Mustafa Serdar Sağ

Comparison of fetuin-A and transforming growth factor beta 1 levels in patients with spondyloarthropathies and rheumatoid arthritis.

We investigated the serum transforming growth factor beta 1 (TGFβ1) and fetuin‐A levels, and determined the relationships between these biomarkers and disease activity, mobility and radiologic progression in patients with spondyloarthropathy (SpA) and rheumatoid arthritis (RA).

Nailfold videocapillaroscopy results in patients with rheumatoid arthritis

We aimed to analyse the nailfold capillaryscopy findings morphologically and examine their relationship with disease activity and demographic characteristics in patients with rheumatoid arthritis. In accordance with the 2010 ACR/EULAR classification criteria, 201 patients diagnosed with Romatoiad artrit (RA) and 50 healthy controls were included. We analysed capillaroscopic abnormalities such asmegacapillaries, haemorrhages, ramifications and avascular areas in patients affected with rheumatoid arthritis. The findings in our study are as follows: in 45.77% of the RA patients, there were nonspecific capillaryscopy findings. When compared to control group, the incidence of tortuosity, dilated capillary and bushy capillary was higher in RA patients (p values, respectively, 0.110, 0.330, 0.440 and 0.516). In RA patients with Raynaud’s phenomenon, the incidence of nonspecific capillaryscopy findings was higher. While there is a weak relationship between tortuosity and the duration of disease, no significant relation was detected between capillaryscopy findings and parameters such as RF, anti-CCP positivity and disease activity score (DAS28). When compared to controls, we have detected that RA patients have more nonspecific capillaryscopic findings. We could not find a relationship between nonspecific capillaryscopic findings and RA’a clinical findings and laboratory parameters. There is a need for a long-term wider-scale follow-up study to investigate whether there is a capillaryscopic pattern that can be correlated with RA’s clinical findings.

Central nervous system involvement in rheumatoid arthritis: possible role of chronic inflammation and tnf blocker therapy

Rheumatoid arthritis (RA) is a chronic disease, the etiology of which has yet to be clarified, which causes activation of proinflammatory pathways that bring about joint and systemic inflammation. Although peripheral nervous system anomalies are observed widely in RA, very few case reports on changes in the central nervous system (CNS) have been published. In recent years, the pathophysiology of CNS involvement that can occur in RA has attracted a great deal of attention. Emphasis has focused on the possibility that CNS involvement occurs due to blood–brain barrier (BBB) damage associated with chronic inflammation. The present study was performed to investigate the possible effects of BBB dysfunction and tumor necrosis factor (TNF) blocker therapy on BBB function, which may cause CNS damage in patients with RA. 58 RA patients [47 (81.0%) females, 11 (19.0%) males] and 34 healthy controls [24 (70.6%) females, 10 (29.4%) males] were included in the study. All RA patients were on synthetic DMARD therapy at the beginning. Thirty patients continued DMARD therapy, and 28 patients with high disease activity were started on TNF blocker therapy. All demographic characteristics of the patients were recorded. Disease activity was evaluated using the Disease Activity Score 28-joint count C reactive protein. The Mini-Mental State Examination was used to evaluate cognitive function, and the Fazekas scale was used to assess cranial lesions visualized by magnetic resonance imaging (MRI). Patients’ peripheral blood S100β, glial fibrillary acidic protein (GFAP), claudin, interleukin (IL)-17, and IL-1β levels were measured at the beginning of the study and after 6xa0months. Demographic characteristics (including sex, age, and body mass index) were similar in the RA and control groups. S100β and GFAP levels were significantly higher in the patient group than in the control group. In the group that was started on TNF blocker therapy, S100β and GFAP levels were significantly decreased 6xa0months after commencement of treatment. No difference was observed between the RA and control groups in terms of hyperintense lesions seen on cranial MRI. The S100β levels increased with lesions in the deep white matter seen on cranial MRI in patients with RA. In conclusion, next to decreasing disease activity and joint erosions by suppressing inflammation, anti-TNF therapy in RA can also suppress potential CNS involvement linked to BBB (blood–brain barrier) dysfunction. Further studies with broader participation and longer patient follow-up are needed to reinforce this hypothesis.

Presence of enthesopathy in patients with primary Sjogren’s syndrome: ultrasonographic study of a local cohort

BackgroundMusculoskeletal findings in Sjögren’s syndrome are arthralgia, arthritis, myalgia, myositis, fibromyalgia, and chronic fatigue. Enthesis zones are important in the formation of pain in the musculoskeletal system. Musculoskeletal ultrasound (US) may show subclinical enthesitis in the synovial joints and in the axial skeleton before joint swelling in inflammatory diseases characterized by arthritis.ObjectiveIn this study, we aimed to determine the presence of enthesopathy using the Madrid sonographic enthesitis index (MASEI) in patients with primary Sjögren’s syndrome (PSS).Patients and methodsConsecutive patients with PSS and age-matched healthy controls were included in this study. All the patients met the 2002 American College of Rheumatology/European League against Rheumatism classification criteria for PSS. The demographic characteristics of the patients were recorded. Six enthesis sites were evaluated using gray-scale and Doppler US with a linear transducer, and they were scored using the MASEI. They were assessed by the EULAR Sjögren’s syndrome disease activity index (ESSDAI).ResultsWe evaluated 40 patients with PSS (average age 48.67xa0±xa011.23xa0years) and 30 healthy controls (average age 45.40xa0±xa08.24xa0years). Patients with PSS had significantly higher MASEI scores than the healthy controls. Plantar fascia, Achilles tendon, and distal patellar tendons were significantly thicker in the PSS group than in the healthy controls. The MASEI total score had a positive correlation with age. There was no correlation between MASEI total score and BMI and ESSDAI.ConclusionIn this study, it was shown that the MASEI scores assessed by US were significantly higher in patients with PSS than in healthy controls. Plantar fascia, Achilles tendon, and distal patellar tendon were significantly thicker in the PSS group than in the healthy controls. This result suggests that PSS may be one of the causes of musculoskeletal pain that can be seen in patients with PSS. Our study was the first study to use an enthesis index ultrasonographically in patients with PSS. In addition, it is the first study to investigate the relationship between the presence of enthesopathy and disease activity by means of US.

Comparison of 25-hidroksi Vitamin D serum concentrations in patients with psoriasis and psoriatic arthritis

BACKGROUND AND OBJECTIVEnRheumatoid arthritis (RA), insulin-dependent diabetes mellitus (IDDM), inflammatory bowel disease, systemic lupus erythematosus (SLE) and multiple sclerosis (MS) are some of the autoimmune diseases related to the decreases in Vitamin D levels. The same immunological properties as psoriasis, such as Th1/Th2 dysregulation, are seen in all of them. This study aims to compare 25-hidroksi Vitamin D (25-OHD) serum concentrations in patients with psoriasis and psoriatic arthritis.nnnMETHODSnThis study includes 91 outpatients; 48 of these patients were chosen randomly among the psoriasis (PS) patients from the dermatology department of the researchers hospital. Forty-three of them were chosen among the psoriatic arthritis (PsA) patients matching the age and gender criteria from the rheumatology department of the researchers hospital. In this study, 25-OHD serum concentrations among the psoriasis and psoriatic arthritis patients were compared.nnnRESULTnThere are more patients in the PsA group with 25-OHD levels lower than 20 ng/ml; however, this finding is insufficient to obtain statistical significance (p= 0.09). PsA and psoriasis groups had similar numbers of patients with 25-OHD levels ranging from 20 to 30 mg/mL and those higher than 30 mg/mL (p> 0.05).nnnCONCLUSIONnThe literature does not show significant differences between the PS and PsA groups in terms of serum 25-OHD levels and a prevalence of Vitamin D deficiency. Besides, PASI scores were higher in the PS group. CRP values in the PsA group were higher than in the PS group. There was a poor negative correlation between CRP and serum 25-OHD levels in the PsA group. This correlation was not found in the PS group.

THU0051 The Levels of Serum Pentraxin 3, IL 6, Fetuin A and Insulin in Patients with Rheumatoid Arthritis

Background The pathogenesis of RA is not well understood, but genetic, environmental and immunologic factors are known to be involved in the development of the disease. The long pentraxin, pentraxin-3 (PTX-3), is an inflammatory marker and a member of pentraxin superfamily which contains CRP and serum amyloid P. There are some published studies showing the relationship between RA and PTX-3. (1–3). We investigated that PTX3, IL 6, fetuin- A, insulin and HOMA-IR might also have a role in the pathogenesis of RA. Objectives The aim of this study was to evaluate the relationship between disease severity and biochemical parameters such as pentraxin-3, fetuin-A, IL-6,insulin and HOMA-IR levels in patients with rheumatoid arthritis. Methods This study included 60 patients with RA and 20 healthy controls. Serum pentraxin-3, fetuin-A, IL-6 and insulin concentrations were determined. Also, HOMA-IR values were calculated. Disease activity was assessed with Disease Activity Score (DAS28). Quality of life was evaluated by the use of the Health Assessment Questionnaire disability index. Results The serum values for ESR, CRP, pentraxin-3 and fetuin-A in patients with RA were elevated than control subjects (p values=0.001, 0.001, 0.000, 0.000, 0.01, 0.02, respectively) A positive correlation was evident between the DAS 28 score and IL6 levels (r =0.263, p=0.045). We found no correlation between the DAS28 score and HOMA-IR, the levels of pentraxin 3, fetuin A, insulin (p<0.05). Fetuin A levels was positively correlated with cumulative steroid dose (r=0.382, p=0.035). A statistically significant correlation was evident between presence of cardiovascular disease and HOMA-IR values in RA patients (r=0.437, p=0.032). In addition, DAS-28 score values were not in correlation with insulin, fetuin-A, HOMA-IR, IL-6 and pentraxin-3 levels (p>0.05). Conclusions Elevated levels of pentraxin-3, fetuin-A, CRP, ESR might play a role in the pathogenesis of RA. Levels of IL-6, fetuin-A, insulin HOMA-IR, pentraxin -3, CRP, ESR concentrations were not associated with clinical severity of the RA. References Dessein PH, Norton GR, Woodiwiss AJ, Joffe BI, Solomon A. Independent role of conventional cardiovascular risk factors as predictors of C-reactive protein concentrations in rheumatoid arthritis. J Rheumatol 2007;34:681–8. Hollan I, Nebuloni M, Bottazzi B, Mikkelsen K, Førre OT, Almdahl SM, Mantovani A, Fagerland MW, Aukrust P, Meroni PL; Feiring Heart Biopsy Study Group.Group. Pentraxin 3, a novel cardiovascular biomarker, is expressed in aortic specimens of patients with coronary artery disease with and without rheumatoid arthritis. Cardiovasc Pathol 2013 Sep-Oct;22(5):324–31. Klimek E, Skalska A, Kwaśny-Krochin B, Surdacki A, Sulicka J, Korkosz M, et al. Differential associations of inflammatory and endothelial biomarkers with disease activity in rheumatoid arthritis of short duration. Mediators Inflamm 2014;2014:681635. Disclosure of Interest None declared

AB0534 The Relationship of Pentraxin-3 Levels in Behcet Disease with IL-17, Disease Activity and Atherosclerotic Risk Factors

Background Several factors have been implicated as contributing to the risk of atherosclerosis in patients with BD. (1) These include inflammatory mediators such as cytokines and adhesion molecules and traditional cardiovascular risk factors such as age, high blood pressure, and dyslipidemia.(2) PTX3 also acts as a modulator of inflammatory processes and is involved in the development of atherosclerotic lesions. It is produced by endothelial cells in atherosclerotic plaques. Objectives With this study we aimed to identify the levels of the proteins like Pentraxin and Fetuin-A which are thought to have a role in the progress of atherosclerotic and cardiovascular disorders in Behçet disease and the relationship of these with disease activity, inflammatory cytokine, insulin resistance and dyslipidemia. Methods This study included 58 patients (36 female, 22 male) with Behçet disease and 20 healthy controls. Serum pentraxin-3, fetuin-A, IL-17 and insulin concentrations were determined. Also, HOMA-IR values were calculated. Disease activity was assessed with Behcets Disease Current Activity Form (BDCAF). Results PTX3 and fetuin-A levels were not correlated with ESR, CRP, and any domains of BDCAF scores. IL-17 levels were significantly positively correlated with arthritis of BDCAF scores. there wasnt any significant relationship between the lipid profile and PTX3, IL17 and fetuin-A levels. There wasnt any correlation between PTX and IL 17, fetuin-A, insulin, HOMA IR levels (p>0.05). Conclusions Just like CRP, PTX3 is an acute-phase reactant and it is considers as an inflammatory and atherosclerotic biomarker. In this study, we presented that PTX3 can increase like IL-17 but there arent any relation between the disease activity and coronary risk factors such as serum lipids, glucose intolerance and obesity. Since this is a cross sectional study, to determine higher levels of pentraxin in BD patients who also have higher cardiovascular disease incidences, the patients have to be followed in the longer run. To identify these long-term studies to quantified atherosclerosis are required. References Pamuk GE, Pamuk ON, Or€um H, et al. Might platelet-leucocyte complexes be playing a role in major vascular involvement of Behcets disease? A comparative study. Blood Coagul Fibrinolysis 2010; 21: 113e117. Seyahi E, Ugurlu S, Cumali R, et al. Atherosclerosis in Behcets Syndrome. Semin Arthritis Rheum 2008; 38:1e12. Disclosure of Interest None declared

AB0154 Comparison of Fetuin-A and Transforming Growth Factor Beta 1 Levels in Patients with Spondyloarthropathies and Rheumatoid Arthritis

Background New bone formation plays an important role in the progression of inflammatory lesions in inflammatory rheumatic diseases. In recent literature, the question of which molecules to use for estimating new bone formation is a particularly interesting research topic. Fetuin-A and transforming growth factor beta 1 (TGFβ1) have been studied in many diseases, including metabolic, cardiovascular, and neoplastic diseases. Objectives We investigated the serum TGFβ1 and fetuin-A levels, and determined the relationships between these biomarkers and disease activity, mobility, and radiologic progression in patients with SpA and RA. Methods The study included 55 patients with SpA and 38 patients with RA, together with 28 healthy subjects. In AS patients, we assessed disease activity using the Bath AS disease activity index (BASDAI), functional ability using the Bath AS functional index (BASFI), and mobility using the Bath AS metrology index (BASMI), radiologic progression using the Bath Ankylosing Spondylitis Radiology Index (BASRI). Serum feutin-A and TGFβ1 were determined using enzyme-linked immunosorbent assay (ELISA) equipment Results Fetuin-A was significantly higher in the axial SpA and RA groups than in healthy subjects (p<0.01). Serum TGFβ1 and fetuin-A levels were similar in the peripheral SpA group and in healthy subjects. A significant positive correlation was found between the fetuin-A and TGFβ1 levels in the axial SpA, peripheral SpA, and RA groups (r =0.293, p=0.009; r =0.215, p=0.04; r =0.223, p=0.05, respectively). Significant correlations were found between fetuin-A and the BASMI and BASRI values in the axial SpA patients (r =0.244, p=0.031; r =0.416, p<0.001, respectively). There were no correlations of TGFβ1 or fetuin-A levels with CRP, ESR, or all of the clinical parameters in the peripheral SpA and RA patients (p>0.05). Conclusions In conclusion, high levels of fetuin-A and TGFβ1 in patients with axial SpA indicate that fetuin-A could be used as a marker for bone proliferation. We hypothesize that fetuin-A may be one of the possible active steps in new bone formation. The data obtained in the present study will contribute to identifying differences between RA and SpA, and in clarifying the disease process, thereby helping to identify specific therapeutic targets. Disclosure of Interest None declared