Introduction. A chronic vascular inflammatory state plays an important role in the pathophysiology of thalassemia. Cross-sectional studies suggest that exercise has anti-inflammatory effects, leading to lower levels of several pro- atherogenic inflammatory markers. However, this has yet to be confirmed by randomized prospective trials.
The present pilot study examined biomarkers inflammation [C-reactive protein (h-CRP) and cytokines] in Beta Thalassemia Major.
Methodology: The present pilot study examined biomarkers inflammation [C-reactive protein (h-CRP) and cytokines] in Beta Thalassemia Major.18 patients with Beta Thalassemia major (mean age 24.64±3.5) that voluntarily divided in two groups of experimental (n=9) and control group (n=9).The subjects of the experimental group attended the concurrent (Resistance- Endurance) exercise for eight weeks. Subjects' blood samples were taken before and after exercise protocol in order to measurement hs-CRP, IL-6, IL-1ᵦ andIL-12 Serum levels.The levels of these markers were measured by using an enzyme-linked Electro immune assay (ELISA) kits. For data analysis the Repeated measures ANOVA, was used. All statistical analysis was performed by SPSS software (V.19). The level of significance was considered p<0.05.
Results: The results indicated the reduction of measurement hs-CRP and IL-6 after eight weeks of concurrent (Resistance-Endurance) exercise compared to the control group (P< 0.05); Indicating IL-1ᵦ and IL-12 ;was increased in exercise group (P> 0.05).
Disscussion: The reduction of hs-CRP and IL-6 serum level and its natural range in the exercise protocol ,can be a regulating response to inflammatory condition in patients under certain exercise conditions without any pathological importance and maybe improved chronic vascular inflammation. We demonstrated that Concurrent (resistance-endurance) exercise is inversely correlated with levels of pro-inflammatory markers in Beta Thalassemia major patients, Therefore, increased production of IL-1β and IL-12 might be contributed to abnormalities in iron metabolism and it is probably due to over stimulation of Th17. The IL-12, as an anti-inflammatory cytokine, and in turn decrease vascular wall inflammation possibly retarding the process of atherosclerosis.