Rheumatology Advance Access originally published online on March 19, 2008
Rheumatology 2008 47(5):732-733; doi:10.1093/rheumatology/ken087
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LETTERS TO THE EDITOR |
Gout and nodal osteoarthritis: a case–control study
Academic Rheumatology, University of Nottingham, Nottingham, UK.
Correspondence to: E. Roddy, Primary Care Musculoskeletal Research Centre, Primary Care Sciences, Keele University, Staffordshire ST5 5BG, UK. E-mail: e.roddy{at}cphc.keele.ac.uk
SIR, The characteristic pattern of joint involvement seen in gout has been attributed to the readiness of MSU crystals to form in osteoarthritic joints [1, 2]. In a recent community-based study, we found that joints that had been sites of acute attacks of gout are frequently also affected by OA [3] suggesting that OA predisposes to local MSU crystal deposition at individual joint sites. However, it is also possible that a general cartilage defect, such as may occur in nodal OA, increases the risk of developing gout. Using the same group of gout sufferers and a separate control group recruited from the same population, we undertook a case–control study to examine this possibility. Approval was gained from Nottingham Local Research Ethics Committee 2.
As reported previously [3, 4], a questionnaire survey was sent to all adults over 30 yrs of age registered with two general practices in Nottingham. Standard demographic information and details of gout were requested. Self-reported nodal OA [5], hallux valgus (HV) [6], knee [7] and big toe pain on most days for at least a month within the last year, joint replacement, diuretic use and previously diagnosed OA, RA or AS were assessed. The primary risk factor of interest was self-reported Heberden's and Bouchard's nodes (recognized central clinical markers of nodal OA): nodal OA was defined as the presence of nodes on at least two rays on each hand [8]. Subjects reporting a diagnosis of gout or acute attacks typical of crystal synovitis were invited to attend a clinical assessment where the diagnosis was confirmed on clinical grounds. A sample size of 326 cases and 1304 controls was required to detect an odds ratio (OR) of 1.4 for nodal OA between cases and controls (power 0.85, significance 0.05, cases: controls 1: 4). Gout cases confirmed at the clinical assessment were each matched to four controls for age (±2 yrs), gender and practice. Crude OR and 95% CI were calculated between gout and manifestations of OA. ORs (95% CI) were then adjusted for BMI (
30 kg/m2 or >30 kg/m2) and diuretic use using a conditional logistic regression model.
Four thousand two hundred and forty-nine completed questionnaire responses were received (adjusted response rate 32%). One hundred and sixty-four cases of gout were confirmed at clinical assessment. Characteristics of the cases have been reported previously [3, 4]. Mean ages of cases and controls were 63.4 yrs (S.D. 11.2) and 63.5 yrs (11.3), respectively. Both groups were predominantly male (81% both groups). Thirty-nine cases (24%) and 86 controls (13%) were obese (BMI > 30 kg/m2) and 23 cases (14%) and 23 controls (4%) had taken diuretics prior to the age at which each index case experienced their first attack of gout. On univariate analysis, gout was associated with knee pain, HV and big toe pain but not nodal OA (Table 1). After adjustment for BMI and diuretic use, significant associations remained between gout and knee pain (OR 2.05; 95% CI 1.37, 3.06), HV (OR 2.10; 95% CI 1.39, 3.18) and big toe pain (OR 2.94; 95% CI 1.62, 5.34).
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Although it may appear that this study is similar to our previous report [3], there are key methodological differences which provide interesting insights into the pathogenesis of gout. Participation in our previous analysis was limited to gout sufferers, the analysis comparing the presence of OA between joints which had and had not been the site of an acute attack of gout, and found a very strong association between sites of acute gout and the presence of OA. In the current patient-based case–control study, we compared self-reported manifestations of OA between gout cases and controls, with a particular focus on whether nodal OA is more common in gout sufferers than controls, and hence may be a risk factor for the development of gout. We were unable to find evidence of such an association although the study was significantly under-powered and therefore may be liable to a type II error. A further caveat is that the instruments used to assess self-reported OA have not been specifically validated in a gout population. The association of knee pain, HV and big toe pain with gout supports the hypothesis that OA at individual sites may predispose to MSU crystal deposition at that site as suggested by previous studies [3, 9]. These associations could equally reflect chronic joint damage from gout rather than OA. However, in our previous study [3], the association between gout and OA at individual joint sites was not influenced by the chronicity of gout, refuting this hypothesis. Further prospective radiographic clarification of this issue is warranted. The findings of this study, taken alongside our previous work, suggest that the association between gout and OA is mediated by local mechanical factors rather than systemic or genetic factors.
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Acknowledgements |
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We would like to thank the staff and patients of Arnold Health Centre and The Calverton Practice in Nottingham, UK.
Funding: We are grateful for funding from the Arthritis Research Campaign, UK (ICAC grant 14851) and unrestricted financial support from Astra-Zeneca-UK, Glaxo-Smith-Kline-USA and Ipsen, France.
Disclosure statement: The authors have declared no conflicts of interest.
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