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AB0039 Interleukin-17 in Systemic Lupus Erythematosus and Rheumatoid Arthritis Patients: Correlation with Clinical Presentation, Laboratory Parameters and Activity Indices
  1. R.F. Moftah1,
  2. E.H.E.-S. Hassan2
  1. 1Clinical pathology
  2. 2Internal Medicine, Rheumatology, Faculty of Medicine, Alexandria University, Alexandria, Egypt


Background Serum interleukin (IL)-17 concentrations have been reported to be increased in systemic lupus erythematosus (SLE), but associations with clinical characteristics are not well understood. Autoimmune diseases such as RA, classically believed to be Th1-mediated, are predominantly driven by a Th17 immune response.

Objectives this study aimed to compare the serum levels of IL-17 in patients with SLE and RA, it is correlation with clinical presentations, laboratory findings and disease activity in both diseases.

Methods The study was carried out on 3 groups. Group I: 20 patients with SLE. Group II: 20 patients with RA. Group III: 10 of age and sex matched healthy subjects as control group.

Results In this study, the mean of age were 43.1±8.98, 46.8±8.17 and 41.98±8.25 for group I (SLE), II (RA) and III (control) respectively, with no statistical significant differences between the studied groups. Also, there were no statistical significant differences between the three studied groups regarding sex, disease duration, disease activity, laboratory investigations (except HB, WBC and platelet count). The mean of IL-17 were 173.2±52.11, 82.6±48.17 and 73.07±41.05 for group I (SLE), II (RA) and III (Control) respectively, group I have values statistically higher than other groups, and group II have values statistically higher than group III. Serum IL-17 levels were significantly higher in SLE patients compared to healthy group.

Conclusions Serum IL-17 concentration correlates with SLE and RA diseases activity but is significantly elevated in patients with SLE disease. The association of other cytokines with serum IL-17 suggests that IL-17 may drive activation of diverse immune pathways in SLE and RA.

Disclosure of Interest None declared

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