Relationship of serum ghrelin, leptin, resistin, adiponectin levels with nutritional status and inflammatory determinants in juvenile idiopathic arthritis

Juvenile idiopathic arthritis is a common chronic disease of childhood in which several proinflammatory cytokines are excessively secreted leading to anorexia and weight loss.In this study, we aimed to investigate the levels of ghrelin, a cytokine which is related to apetite and inflammation; adipose tissue cytokines (leptin, adiponectin and resistin) and proinflamatory cytokines (IL-6 and TNF-?) in JIA patients. Besides, we further aimed to investigate the relationship between this adipokines and cytokines with patients? apetite and nutritional status.Patients and method: In this crossectional study, we investigated 40 JIA patients (19 active, 21 inactive patients) and 32 healthy controls. The sociodemographic data, JIA subgroups, antirheumatoid treatments, duration of signs and symptoms of the disease of the patients were recorded. Body weight, length, body mass index, weight for height, and Tanner staging of the patients and controls were also recorded after a complete physical examination. A-24-hour food intake record of the patients and controls were also required.After a 12-hour hunger period, blood samples were taken for ghrelin, proinflamatory cytokines (IL-6, TNF-?), and adipose tissue cytokines (leptin, adiponectin, resistin). The serum samples were studied by ?sandwich ELISA?. The adipose tissue cytokines were proportioned to BMI in order to measure relative values.Results: There was not a significant difference between patients and the controls regarding the weight, length, body mass index, and weight for height. 26 patients and 10 controls gave the 24-hour food intake list; there was not a significant difference between these 2 groups. There was not a significant difference between patients and the controls regarding the levels of ghrelin, TNF-?, IL-6 and resistin. There was a statistically significant difference between patients and controls regarding the levels of relative adiponectin (0.26 ± 0.04; 0.39 ± 0.04, respectively; p=0.041) and relative leptin (0.39 ± 0.05; 0.62 ± 0.07, respectively; p=0.011). Regarding relative adiponectin, the difference between active group (0.21 ± 0.02) and inactive group (0.30 ± 0.08) was not statistically significant (p=0.507); however, there was a significant difference between controls (0.39 ± 0.04) and either active or inactive disease group (p=0.004 ve p=0.025, respectively). Relative leptin levels were statistically significant between control group and inactive disease group (0.62 ± 0.07 vs 0.32 ± 0.05, p=0.000). We also compared the patients whose weight for height were 90-110 with healthy controls in order to make a comparement independent from the effects of adipose tissue on levels of leptin and adiponectin: levels of adiponectin were significantly lower in patients than controls (3.6 ± 0.34 vs 6.4 ± 0.80; p=0.005), levels of leptin were significantly lower in patients than controls (5.1 ± 0.74 vs 10.7 ± 1.44; p=0.000), levels of relative adiponectin were significantly lower in patients than controls (0.22 ± 0.02 vs 0.38 ± 0.04; p=0.007) and levels of relative leptin were significantly lower in patients than controls (0.30 ± 0.04 vs 0.61 ± 0.07; p=0.000).Conclusion: In this study, we showed that levels of relative leptin and adiponectin of JIA patients were lower than controls. This may be related to the inhibition of leptin and adiponectin production per unit of fat mass in the existence of disease. Further prospective studies including larger number of patients are required to demonstrate the effect of the disease and the treatments on adipokines in JIA patients.