Background RA is a chronic disease with a yet unclarified etiology, which causes the activation of pro-inflammatory pathways that bring about joint and systemic inflammations (1).In recent years, the pathophysiology of brain damage that can occur in RA has drawn attention. Emphasis is being put on the possibility that brain damage occurs due to blood-brain barrier (BBB) damage that is linked to chronic inflammation

Objectives In this study, we aimed to investigate the peripheral blood levels of brain-specific proteins such as S100 beta and GFAP (glial fibrillary acidic protein), the differences in these proteins in patients who did and did not undergo TNF blocker therapy and their relationship with cranial MR lesions, disease activity and cognitive functions with the purpose of determining CNS (central nervous system) damage in patients with rheumatoid arthritis (RA).

Methods 58 RA patients (47 (81.0%) females, 11 (19.0%) males) and 34 healthy controls (24 (70.6%) females, 10 (29.4%) males) were included in the study. All RA patients were on synthetic DMARD therapy at the beginning. While 30 patients continued sDMARD therapy, 28 patients with high disease activity were started on TNF blocker therapy. All demographic characteristics of the patients were recorded. Disease activity was evaluated using DAS28. The Mini-Mental State Examination (MMSE) was used to evaluate cognitive functions, and the Fazekas Scale was used to assess the cranial MRI lesions. The peripheral blood S100 beta, GFAP, claudin, IL-17, IL-1 beta levels of the patients were measured at the beginning and on the 6th month.

Results Demographic characteristics were similar between the two groups and no statistical difference was detected between the patient group and the control group in terms of sex, age, and BMI. (p>0.05) S100 beta and GFAP levels were higher to a significant degree compared to the control group. (p<0.05) In the group that was started on TNF blocker therapy, S100 beta and GFAP levels were detected to have decreased significantly 6 months after treatment compared to the start of treatment. (p<0.05) No difference was found between the RA and control groups in terms of hyperintense lesions seen in the cranial MRI. (p>0.05) As the lesions in the deep white matter seen in the cranial MRI of RA patients increased, their S100 beta levels were also seen to increase. (p<0.05)

Conclusions In conclusion, next to decreasing disease activity and joint erosions by suppressing inflammation, anti-TNF therapy in RA can also suppress potential brain damage linked to subclinical BBB (blood-brain-barrier) dysfunction. Further studies with broader participation and longer patient follow-up are needed to reinforce this hypothesis.

References

1. McInnes, I.B. and Schett, G. (2011). Thepathogenesis of rheumatoidarthritis. N Engl J Med 365, 2205 2219.doi:10.1056/ NEJMra1004965.

References

Disclosure of Interest None declared