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Background:Although Familial Mediterranean Fever (FMF) is a monogenic disease, microbiota composition may play role in the pathogenesis or phenotypic expression.Objectives:We aim to evaluate the intestinal microbiota composition in patients with FMF and to compare with healthy controls.Methods:In this prospective cohort study, a group of 10 adult patients with FMF and 10 age-appropriate healthy controls, for which there was strict inclusion/exclusion, were enrolled. Fecal samples were stored at -80°C until DNA extraction. A region of the 16S rRNA gene (V3-V4) was selected and sequencing was performed on the Illumina MiSeq platform at the Sequencing and Bioinformatics Service of FISABIO foundation.Results:Alpha and beta diversity tests were similar between FMF and control groups except that Chao1 index. Chao1 index was modestly decreased in FMF group comparing the healthy controls (pEggerthella, at genus level. At species level,Eggerthella sinensisandEggerthella lentawere more abundant in patients with FMF.Conclusion:Eggerthella lentawas previously shown to be higher in type II diabetes, multiple sclerosis, rheumatoid arthritis and some disseminated infections. In this study we firstly showed abundance ofEggerthellain patients with FMF, especially inE. sinensisandE. lenta;in addition to. Whether any of observed associations are causal, or the direction of causality is unclear yet and further studies with patients with FMF at the first diagnosis might clarify this issue.Disclosure of Interests:None declared

Background:Serum autoantibodies closely reflect patterns of organ involvement and disease progression in systemic sclerosis (SSc). The entire autoantibody profile is less well defined in many cohorts and the data regarding their clinical associations and frequencies is limited.Objectives:To determine the autoantibody profile of patients with SSc, as well as their clinical associations, in well-characterized inception- cohort with disease duration less than 3 years.Methods:Serum samples of 100 patients out of 105 enrolled in the study were analyzed for ANA patterns with indirect immunofluorescence (IIF) assay using HEp-20-10/primate liver mosaic IIFT kit. Sera of 96 patients were subjected to commercial line immunoassay to quantify autoantibodies against 13 different autoantigens.Results:92 (92%) out of 100 patients were positive for ANA by IIF (Table 1). The speckled staining was the most pattern followed by nucleolar in 10 patients, centromere in 4, reticular in 1, nuclear in 2 and homogenous in 1. All patients (n= 96) patients were positive for at least 1 autoantibody by immunoblotting (Table 2). Twenty-two (49%) of patients with antiTopo I, 12 (44%) of the patients with antiCENP and 4 (22%) of the patients with antiRNAPIII were single positive. There was no difference in terms of the clinical findings when the patients with single and coexpression of these antibodies were compared. The distributions of the most frequent autoantibodies are shown in Figure 1. Interstitial lung disease was more frequent in the patients positive for anti-Topo I (78.8%) and anti-RNAPIII (27.3%). One of the two patients with breast cancer was anti-RNAPIII positive and none of the patients have diagnosed scleroderma renal crisis. Anti-Topo I was more common in patients with dcSSc (75%) and anti-CENP in lcSSc (46.4%).Table 1.Demographic, clinical and laboratory characteristics of the SSc patients.Sex Female N, %91 (86.7%) Male N, %14 (13.3) Female-to-male ratioAge, mean±SD years48.6±12.7Disease duration, mean±SD years2±1.4Disease classification N, % Diffuse39 (36.5%) Limited65 (62.5%) Sine scleroderma1 (1%)Interstitial lung disease37 (34.3%)Pulmonary arterial hypertension3 (2.8%)Scleroderma renal crisis0Digital ulcer14 (13.3%)Raynaud phenomenon105(100%)Telengiectasia31 (28.8%)Calcinosis1 (1%)Malignancy3 (2.9%)Antinuclear antibody profile N*, % Positive92 (92%)Staining pattern Speckled65 (65%) Nucleolar13 (13%) Centromere29 (29%) Homogeneous3 (3%) Reticular3 (3%)Table 2.Numbers and combinations of autoantibodies identified in the 96 SSc patients.Topo-ICENPRNAP IIIFibrillarinNOR90Th/ToPm/SclKuPDGFRRo52Topo-I22170159507CENP12202222011RNAPIII40121307Fibrillarin0000000NOR90011002Th/To04202Pm/Scl4306Ku102PDGFR00Ro522Single positive221240004102Total452718058179024Figure 1.Diagram of disease-related antibodies against the four main autoantibodies [anti-centromere (antiCENP) anti-Topoisomerase I (antiTopo I), anti-RNA polymerase III (antiRNAP III) and anti-Ro52).Conclusion:We presented the clinical and serologic features of the Turkish SSc patients from a new inception cohort. Clinical features of the SSc patients with single or multiple antibody positivity were not different.References:NoneDisclosure of Interests:None declared

Background Rheumatoid Arthritis (RA) is a chronic, inflammatory, autoimmune disease (1). Adiponectin is an adipocytokin which has anti-atherogenic, anti-angiogenic, anti-inflammatory and anti-tumor effects (2). Adiponectin also increases the sensitivity to insulin (3). Objectives The aim of this study was to investigate the relationship between disease activity, acute phase response, insulin resistance and adiponectin levels, known to have antiinflammatory effects in RA. Methods Sixty-five patients with RA and thirty patients with osteoarthritis (OA) who fulfilled the American College of Rheumatology (ACR) classification criteria for each disease were included for this study. Patients who have a previous history of diabetes mellitus or recieving oral anti-diabetic agents, insulin, anti-obesity drugs or disease modifying anti-rheumatismal drugs were excluded. Body mass index, acute phase reactants, DAS-28, fasting blood glucose, insulin levels and adiponectin levels were measured at the beginning (0. month) and 3th month of the therapy in RA patients. Results Adiponectin levels at the third month of the therapy were significantly increased compared with baseline levels. However there was no correlation between adiponectin levels and disease activity or acute phase reactans in both baseline and third month of the therapy. Acute phase response and DAS-28 decreased at the end of the 3rd month, as expected. The decrease in insulin resistance was statistically non-significant.There was no correlation between adiponectin levels and insulin resistance at the begining of the therapy but there was an inverse correlation at the end of 3rd month. Conclusions We believe that the cause of elevation in adiponectin levels and the decrease in insulin resistance are the results of immunsupresive therapy used in treatment of RA. References Scott DL, Wolfe F, Huizinga TWJ. Rheumatoid arthritis. Lancet 2010; 376: 1094-1108 Diez JJ, Iglesias P. The role of the novel adipocyte-derived hormone adiponectin in human disease. Eur J Endocrinol 2003; 148:293-300 Kadowaki T, Yamauchi T. Adiponectin ve adiponectin receptors. Endocrine Reviews 2005; 26(3): 439-451 Disclosure of Interest None Declared