Serum leptin, IL-6, hepcidin and bone markers in patients with spondyloarthritis and their correlation with disease activity and aerobic exercise

Objective: To assess the association of serum leptin, IL-6, hepcidin and bone metabolism markers including sclerostin and dickkopf-1 levels with aerobic exercise and disease activity in patients with spondyloarthritis Material and Method: Twenty five patients diagnosed with ankylosing spondylitis, twenty five patients diagnosed with nonradiographic axial spondyloarthritis and twenty healthy volunteers were included to this study. Ten patients in ankylosing spondylitis group were performed 30 min of cycling followed by stretching exercises totally 15 seans. For analysis leptin, IL-6, hepcidin, sclerostin and dickkopf-1 levels and also for determine disease activity markers as C-reaktif protein and Erythrocyte sedimentation rate blood samples were taken and Bath Ankylosing Spondylitis Disease Activity Score (BASDAI), Bath Ankylosing Spondylitis Functional Index (BASFI), visual analog scale (VAS) were calculated before and after exercise. Anthropometric measurements such as body weight, height, waist and hip circumference were evaluated. With the results of these measurements body mass index, waist-to-hip ratio were calculated before and after exercise. Biochemical blood samples and anthropometric measurements were assessed for once in non-exercise groups. Results were compared between groups with AS, nr-aksSpA patients and healty controls. Whether the difference between healty control and both AS and nr-aksSpA patients groups were evaluated. In patients groups results with before and after exercise were compared and a the same time results were assessed in terms of association with disease activity. Results: No significant difference was observed between the three groups with regards to leptin, IL-6, hepcidin. Serum sclerostin levels were statistically significant higher in AS patients than patients with nr-aksSpA (p=0,008). Also symptom onset time was statistically higher in AS patients than patients with nr-aksSpA (p=0,007) and there was a positive corelation between sclerostin levels and symptom onset time (p=0,039, r= ,293). Serum dickkopf-1 levels were also relatively higher in patients with AS and nr-aksSpA than healty control however did not statistically significant. There was a positive correlation between CRP as a disease activity marker and serum hepcidin levels (p=0,11, corelation coefficient=,301). In patients with AS who performed exercise, postexercise VO2max and walking distance were statistically increased (p=0,036, p=0,036 respectively) and scores of clinical disease activity and functionality markers such as BASDAI, BASFI were relatively declined however did not statisticially sinificant. In addition, VAS scores were statistically reduced meanwhile statistically decreases were detected with regard to serum leptin levels (p=0,047). Conclusions: In this study, we showed that VO2max and walking distance of AS patients increased with aerobic exercise. Thus, we increased the cardiopulmonary endurance of the patients. But we could not show a clear relationship between aerobic exercise and inflammation and disease activity. We considered that there may be a relationship between reduced leptin levels after exercise and disease activity, but the methods used in this matter were insufficient. Relation between leptin levels and disease activity can be illuminated by better designed studies. We have not found any relationship between disease activity markers and serum IL-6, sclerostin, dickkopf-1 levels that could be markers of inflammation for assess disease activity. However, we found positive correlation between CRP level which is acute phase reactant and hepcidin. Thus, we thought that hepcidin could be an objective marker to assess disease activity. Due to limited data on this subject, this relationship can be clarified more clearly with more patients. In patients with Nr-AxSpA and AS, we found both serum sclerostin levels and initial onset of first symptoms statistically significantly higher in patients with AS. As a result, we think that sclerostin level, which is osteoproliferation inhibitor, could support the hypothesis in the literature which is different process of the same disease for nr-aksSpa and AS classification. Although spondyloarthritis is thought to be partially associated with inflammation and new bone formation, we believe that sclerostin contributes to the new bone formation independent from inflammation. In the context of all these results, we believe that the pathways involved in disease activity and the relationship of disease activity and exercise can be clarified in the studies to be performed in the future with a larger number of patient.