Abstract
Enhanced epidermal turnover is believed to increase uric acid synthesis in psoriasis. Fifteen patients with psoriasis (less than 30% skin surface involvement) showed normal serum urate concentrations and urinary hypoxanthine and xanthine excretion but increased uric acid excretion (patients vs. controls, 3.2 ± 0.1 vs. 2.0 ± 0.1 mmol/g creatinine, P<0.01). The reanl physiological response to RNA loading is to increase uric acid excretion due to reduced tubular urate postsecretory reabsorption. To test whether increased uric acid excretion in psoriasis indicates enhanced purine nucleotide degradation we examined the intrarenal handling of uric acid and the capacity of the nucleotide catabolic pathway to accelerate in response to fructose infusion. The probenecid test evidenced a significantly diminished tubular urate postsecretory reabsorption in psoriatic patients. Intravenous fructose promoted a mean increase in hypoxanthine and xanthine excretion, with respect to mean baseline values, of 1257 and 1387 percent vs. 342 and 380 percent in patients vs. controls, respectively (P<0.001) These data indicate accelerated purine nucleotide degradation in psoriasis. A diminished tubular urate postsecretory reabsorption with normal serum urate levels may reflect increased uric acid synthesis.
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Puig, J., Mateos, F., Gómez, P. et al. URIC ACID METABOLISM IN PSORIASIS: 166. Pediatr Res 19, 771 (1985). https://doi.org/10.1203/00006450-198507000-00186
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DOI: https://doi.org/10.1203/00006450-198507000-00186