Background We aimed in this study to investigate blood-brain barrier (BBB) dysfunction in RA patients who had no neurological symptoms, and were receiving synthetic DMARD treatment.
Objectives We investigated correlations between cranial MRI images and brain specific proteins (S100 Beta, GFAP), cytokines (IL-1 beta, IL-17) in plasma which had important roles in disease activity.
Methods In our study, 57 patients (46 females and 11 males) were included included in RA group, and 34 patients (24 females and 10 males) in the control group. All of RA patients were receiving synthetic DMARD treatment. Demographic characteristics of all patients were recorded. Disease activity was evaluated by using DAS-28. Mini-mental test (MMT) was used for evaluation of cognitive functions, and Fazekas scale was used to evaluate cranial MR lesions. S100 beta, GFAP, claudin, IL-17, and IL-1 beta levels were measured in peripheral blood of both groups.
Results Demographic characteristics were similar between the groups, and there was no statistically significant difference in gender, age, and body mass index (BMI) between patient and control groups (p>0.05). S100 beta, and GFAP levels were significantly higher in RA group (p<0.05). No difference was determined in hyperintense lesions diagnosed in cranial MR between patient and control groups (p>0.05). There were positive correlations between IL-17 S100 beta and GFAP, and IL-1 beta and S100 beta.
Conclusions In our study, we have shown that blood-brain barrier may be damaged subclinically in RA patients, brain specific proteins related to BBB dysfunction may be increased in the peripheral blood, and BBB dysfunction may be related to cytokines which play an important role in disease pathogenesis. In conclusion, cytokines which circulate in the peripheral blood in RA may cause subclinical BBB damage. Further large scale studies with long-term follow-up are required which will support this hypothesis.
Disclosure of Interest None declared