# Impact of Brodalumab on Serum Levels of IL-6, IL-17A, IFN-α, IFN-γ, and TNF-α in Patients with Psoriasis Who Failed Treatment with TNF-α Inhibitors

## TL;DR

This study examines how brodalumab affects specific immune markers in psoriasis patients who did not respond to TNF-α inhibitors.

## Contribution

The study provides new insights into the impact of brodalumab on serum cytokine levels in TNF-α inhibitor-resistant psoriasis patients.

## Key findings

- Brodalumab significantly increased IL-17A levels in patients.
- Changes in IL-6, IFN-α, IFN-γ, and TNF-α were not statistically significant.
- No strong correlation was found between cytokine changes and clinical improvement.

## Abstract

Psoriasis is a chronic, immune-mediated inflammatory skin disorder that significantly impacts patients’ quality of life. While TNF-α inhibitors are frequently used to treat moderate-to-severe cases, not all patients respond adequately. Brodalumab, a monoclonal antibody targeting the IL-17 receptor A, has emerged as an alternative for individuals unresponsive to prior therapies. This prospective study investigated the effects of brodalumab on serum cytokine levels—specifically IL-6, IL-17A, IFN-α, IFN-γ, and TNF-α—and their correlation with disease severity as assessed by Psoriasis Area and Severity Index (PASI). Eighteen patients with moderate-to-severe psoriasis who were unresponsive to TNF-α inhibitors received brodalumab for 12 weeks. Cytokine concentrations were measured at baseline and week 12 using an automated immunoassay (ELLA), and clinical outcomes were evaluated using PASI. The results showed a significant increase in IL-17A levels, while changes in IL-6, IFN-α, IFN-γ, and TNF-α did not reach statistical significance. No significant correlations were found between changes in cytokine levels and PASI improvement. However, the small number of available serum samples at week 12 (n = 11) limited the statistical power to detect treatment-related changes in cytokine levels. These findings suggest that while brodalumab influences specific immune markers, the clinical response may not be directly reflected by serum cytokine levels. This highlights the multifactorial nature of psoriasis pathogenesis and underscores the need for further studies to clarify the role of cytokine biomarkers in treatment response.