Journal Article
Observational Study
Research Support, Non-U.S. Gov't
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Subsets of symptomatic hand osteoarthritis in community-dwelling older adults in the United Kingdom: prevalence, inter-relationships, risk factor profiles and clinical characteristics at baseline and 3-years.

OBJECTIVE: To compare the population prevalence, inter-relationships, risk factor profiles and clinical characteristics of subsets of symptomatic hand osteoarthritis (OA) with a view to understanding their relative frequency and distinctiveness.

METHOD: 1076 community-dwelling adults with hand symptoms (60% women, mean age 64.7 years) were recruited and classified into pre-defined subsets using physical examination and standardised hand radiographs, scored with the Kellgren & Lawrence (K&L) and Verbruggen-Veys grading systems. Detailed information on selected risk factors was obtained from direct measurement (Body Mass Index (BMI)), self-complete questionnaires (excessive use of hands, previous hand injury) and medical record review (hypertension, dyslipidaemia, type 2 diabetes). Hand pain and disability were self-reported at baseline and 3-year follow-up using Australian/Canadian Osteoarthritis Hand Index (AUSCAN).

RESULTS: Crude population prevalence estimates for symptomatic hand OA subsets in the adult population aged 50 years and over were: thumb base OA (22.4%), nodal interphalangeal joint (IPJ) OA (15.5%), generalised hand OA (10.4%), non-nodal IPJ OA (4.9%), erosive OA (1.0%). Apart from thumb base OA, there was considerable overlap between the subsets. Erosive OA appeared the most distinctive with the highest female: male ratio, and the most disability at baseline and 3-years. A higher frequency of obesity, hypertension, dyslipidaemia, and metabolic syndrome was observed in this subset.

CONCLUSION: Overlap in the occurrence of hand OA subsets poses conceptual and practical challenges to the pursuit of distinct phenotypes. Erosive OA may nevertheless provide particular insight into the role of metabolic and cardiovascular risk factors in the pathogenesis of OA.

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