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Axial spondyloarthritis (axSpA) is a chronic inflammatory disease that mainly affects the axial skeleton. Peroxisome proliferator activated receptor alpha (PPARA) is an intracellular transcription factor, which play a role in inflammation and osteoblasting activity. This study is designed to investigate the relationship of NG_012204.2:p.Ala268Val polymorphism of PPARA with axSpA risk and its role in disease development.

Objectives: The study aimed to investigate serum tenascin-C levels and its relationship with pathogenesis of Behçet's disease (BD) with inflammatory processes. Patients and methods: This prospective and analytical study included 34 BD patients (19 males, 15 females; mean age: 31.5±8.2 years; range, 18 to 48 years) who met the 2014 International Criteria for Behçet's Disease and had no comorbidities and 37 healthy volunteers (21 females, 16 males; mean age: 29.6±5.3 years; range, 21 to 45 years). Sex, age, age at diagnosis, clinical and laboratory data, medication use, and smoking history of the participants were recorded. Serum tenascin-C levels were measured using a commercially available tenascin-C enzyme-linked immunosorbent assay kit. Results: There was no significant difference between the groups in terms of age (p=0.262) and sex (p=0.287). Serum tenascin-C levels were significantly lower in the BD group (10,824±7,612 pg/mL) compared to the control group (27,574±14,533 pg/mL, p<0.001). In the receiver operating characteristic analysis performed for the diagnostic value of tenascin-C level in BD, the sensitivity was determined as 79.4% and the specificity as 82.5% (p<0.001). No statistically significant difference was observed in tenascin-C levels in correlation with clinical characteristics, laboratory values, medication use, and smoking in the BD group. Conclusion: In contrast to other chronic inflammatory diseases, lower levels of tenascin-C were observed in patients with BD than in the healthy individuals, which can be attributed to the absence of prolonged chronic inflammatory course in BD. The fact that tenascin-C levels are high in other rheumatic inflammatory diseases but low in BD may be useful in the differential diagnosis of BD. [ABSTRACT FROM AUTHOR]

Scleroderma (systemic sclerosis) is a chronic inflammatory disease that progresses with vascular damage, immunological abnormalities, and extensive fibrosis. Rituximab, an antibody against the Blymphocyte- specific CD20 surface marker leads to depletion ofB cell counts and functions. This study aims to investigate the protective efficacy of rituximab on skin fibrosis in bleomycin (BLM) -induced experimental scleroderma model.This study included 4 groups of (n=7 for each group) Balblc mice. Group I mice were treated with subcutaneous 100 μl/day phosphate-buffered saline (PBS); while mice in Groups II, III, and IV were treated with subcutaneous 100 μl/day BLM. Mice in Group III and Group IV were treated, intraperitoneally, with 50 μg and 250 μg rituximab, respectively; on the 1st and 14th days of the experiment. Mice in all groups were sacrificed at the end of the 4-week experimental period and tissue specimens were obtained. Serum levels of transforming growth factor (TGF)-p1, dermal thickness, the number of dermal inflammatory cells, and the number of a smooth muscle actin positive cells (a-SMA+) were determined.The administration of BLM increased the inflammatory cell infiltration of the dermis, a-SMA+ cell counts in the dermis, and dermal thickness. However, rituximab treatments decreased inflammatory cell infiltrations, a-SMA+ cell counts and dermal thickness, in the BLM injected mice. Both rituximab doses had similar antifibrotic efficacy. Rituximab prevents the development of fibrosis in a BLM-induced experimental scleroderma model. This result suggests that rituximab may be a effective therapeutic agent in patients with early-stage scleroderma. [ABSTRACT FROM AUTHOR]

This study aimed to present our single-center experience of anakinra and canakinumab treatment in patients with Familial Mediterranean fever (FMF). This study included 48 patients who were treated with anti-interleukin-1 (anti-IL-1) treatment for at least six months. Initially, all patients with colchicineresistant or intolerant FMF were received anakinra treatment. Then those resistant to anakinra were given canakinumab treatment. Of the 48 (female/male:29/19) patients using anti-IL-1, their age was 31.2 ± 10.7 years, the duration of drug use was 15±8 months. 30 patients were already using anakinra and 18 patients were using canakinumab. Treatment was found to be switched to canakinumab in 9 patients due to non-adherence to daily injection, and inadequate response to anakinra in 9 patients. After the anti-IL-1 treatment the number of attacks, erythrocyte sedimentation rate, C-reactive protein, fibrinogen levels, colchicine dose and proteinuria (for all p<0.001) were decreased. Anti-IL-1 treatment is effective for controlling attacks and reducing proteinuria in patients with colchicine-resistant or intolerant FMF. In addition, canakinumab appears to be an alternative treatment option when there is a inconvenience to daily injection or resistance to anakinra treatment. [ABSTRACT FROM AUTHOR]

Epigallocatechin 3‐gallate (EGCG) is a polyphenol that has been shown to have antioxidant and anti‐inflammatory effects. In this study, collagen‐induced arthritis (CIA) model, in Wistar albino rats, was used to elucidate the effect of EGCG on pathogenetic pathways in inflammatory arthritis. The levels of serum TNF‐α, IL‐17, malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx); the expression levels of tissue heme oxygenase‐1 (HO‐1) and nuclear factor erythroid 2‐related factor 2 (Nrf2); histopathologically, perisynovial inflammation and cartilage‐bone destruction were examined. In the sham group, serum TNF‐α, IL‐17, and MDA levels increased, while SOD, CAT, GPx levels, and the expressions of Nrf2 and HO‐1 decreased. On the other hand, in the EGCG administered groups, serum TNF‐α, IL‐17, and MDA levels improved, while SOD, CAT, GPx levels and the expressions of Nrf2 and HO‐1 increased. Moreover, histopathological analysis has shown that perisynovial inflammation and cartilage‐bone destruction decreased in the EGCG administered groups. These results suggest that EGCG has an antiarthritic effect by regulating the oxidative‐antioxidant balance and cytokine levels in the CIA model, which is a surrogate experimental model of rheumatoid arthritis. [ABSTRACT FROM AUTHOR]