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GRAEME J. CARROLL ABSTRACT. Methods. HFE genotyping was performed in 87 patients with radiologically proven OA in 3 joint regions: index or middle finger metacarpophalangeal joints (MCP2,3; n = 52), elbow joints (n = 8), ankle, intertarsal or tarsometatarsal joints (ankle/IT/TMT; n = 27); and in 56 patients with radiologically proven OA in finger interphalangeal (IP) joints, but not MCP2,3 joints (IP OA control group). HFE mutation frequencies in these groups were also compared to those in a similar population (Busselton population control group). Results. A statistically significant association between HFE mutations and OA was observed for the MCP2,3 joints (p = 0.0001) and the ankle/IT/TMT joint group (p = 0.002) as well as for the 3 joint regions collectively (p = 0.0001), but not for the elbow joints (p = 0.062). Comparison with the Busselton population controls showed similar statistically significant associations, except for the elbow and ankle/IT/TMT groups, where similar trends were observed. Conclusion. HFE gene mutations are associated with OA in the MCP2,3 joints. These mutations may be markers for a polyarticular OA phenotype. (J Rheumatol 2006;33:741–3)
Key Indexing Terms: OSTEOARTHRITIS
From the University Department of Medicine, University of Western Australia; Department of Rheumatology, Fremantle Hospital; and ArthroCare Pty. Ltd., Perth, Western Australia. G.J. Carroll, MD, FRACP, Honorary Research Fellow, University Department of Medicine, University of Western Australia, Consultant Rheumatologist, Department of Rheumatology, Fremantle Hospital; Medical Director, ArthroCare Pty. Ltd. Address reprint requests to Dr. G.J. Carroll, ArthroCare, PO Box 6, Mount Lawley, Western Australia 6929. E-mail: md@arthrocare.com.au Accepted for publication November 25, 2005.
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