Biological Therapy Leads to a Reduction in Systemic Inflammation but Leaves Serum Uric Acid Unmodified in Moderate-to-Severe Plaque Psoriasis: A Prospective Longitudinal Cohort Study.

Background/

Objective

Psoriasis is a systemic inflammatory disease often associated with metabolic comorbidities, including hyperuricemia. While biological therapies effectively target inflammatory pathways, their specific impact on serum uric acid (SUA) levels remains debated. This study aimed to evaluate whether biological therapy, while reducing systemic inflammation, influences SUA levels in patients with moderate-to-severe plaque psoriasis.

Methods

A prospective longitudinal cohort study was conducted involving 30 patients with moderate-to-severe plaque psoriasis. Patients received biological treatment (adalimumab, secukinumab or ustekinumab) and tsDMARDS (apremilast). Clinical severity was assessed using the Psoriasis Area and Severity Index (PASI). C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), SUA levels and other laboratory markers were measured at baseline and after 48 weeks of therapy.

Results

Biological therapy led to a significant reduction in PASI scores (from 21.6 ± 10.7 at baseline to 0.4 ± 0.86 after 48 weeks of therapy, p < 0.001), and CRP decreased from a median of 5.75 mg/L at baseline to 3.55 mg/L, p < 0.001. ESR also declined from 26.2 ± 11.4 mm/h to 19.0 ± 8.06 mm/h, p < 0.001. However, no statistically significant change was observed in mean SUA levels 5.49 ± 1.55 vs. 5.55 ± 1.60 mg/dL; p = 0.758. Subgroup analysis revealed that SUA levels remained stable regardless of the specific biological agent used or the degree of clinical improvement.

Conclusions

Our findings suggest that while biological therapy is highly effective in controlling skin and systemic inflammation in psoriasis, it does not modify SUA levels. These results imply that hyperuricemia in psoriasis may be driven by metabolic factors independent of the primary inflammatory pathways targeted by current biologics.