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Published on: September 15, 2023
Relationship between biologic therapy and cytokine levels in patients with inflammatory arthritis
Ze Zhang1, Bing-He Zhou, Liang Hu
1Department of Clinical Laboratory, Shanghai Pudong Hospital, Fudan University, Shanghai, China.
Abstract:
Biological agents are frontline treatments for ankylosing spondylitis (AS) and rheumatoid arthritis (RA); however, their efficacy varies owing to differences in patient autoimmune status. This study aimed to evaluate peripheral blood cytokine profiles in patients with AS and RA and assess the impact of different treatment modalities. Data from 145 patients with AS, 491 patients with RA, and 125 healthy controls were collected. Cytokine levels (tumor necrosis factor [TNF]-α, interleukin [IL]-6, IL-8, IL-17, IL-5, etc) were analyzed in healthy controls and patients with AS and RA, with a focus on patients with AS treated with or without biologics. The effects of biologic therapy on cytokine levels in patients with AS and RA were evaluated, along with the impact of disease-modifying antirheumatic drug (DMARD) monotherapy or combination therapy with biologics in patients with RA. Significant differences in interferon (IFN)-α, IFN-γ, IL-10, IL-12P70, IL-2, IL-4, IL-5, IL-6, IL-8, TNF-α, and IL-1β were found among the AS, RA, and HC groups (P < .001); however, no significant difference was noted in IL-17A levels. In patients with RA treated with biologics, IL-1β levels significantly increased (P = .013). In patients with AS treated with biologics, TNF-α levels were correlated with IL-6 and IL-8 levels, and IL-17A levels were correlated with IL-5 and IL-8 levels. Combination therapy with DMARDs and biologics significantly increased IL-1β (P = .016) and IL-6 (P = .047) levels in patients with RA. Overall, biological agents affect cytokine levels in patients with AS and RA, and combination therapy with DMARDs upregulates these levels. Drug choice and combination may significantly influence treatment outcomes in patients with AS and RA treated with biological agents.
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