Elucidation of the causes of inflammation has vital importance in the development of new approaches for the treatment of arthritic diseases. The degradation of aggrecan by upregulated disintegrin and metalloproteinase with trombospondin motifs (ADAMTSs) is the key event in the development of both rheumatoid arthritis (RA) and osteoarthritis (OA). Increased levels of leptin in both RA and OA have been demonstrated, thus linking leptin to arthritic diseases, but the mechanism has not been clarified. This study investigated the putative role of signaling pathways (p38, JNK, MEK1, NF-ĸB, and PI3) involved in leptin-induced cartilage destruction. Normal human articular chondrocytes were cultured with recombinant human leptin at 100, 250, 500, and 1000 ng/mL doses for 6, 12, 24, and 48 h, after which ADAMTS-4, -5, and -9 genes expression were determined by real time-polymerase chain reaction (RT-PCR) and Western Blot methods. The signaling pathways involved in leptin-induced ADAMTSs upregulation were also investigated by using inhibitors of signaling pathways. It was demonstrated that ADAMTSs expression level was peaked at 1000 ng/mL doses for 48 hours, and MAPKs (p38, JNK, and MEK) and NF-ĸB signaling pathways involving in leptin triggered ADAMTSs upregulation. Obesity as a risk for RA and OA may contribute to the inflammation of both RA and OA diseases by secreting adipokines like leptin. We hypothesize that leptin is involved in the development of RA and OA accompanied with obesity by increasing ADAMTS-4, -5, and -9 genes expression via MAPKs and NF-ĸB signaling pathways.

We have shown that clinically diagnosed RLS was associated with the nondipping pattern, which has been shown to be an independent predictor of cardiovascular risk.

The objective of this study was to adapt the Shoulder Disability Questionnaire (SDQ) for use in Turkey, and to test its reliability and validity. Eighty patients with shoulder pain were included in the study. Pain severity at rest, with motion and during sleeping was assessed by using a numeric pain scale. The shoulder's active and passive range of motion were measured by a goniometer and recorded. The Constant-Murley scale was used for functional assessment. The Turkish version of the SDQ, which was adapted by using guidelines, was completed by the patients. To assess reproducibility, the SDQ was completed by 32 patients who did not improve 1 week later. The reliability of the adapted version was good, with high internal consistency (Cronbach's alpha=0.76) and test-retest reliability (Pearson's correlation coefficient=0.88). The Turkish version of the SDQ was found to have a moderate correlation with pain at rest, with motion and during sleeping. The Turkish version of the SDQ was found to be reliable and valid. The moderate correlation of the questionnaire with clinical parameters including pain shows its validity, but the questionnaire should be tested extensively for detecting changes within time, for use in the follow-up and clinical practice.

OBJECTIVE:The aim of this study was to investigate whether there is a correlation between serum leptin level, disease activity and inflammation markers in patients with fibromyalgia syndrome (FMS).METHODS:A total of 48 patients with FMS diagnosed according to the 1990 American College of Rheumatology criteria were included in the study, as well as 36 healthy women as controls. The Visual Analogue Scale was used to gauge pain severity, the Fibromyalgia Impact Questionnaire was used to assess physical function, the 36-Item Short Form Health Survey was used to examine quality of life, and depression was measured with the Beck Depression Inventory. Blood samples were examined for erythrocyte sedimentation rate (ESR), C-reactive protein level (CRP), high-sensitivity CRP level (hsCRP), the neutrophil-to-lymphocyte ratio (NLR), and the serum leptin level was determined using the enzyme-linked immunosorbent assay method.RESULTS:The serum leptin level in patients with FMS was significantly higher than in the healthy group. However, no significant relationship was found between leptin level and clinical and inflammatory parameters. In addition, there were no significant differences between the patients and the control group in measurements of ESR, CRP, hsCRP, or NLR.CONCLUSION:A higher serum leptin level in patients with FMS suggested that leptin may play role in the pathogenesis of FMS, yet there was no relationship between leptin and clinical and inflammatory parameters, suggesting that leptin is not an indicator of disease activity in FMS. Additional research should be performed with larger patient groups.