TNF ınhibitor resistance in ankylosing spondylitis: is Helicobacter pylori the overlooked culprit?

Ankylosing spondylitis (AS) is a chronic inflammatory disease that poses challenges in treatment due to resistance to anti-tumour necrosis factor (anti-TNF) therapies. This study investigates whether Helicobacter (H. pylori) infection contributes to reduced anti-TNF treatment response in AS patients.

A cross-sectional study was conducted on 159 patients with AS. H. pylori infection was assessed using serological assays (ELISA for Iga and Igg), histopathological examination of gastric biopsies, and stool antigen testing. Disease activity and functional impairment were evaluated using ESR, CRP, BASFI, and ASDAS-CRP scores.

Patients with anti-TNF therapy resistance exhibited significantly higher H. pylori Iga seropositivity (p = 0.01) and histopathological positivity (p = 0.03). Additionally, they had longer anti-TNF treatment duration and higher inflammatory markers, including ESR, CRP, BASFI, and ASDAS-CRP scores, indicating a more significant inflammatory burden and functional impairment.

Our findings suggest chronic H. pylori infection may contribute to anti-TNF therapy resistance in AS by promoting systemic inflammation and gut barrier dysfunction. These results underscore the importance of early, aggressive treatment strategies and suggest that H. pylori eradication may potentially enhance the efficacy of anti-TNF drugs. Future interventional studies are required to validate these findings and explore H. pylori screening as a therapeutic approach in AS management.

• Resistance to anti-TNF therapy in AS presents a significant challenge, with the underlying mechanisms not yet fully understood. • This study identifies Helicobacter pylori (H. pylori) infection as a potential contributor to anti-TNF drug resistance in ankylosing spondylitis (AS), with Iga seropositivity and histopathological positivity being markedly higher in resistant patients. • Chronic H. pylori infection may promote systemic inflammation and gut barrier dysfunction, hindering immune responses to anti-TNF therapies. Patients exhibiting therapy resistance showed a more substantial inflammatory burden, including elevated ESR, CRP, BASFI, and ASDAS-CRP scores, which reinforces the connection between persistent inflammation and treatment failure. • Targeting H. pylori through screening and eradication could enhance the efficacy of anti-TNF drugs and improve treatment outcomes for patients with AS.