Use of TNF-alpha inhibitors reduces inflammation and increases levels of eosinophils — a type of immune cell that protects the body from infections — in patients with ankylosing spondylitis, a study shows.
Anti-TNF-alpha agents are widely used to treat patients with active ankylosing spondylitis who are unable to manage their condition with nonsteroidal anti-inflammatory drugs (NSAIDs) as a first-line treatment. There are a variety of anti-TNF agents available, including infliximab (brand names Remicade, Remsima), adalimumab (brand namesHumira, Imraldi), Simponi (golimumab), Cimzia (certolizumab), and Enbrel (etanercept).
This therapeutic strategy can improve clinical symptoms and quality of life of patients with ankylosing spondylitis by reducing inflammation. However, TNF-alpha inhibitors can also affect immune cells, changing their levels and responsiveness.
In this study, Turkish researchers evaluated the impact of long-term use of anti-TNF-alpha therapies in peripheral blood eosinophil counts in patients with ankylosing spondylitis.
Eosinophils are a type of immune cell that have a major role in the body’s protection from infections and cancer, but are also involved in allergic reactions. Peripheral blood eosinophil count is a valuable biomarker for allergic diseases, parasitic infections, asthma, and sepsis (generalized inflammation). Importantly, the formation and migration of eosinophils are suppressed due to inflammation in bone marrow.
TNF-alpha has been found to play a dual role in these cells, mediating their death as well as their survival, so the effect of anti-TNF-alpha agents on these cells is unclear.
The study enrolled 75 patients with ankylosing spondylitis, who were evaluated before and three and six months after they started treatment with TNF-alpha inhibitors. Therapies used included Remicade (32%), Humira (20%), Enbrel (18.7%), Simponi (18.7%), and Cimzia (10.7%).
Treatment with TNF-alpha inhibitors significantly reduced the blood levels of C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), two recognized hallmarks of active inflammation. This positive result was accompanied by a progressive reduction of disease activity, as measured by Bath Ankylosing Spondylitis
Disease Activity Index (BASDAI) scores, from a mean value of 5.4 down to 2.8 after six months of treatment.
Analysis revealed that blood eosinophil levels increased significantly by about 46% after six months of anti-TNF-alpha therapy compared with before treatment initiation. Eosinophil number changes were not found to correlate with BASDAI score, nor with ESR and CRP values.
The median eosinophil count was determined within normal ranges before and after (in the third and sixth months) anti-TNF-alpha therapy. More pronounced alterations in eosinophil counts were reported in patients taking Remicade, Enbrel, and Humira.
“To the best of our knowledge, our study is the first to evaluate blood eosinophil counts, disease activity with anti-TNF-alpha therapy,” the researchers wrote. “Blood eosinophil count may be affected by TNF-alpha inhibition in patients with ankylosing spondylitis.” However, they also noted that “eosinophil count cannot be used as a biomarker that reflects disease activity.”
Additional comprehensive prospective studies are still warranted to further explore the potential relationship between disease activity and blood eosinophil count.