Abstract

Introduction: Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) are chronic inflammatory conditions that damage joints and impair patient’s physical fitness. Despite sharing many drugs in their treatment guidelines, they have many differences in their pathogenicity. It is generally understood that a mismatch between pro-and anti-inflammatory cytokine activity promotes autoimmune and chronic inflammation. However, it is still unclear how cytokines are arranged within such complex signaling pathways, and hence which cytokine would be the better target for the evolution of treatments.Methods: This cross-sectional study included 71 patients, 45 with RA, and 26 with AS. According to the type of the treatments, RA patients were divided into three groups (1,2,3), and AS patients were divided into 2 groups (4,5) Data collection was made by clinical examination and specially designed questionnaire form. Five to seven milliliters of blood were collected, centrifuged and the serum was stored at -24 C till the time of assay. Serum TNFa, CXCL13, and ICAM1 were determined by the ELISA. CRP is measured by the photometric method, and ESR by the Wintrobe method. Data were analyzed statistically utilizing the SPSS program (version 26).Results: Eighty-two percent of patients with RA were females, and (18%) were males, their mean age was (51.84 ± 10.74) years and their mean weight was (73.28 ± 13.17) Kg. Regarding AS, (4%) of the patients were females and (96%) were males, with a mean age was (41.88 ± 10.95) years and mean weight was (78.67 + 13.4) Kg. Serum inflammatory parameters except ICAM1 were significantly higher in patients with RA than in those with AS, regardless of the treatment type.Conclusion: TNFa is significantly correlated with DAS-CRP, ASDAS in patients with RA and AS but its level is significantly higher in patients with RA. Serum CXCL13 correlates with disease activity in patients with RA and could be used as a target for the evolution of new treatments while it has a minor role in patients with AS.

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