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Psoriasis is a chronic autoinflammatory disease that affects 2 % of the population in Western countries.1,2 Its pathogenesis includes an immune cascade of pro-inflammatory cytokines that results in a state of persistent inflammation and increased epidermal cell turnover.3 Its spectrum includes different cutaneous manifestations that can coexist in a single patient, although they all share essential characteristics: erythema, thickening and scales. The persistent inflammatory state has been associated with extracutaneous manifestations: increased cardiovascular risk, psoriatic arthritis secondary to oxidative stress increase and antioxidant capacity decrease. Epidermal turnover is accentuated, with the clinical and diagnostic histopathological features of the disease.4,5 The increase in the keratinocyte cell cycle induces an increase in purine metabolism, which elevates serum uric acid levels.6 Since 1948, Lobitz and Brunsting described for the first time the relationship between hyperuricemia and psoriasis;7 recently, Gisondi et al.8 confirmed this relationship, identifying psoriasis as the most important risk factor in a multivariate analysis when compared with other known risk factors for hyperuricemia, such as obesity or metabolic syndrome. In 2016, Li et al., in a meta-analysis that assessed data from 14 clinical trials and included 29 416 patients with psoriasis, concluded that the correlation between psoriasis and hyperuricemia shows an ethnic pattern associated with genetic components and different lifestyles.9 The increase in serum uric acid has been associated with an increase in the carotid intima thickness in patients with psoriatic arthritis, whereas in patients Abstract

Uric acid as a marker of clinical severity and comorbidities in plaque psoriasis