Keywords: Familial Mediterranean fever, inflammation, microribonucleic acid, periodic fever. Objectives: This study aims to evaluate the plasma expression of microribonucleic acids miRNAs that may be associated with the pathogenesis of familial Mediterranean fever FMF. Patients and methods: Thirty patients with FMF 18 males, 12 females; mean age 9. The plasma levels of miRNAs were analyzed with real- time polymerase chain reaction in attack and remission periods of patients and healthy controls HCs. Further comprehensive and functional researches may help to clarify the role of miRNAs in FMF and elucidate the pathogenesis of the disease. Familial Mediterranean fever FMF is an autosomal recessive inherited autoinflammatory disease characterized by short 6 hours to 3 daysrecurrent and self-limiting episodes of fever with sterile polyserositis, arthritis or erysipeloid skin rash. The MEFV mutations cause impaired function of a protein called pyrine by incorrect coding and that process results in uncontrolled inflammation. Microribonucleic acids miRNAs are small nucleotidesnon-coding RNA molecules that have roles on the regulation of gene expression at the post-transcriptional stage. These molecules have many roles in different biological processes in the body such as cellular proliferation, differentiation, metabolism and apoptosis. These molecules can be measured in blood and different body fluids; therefore, it has been suggested in the literature that miRNAs can be used as a biochemical marker in different diseases. The plasma expression of miRNAs differs in various autoimmune and autoinflammatory diseases. Thus, miRNAs may have a role in the pathogenesis of inflammation and be useful in diagnosis and follow-up of these diseases. These candidate miRNAs have been selected based on the previous studies which showed their association with autoimmunity and inflammation by effects over inflammatory cytokines. Therefore, in this study, we aimed to evaluate the plasma expression of miRNAs that may be associated with the pathogenesis of FMF. We recruited 30 patients 18 males, 12 females; mean age 9. Patients using steroid or non-steroidal anti-inflammatory drugs before diagnosis or those with other chronic diseases were excluded. Patients were evaluated in two periods: with attack manifestations serositis, arthritis or erysipeloid skin rash together with fever on admission and remission period at sixth month of treatment. Age- and sex-matched 30 healthy children 18 males, 12 females; mean age 9. All of them underwent detailed clinical and laboratory examination to rule out inflammatory, infectious and chronic diseases. All participants were of Caucasian and Turkish origins. A written informed How To Become An Escort 2017 was obtained from the legal guardians of each participant. The study was conducted in accordance with the principles of the Declaration of Helsinki. Blood samples were obtained from FMF patients during attack and remission periods, and at the time of admission to social pediatrics outpatient clinic from HC group. During the remission period, all patients were under colchicine treatment. Patients were divided into two groups based on carrying or not carrying the MV mutation. Peripheral blood samples were taken into ethylenediaminetetraacetic acid tubes and miRNA isolation was carried out on the same day. Manually mixed tubes were centrifuged at 4, rpm for 15 minutes and then totally 1, μL volume was picked up via μL graduated pipette from the top of the obtained plasma. This 1, μL accumulated plasma was again centrifuged at 13, rpm for five minutes and just μL volume was picked up from upper centrifuged plasma and filled into another Eppendorf tube. We used Caenorhabditis elegans cel-miR as an endogenous reference gene to normalize the miRNA expression levels. To How To Become An Escort 2017 the data, global Ct mean of expressed miRNAs, available in the same analysis center, was used. ΔCt mean ± standard deviation [SD] values were found. Qualitative data were presented with numeric and percentage values and measurement data were presented with mean value ± standard deviation SD or median value. Demographic characteristics and laboratory findings white blood cell count, C-reactive protein and erythrocyte sedimentation rate [ESR] of all subjects were shown in Table 1. As expected, acute phase reactants were found to be statistically significantly higher in patients in attack period p Table 1. Although miRNA levels were 1. Plasma miR expressions were 1. These levels were 1. Plasma miRNA expressions were 6. These levels were 7. Recent studies have shown that plasma expression of miRNAs is altered in various autoimmune and autoinflammatory diseases, and miRNAs may also have effects in the pathogenesis of these diseases. Wada et al. They have also suggested that these molecules could be used as a biomarker to identify FMF subgroups. To date, the role of miRNAs in the pathogenesis of inflammation has been shown mostly in studies including patients with autoimmune diseases such as systemic lupus erythematosus SLERA and Sjögren's syndrome. Ma et al. Similar to this study including patients with systemic onset JIA, we have demonstrated that plasma miRNA levels were increased in FMF patients during both attack and remission periods.
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