Background/Purpose: We recently reported an association between gout and osteoarthritis (OA) presence and severity, and a possible association between hyperuricemia and OA severity (Howard et al, JCR 2014).  Others have reported that synovial fluid uric acid levels among non-gout patients correlate with OA severity (DeNoble et al, PNAS 2011).  To date however, the possibility that serum UA (sUA) levels may be associated with OA progression has not been assessed.  We therefore asked whether higher levels of sUA were associated with OA progression, determined as joint space narrowing (JSN), in a natural history cohort of non-obese symptomatic knee OA (SKOA) patients.

Methods: The NYU SKOA cohort consists of subjects followed for clinical, imaging and laboratory parameters for 24 months. Only patients with BMI<32 are included. From 144 completers we selected the first 80 subjects enrolled, and measured a single-point sUA level by ELISA (in duplicate) using previously banked and frozen serum. At entry and 24 months, patients underwent standardized weight-bearing fixed-flexion posteroanterior knee radiographs using the SynaFlexer™ methodology. Diseased compartment joint space width (dcJSW) and Kellgren-Lawrence (KL) grades in the signal (more painful) knee were determined by a musculoskeletal radiologist blinded to patient information (LR). Our primary outcome was extent of progression of JSN (decline in JSW in mm) over 24 months, as a function of sUA. 

Results: Mean baseline KL score for all 80 subjects was 2.2, and mean baseline dcJSW was 3.5 ±1.3mm.  Patients were 62% female, with a mean age of 61±10 years and mean BMI of 26.7±3.6kg/m².  Most sUAs were <7.0 mg/dL, consistent with a non-obese, predominantly female population. Consistent with prior reports, sUA levels correlated with age (p=0.02) and BMI (p=0.04).  We observed no significant associations between sUA and baseline JSW or KL score. In contrast, we observed a modest but statistically significant correlation between sUA and JSN across all patients (R=0.22;p=0.048). Additionally, when dichotomized by JSN (≥0.5 or <0.5mm/24mo), progressors demonstrated significantly higher sUA levels vs non-progressors (2.35 vs 2.92mg/dl, p=0.004).  Conversely, patients with above-median sUA levels experienced more JSN compared with those below the median, though these differences did not achieve significance (0.41 vs 0.63 mm, p=0.30).  When analyzed according to baseline severity (either KL grade or dcJSW quartiles) we observed non-significant trends of increasing JSN with increasing sUA in all but the KL3 and third quartile of dcJSW groups.

Conclusion: Our data suggest that increasing sUA concentrations may be associated with increased rates of JSN among non-obese patients with SKOA. If confirmed in other populations, these data would warrant investigation into the mechanisms/directions of the association, and possibly into the question of whether urate lowering in patients with early OA may be a strategy to reduce and/or prevent progression.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/association-between-serum-urate-and-osteoarthritis-progression-in-a-non-obese-cohort/