Gout Increases Risk of Developing AMD

In vitro studies have supported the idea that uric acid-lowering therapy may reduce toxic effects on the retina in patients with gout as well as promote retinal recovery. Photo: Cleveland Clinic. Click image to enlarge. Research in eye care has been circulating the hypothesis that chronic inflammation in hyperuricemia may be associated with pathogenesis of one very prominent ocular condition: age-related macular degeneration (AMD). A paper newly published in Retina involved researchers examining whether an association between gout and subsequent AMD development and progression holds any validity.The retrospective investigation used a multicenter healthcare research network to identify patients with idiopathic gout who had a prescription for a uric acid-lowering agent (n=23,225)—this was the gout cohort. These individuals were then matched to a cohort without a gout diagnosis (n=1,779,378), serving as the control group, and looked at ophthalmic outcomes of both.Doing so yielded the result that those with gout had increased risk of developing dry AMD, with a relative risk (RR) of 2.73. The gout group also had increased risk of developing advanced dry AMD (RR 2.64), wet AMD (RR 2.48), and needing subsequent anti-VEGF therapy (RR 2.80) compared to the control group at five years. What’s more, the gout group also displayed increased risk for macular hemorrhage as well as needing anti-VEGF injections at one, three and five years compared to controls. A separate analysis of those specifically with early dry AMD determined that those with gout had increased risk for early AMD progression to advanced dry or wet stages or developing macular hemorrhage.The authors further elaborate in their discussion of the paper about the possible reason for this observed relationship. As they explain, upregulated inflammatory status underlies the pathogenesis of both gout and AMD. In the context of hyperuricemia, gout flares result from monosodium urate crystal deposition in joints, ultimately causing monocyte recruitment, NOD-like receptor protein 3 (NLRP3) inflammasome activation and release of inflammatory cytokines of interleukin-1β, interleukin-6 and tumor necrosis factor α.With AMD, drusen presence also triggers NLRP3 inflammasome activation in the retinal pigment epithelium cells. Also with AMD pathogenesis, oxidative stress and inflammation promote the death of retinal pigment epithelium cells and photoreceptor dysfunction. Relating this to gout, both conditions share downstream activation of inflammation and oxidative stress, thus sharing risk factors. For this reason, the authors posit that “modulation of hyperuricemia and treatment of gout may result in improved ocular outcomes among patients with gout and AMD.”While the authors also point out that antioxidant-rich foods and supplements have been shown to prevent flares in patients with gout, whether a combined efficacy exists for vitamins and supplements that may downregulate the inflammatory response in those with gout and AMD is unclear.The researchers more generally believe that “these findings support prior hypotheses suggesting chronic inflammation in hyperuricemia may play a role in AMD pathogenesis.”Click here for the journal source. Alshaikhsalama AM, Alsoudi AF, Wai KM, et al. Gout and risk of age-related macular degeneration. Retina. July 3, 2025. [Epub ahead of print].