Experimental findings suggest hyperuricemia may influence atherosclerotic plaque in psoriatic arthritis, highlighting key inflammatory pathways.
Hyperuricemia has long been recognized as the biochemical substrate for gout, but growing evidence suggests that it may also contribute to cardiovascular (CV) disease. Psoriatic inflammation, dominated by interleukin (IL)-23/IL-17 and tumor necrosis factor, amplifies endothelial activation (increase in vascular cell adhesion molecule 1), oxidative stress, and neutrophil extracellular trap formation (ie, NETosis), priming the arterial wall for atherogenesis.
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Queiro et al. (2026) studied this question.
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