Influence of adipocytokines and IL-6 on ankylosing spondylitis disease activity and functional status |
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Authors: | Gehan Gamal Elolemy Sahar Saad Ganeb Ahmed Taha Abou Ghanima Eman Ramadan Abdelgwad |
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Institution: | 1. Department of Rheumatology and Rehabilitation, Faculty of Medicine, Benha University, Egypt;2. Department of Clinical Pathology, Faculty of Medicine, Benha University, Egypt |
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Abstract: | Aim of the workThis study aimed to assess serum levels of some adipocytokines (leptin, adiponectin and resistin) and IL-6 in patients with ankylosing spondylitis (AS) to evaluate their relationship to disease activity and functional capacity.Patient and methodTwenty-five AS patients were enrolled. Body mass index (BMI), Bath AS Disease Activity Index (BASDAI), Bath AS Functional Index (BASFI) and acute phase reactants, such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels, were assessed. Serum leptin, adiponectin, resistin and interleukin (IL)-6 levels were determined using enzyme-linked immunosorbent assay (ELISA).ResultsThe mean levels of leptin (9.1 ± 3.9 ng/ml), resistin (2.27 ± 1.15 ng/ml) and IL-6 (9.2 ± 5.8 pg/ml); were significantly elevated in patients with AS compared to the controls (p = 0.000, p = 0.0028 and p = 0.000, respectively). Only serum leptin levels correlated significantly with IL-6 (p = 0.004), and both serum leptin and IL-6 levels correlated significantly with BASDAI (p = 0.02 and p = 0.005, respectively), ESR (p = 0.04) and CRP (p = 0.01 and p = 0.006, respectively) in AS patients. Serum resistin did not correlate with any of the AS disease parameters, whereas, serum adiponectin neither significantly elevated nor correlated with any of these parameters.ConclusionThe associations of significantly increased levels of serum leptin and IL-6 with AS disease activity parameters give clues to their role in the inflammatory process of the disease. Failure to find any correlation between high serum resistin levels and AS disease activity parameters is suggestive of its role in the pathogenesis rather than disease activity. |
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