METHODS: All inhabitants ≥ 20 years old from the county of Nord-Trøndelag were invited. Data from 70,805 unique participants from HUNT2 (1995-1997) and HUNT3 (2006-2008) were included. For participants who self-reported RA or AS, case files from all 3 hospitals in the catchment area were evaluated using standardized diagnostic criteria. RESULTS: Of 2703 self-reported cases of RA, 19.1% were verified in hospital files. Of 1064 self-reported cases of AS, 15.8% were verified. Of 259 cases self-reporting both RA and AS, 8.1% had RA and 5.4% had AS. Overall, a self-report of 1 or both diagnoses could not be verified in 82.1%, including 22.8% with insufficient information or no case file. The prevalence of RA was 768 (95% CI 705-835) per 100,000. The incidence of RA from HUNT2 to HUNT3 was 0.48 (0.41-0.56) per 1000 per year. The prevalence of AS was 264 (228-305) per 100,000. The incidence of AS from HUNT2 to HUNT3 was 0.19 (0.15-0.24) per 1000 per year. CONCLUSION: Self-reported diagnoses of RA and AS are often false-positive. The prevalence and incidence of RA were comparable to reports from similar populations. The incidence of AS was higher than previously reported in a mixed population from Norway.
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