Involvement of different risk factors in clinically severe large joint osteoarthritis according to the presence of hand interphalangeal nodes
Valdes, Ana M., McWilliams, Daniel, Arden, N. (Nigel), Doherty, Sally A., Wheeler, Margaret, Muir, Kenneth (Kenneth R.), Zhang, Weiya, Cooper, Cyrus, Maciewicz, Rose A. and Doherty, M., M.D.. (2010) Involvement of different risk factors in clinically severe large joint osteoarthritis according to the presence of hand interphalangeal nodes. Arthritis & Rheumatism, Vol.62 (No.9). pp. 2688-2695. ISSN 0004-3591Full text not available from this repository.
Official URL: http://dx.doi.org/10.1002/art.27574
Objective. To quantify the differences in risk factors influencing total hip replacement (THR) and total knee replacement (TKR) based on the presence versus absence of multiple interphalangeal nodes in 2 or more rays of the fingers of each hand in patients with large joint osteoarthritis (OA). Methods. A group of 3,800 patients with large joint OA who underwent total joint replacement (1,201 of whom had the nodal phenotype) and 1,906 control subjects from 2 case-control studies and a population-based cohort in the UK were studied. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated for the risk of total joint replacement in association with age, sex, body mass index (BMI), height, and prevalence of the T allele in the GDF5 rs143383 polymorphism. ORs for total joint replacement were compared between cases of nodal OA and cases of non-nodal OA and between patients who underwent TKR and those who underwent THR. Results. Age, sex, and BMI had significantly higher ORs for an association with total joint replacement in nodal OA cases than in non-nodal OA cases. The GDF5 polymorphism was significantly associated with THR in cases of nodal OA, but not in cases of non-nodal OA, and increased height was a risk factor for THR in non-nodal OA cases only. Female sex was a protective risk factor for TKR in non-nodal OA cases (OR 0.60, 95% CI 0.52-0.70) but was predisposing for TKR in the nodal form of OA (OR 1.83, 95% CI 1.49-2.26). The nodal phenotype was associated with a significantly higher risk of undergoing both THR and TKR (OR 1.46, 95% CI 1.09-1.94) and also a significantly higher risk of bilateral TKR (OR 1.70, 95% CI 1.37-2.11), but, paradoxically, was associated with a lower risk of bilateral THR (OR 0.72, 95% CI 0.56-0.91). Conclusion. Nodal and non-nodal forms of large joint OA have significantly different risk factors and outcomes, indicating a different etiology for the 2 forms of OA. With regard to the likelihood of undergoing THR, this appears to be, at least in part, genetically determined.
|Item Type:||Journal Article|
|Subjects:||R Medicine > RC Internal medicine|
|Divisions:||Faculty of Medicine > Warwick Medical School|
|Journal or Publication Title:||Arthritis & Rheumatism|
|Publisher:||John Wiley & Sons, Inc.|
|Number of Pages:||8|
|Page Range:||pp. 2688-2695|
|Access rights to Published version:||Restricted or Subscription Access|
|Funder:||European Union, Medical Research Council (UK), Oxford National Institute for Health Research Musculoskeletal Biomedical Research Unit. AstraZeneca UK, Arthritis Research Council UK|
|Grant number:||200800, 17661, 14581|
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