Abstract
ObjectivesWith the present study we wanted to explore the impact of treatment with a tumor necrosis factor-α -inhibitor (TNFi) on levels of soluble biomarkers in rheumatoid arthritis (RA) patients and to identify predictors of impaired drug levels and development of anti-TNFi antibodies (anti-TNFi Abs).MethodsBlood samples from 26 patients with established RA were taken at baseline and following 6 months of treatment with adalimumab or infliximab. Samples were analyzed for levels of TNFi, interleukin (IL)-6, and soluble TNF-receptors 1 and -2 (sTNF-R1 and -2) and for presence of anti-TNFi Abs. Clinical and demographic data were recorded as well.ResultsDuring the initial 6 months treatment, DAS28(CRP) (Disease activity score in 28 joints using C-reactive protein) and levels of IL-6 and sTNF-R2 decreased significantly in patients without anti-TNFi Abs and in patients retaining detectable drug levels. The levels of other tested cytokines (TNF-α, TNF-β, IL-1ra, IL-1b, IL-8, IL-10, IL-12(p70), IL-13, IL-17A, IL-17F, and IL-33) were generally below detection limits. Higher baseline levels of IL-6 associated with undetectable levels of TNFi at follow-up. Anti-TNFi Abs were associated with decreased drug levels, but no predictors for anti-TNFi Ab development could be found.ConclusionThe effect of treatment with TNFi on RA disease activity depends on levels of active drug, and by presence of anti-TNFi Abs. In patients who retain detectable drug levels, and in the absence of anti-TNFi Abs, clinical outcome is improved during treatment, and circulating levels of IL-6 and sTNF-R2 decrease. Baseline levels of IL-6 may predict depletion of TNFi and may identify patients at risk of treatment failure.
Highlights
Biological TNF-α inhibitors (TNFi) have revolutionized the treatment of rheumatoid arthritis (RA) and other autoimmune inflammatory diseases, only one third of RA patients will experience a sustained treatment response [1,2,3]
The effect of treatment with TNFi on RA disease activity depends on levels of active drug, and by presence of anti-TNFi Abs
In patients who retain detectable drug levels, and in the absence of anti-TNFi Abs, clinical outcome is improved during treatment, and circulating levels of IL-6 and sTNF-R2 decrease
Summary
Biological TNF-α inhibitors (TNFi) have revolutionized the treatment of rheumatoid arthritis (RA) and other autoimmune inflammatory diseases, only one third of RA patients will experience a sustained treatment response [1,2,3]. Anti-TNFi Abs may develop in patients treated with a TNFi, and their presence in the patient is associated with lower levels of bioactive TNFi, impaired clinical efficacy, and adverse reactions [6;10,11,12,13,14]. Anti-TNFi Abs are more often detected in patients treated with adalimumab (Humira1) and infliximab (Remicade1) than in patients treated with other available TNFi [13]. It is, still unknown why some patients develop anti-TNFi Abs, while others do not. Patients developing anti-TNFi Abs most often do so within the first 6–12 months of treatment, but measurable anti-TNFi Abs may develop after several years of treatment [11]
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