Clinical and laboratory evaluation of response to biological agents in Rheumatoid Arthritis and Ankylosing Spondylitis

Abstract

Our aim was to evaluate the anti-tumor necrosis factor (TNF) response to treatment, which has been in place in the treatment of Rheumatoid Arthritis(RA) and Ankylosing Spondylitis(AS) patients in recent years and has achieved successful results. In this regard, the follow-up of the disease is more predictable after the initiation of anti-TNF therapy; it is aimed to interpret the parameters used in follow-up more correctly. This cross-sectional, retrospective study was performed in auniversity hospital between 2010-2016. Files of 24 patients with AS and 53 patients with RAwere retrospectively screened. Their clinical situations and laboratory levels were compared before and after the biological agent treatment. Treatment response with RA was evaluated by Disease Activity Score-28 (DAS28) scale and AS patients’ treatment response was evaluated by Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) scale. A total of 77 patients were included in the study. Of the participants, 53 were diagnosed as RA and 24 were diagnosed as AS. After our study we have determined statistically reasonable decrease in C-Reactive protein (CRP), white blood cell (wbc), Platelete, erythrocyte sedimentation rate (ESR) levels but an increase in blood urea nitrogene (BUN), haemoglobine (Hb), Albumin levels. The mean baseline score of BASDAI assessed before the treatment in 24 patients with AS was 6.08 and after the treatment was 3.42; DAS-28 assessed before the treatment was 5,77 and after the treatment was 3,58 and these differences was statistically significant. Patients treated with biological agents showed a significant improvement in clinical assessment evaluated by BASDAI in patients with AS and DAS28 in patients with RA. Significant decrease in CRP, ESH, wbc levels, improvement in chronic disease anemia, increase in albumin level as a negative acute phase reactant and decrease in thrombocyte levels were determined because of acute phase response and regression of inflammation.