Background/Purpose: Familial Mediterranean fever (FMF) is an autoinflammatory disease which has self-limiting inflammatory attacks placing in polyserositis. Hepcidin is a protein in peptide structure and it is synthesized from the liver. Hepcidin plays a role in iron metabolism. Especially hepcidin increased at the during inflammation and it decreases the serum level of iron. IL-6 stimulation increases the level of hepcidin. The cause of anemia in chronic diseases is associated with hepcidin. Calprotectin is a recently defined cytokine released from monocytes and neutrophils in response to tissue trauma and inflammation..To compare the levels of hepcidin and calprotectin in healthy individuals and FMF patients with attack-free period and to show the relation with genetic mutations.Methods: Between July 2017-December 2017, sixty patients diagnosed with FMF and sixty healthy volunteers enrolled in this study. All of FMF patients were used colchicine (1-1.5mg/day). Clinical findings and PRAS scores of all patients and were recorded. The blood from a peripheral vein using  suitable blood tubes was withdrew to measure serum prolidase and HIF-1α levels. Blood tests were examined by Elisa. The study protocol was approved by the local ethics committee.Results: Laboratory findings and basic characteristics of FMF and healthy control group are shown in Table1. Mean serum hepcidin level was measured as 468.1(210.3-807.8) pg/ml in FMF group and 890.0 (495.0-1716.9) pg/ml in healthy control (HC) group (p<0.001).The mean serum levels of calprotectin in the FMF group were measured as 1331.4 (969.3-1584.6pg/ml and73.8(45.0-147.9)pg/ml in the HC group (p<0.001). Accoding to ROC analysis optimal levels of serum hepcidin(<581.25 pg/ml; sensitivity was 66.7% and specificity was 71.7%, p<0.05) and calprotectin (>238 pg/ml; sensitivity was 96.7% and specificity was 100%, p<0.05). There was no significant difference between serum hepcidin and calprotectin levels in FMF patients with M694V homozygous and M694V heterozygous (p>0.05). There was no significant difference in serum hepcidin levels between FMF patients with and without arthritis, proteinuria and amyloidosis (p>0.05). There was no significant correlation between laboratory findings, sex, age, and serum calprotectin and hepcidin levels (p>0.05 r<0.25).Conclusion: Serum calprotectin levels in FMF patients with attack-free period were significantly higher than in the healthy control group. Serum hepcidin levels in FMF patients were significantly lower than in the healthy control group. Low levels of hepcidin may be explained that including FMF patients with attack-free period in to the study. Calprotectin may be an important biomarker in FMF. To understand the role of these biomarkers in the diagnosis of FMF are needed to evaluate in more comprehensive studies.

The data are expressed as mean ± standard deviation, median (1th quarter-3th quarter) and n (%).