Immunity, Inflammation and Disease · 5 authors, 1 centre
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This study found that patients with hyperuricemia and gout have significantly higher uric acid and interleukin-1β (IL-1β) levels in their tear fluid compared to healthy controls. Tear uric acid was independently and positively associated with tear IL-1β, suggesting a link between hyperuricemia and ocular inflammation. These findings indicate that eye inflammation may begin even in asymptomatic hyperuricemia, highlighting the need for early attention to ocular health in these patients.
**Background:** Uric acid is the end product of purine catabolism, and hyperuricemia affects up to 21% of the general population. While hyperuricemia is a key risk factor for gout and is associated with comorbidities like hypertension and diabetes, its impact on ocular health is poorly understood. Urate crystal deposition can occur in ocular structures, and inflammation mediated by cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-α) is central to gout pathogenesis. Tear fluid composition can reflect ocular inflammation, but cytokine levels in tears of hyperuricemia and gout patients had not been studied. This study aimed to compare tear uric acid and pro-inflammatory cytokine levels between hyperuricemia/gout patients and healthy controls, and to explore correlations between tear uric acid and these cytokines.
**Methods:** A total of 58 control subjects and 58 hyperuricemia patients (40 asymptomatic hyperuricemia, 18 with gout) were recruited from the Affiliated Suzhou Hospital of Nanjing Medical University between June 2020 and October 2021. Exclusion criteria included any ophthalmological condition, severe liver or kidney impairment, pregnancy, and use of uric acid-lowering therapy, NSAIDs, colchicine, corticosteroids, or diuretics within 1 month. Reflex tears were collected using capillary microcaps after sneeze reflex stimulation. Tear uric acid was measured by chemiluminescence, and tear and serum IL-1β and TNF-α were measured by ELISA. Clinical and laboratory data including BMI, blood pressure, liver and kidney function, and serum uric acid were recorded. Statistical analyses included Student's t-test, chi-square test, Spearman correlations, and multivariable linear regression.
**Key Results:** Tear uric acid levels were significantly higher in the hyperuricemia group compared to controls (98.2 ± 51.5 vs. 42.7 ± 24.0 µmol/L, p < .001). Tear IL-1β concentrations were also significantly elevated in hyperuricemia patients (210.2 ± 113.9 vs. 142.6 ± 29.8 pg/mL, p < .001), while tear TNF-α levels did not differ significantly (130.5 ± 50.5 vs. 134.7 ± 54.8 pg/mL, p = .665). Spearman correlation analysis showed a significant positive correlation between tear uric acid and tear IL-1β in the total population (r = 0.597, p < .001) and in the hyperuricemia group, but not in controls. No significant correlation was found between tear uric acid and tear TNF-α. Multivariable linear regression revealed that tear uric acid was independently associated with serum uric acid (B = 0.177, 95% CI 0.118–0.256, p < .001) and tear IL-1β (B = 0.192, 95% CI 0.111–0.273, p < .001). Among hyperuricemia patients, those with asymptomatic hyperuricemia had higher tear uric acid than gout patients (109.3 ± 54.5 vs. 73.5 ± 33.7 µmol/L, p = .013), but this difference was not significant after adjusting for serum uric acid (p = .076). No significant differences in tear IL-1β or TNF-α were found between asymptomatic hyperuricemia and gout groups.
**Clinical Implications:** This study demonstrates that hyperuricemia and gout patients have elevated uric acid and IL-1β levels in tear fluid, with a strong independent association between tear uric acid and IL-1β. This suggests that hyperuricemia may contribute to ocular inflammation via IL-1β-mediated pathways, even in the absence of symptomatic gout. The finding that asymptomatic hyperuricemia patients have similar tear cytokine levels to those with gout flares indicates that ocular inflammation may begin early, before gout symptoms appear. These results highlight the potential for tear fluid analysis as a non-invasive tool to assess ocular inflammation in hyperuricemia, and suggest that IL-1β could be a therapeutic target for preventing hyperuricemia-related ocular complications. However, the cross-sectional design and small sample size limit causal inferences, and further prospective studies with larger cohorts are needed to confirm these findings and explore clinical ocular outcomes.