included 17 oligoarticular cases (27.4 2%), 15 polyarticular cases (24.19%) and ... The oligoarticular cases and polyarticular cases didn't have obvious ...
Methods: Randomized principle was applied to divide the 124 JIA cases into control and treatment group. Slow-acting antirheumatic, nonsteroidal drugs or adrenocortical hormone were applied in these cases as basic drugs. There are no signiﬁcant differences (P>0.05) of clinical classiﬁcation and basic treatment between the two groups.62 cases of treatment group achieved subcutaneous Etanercept, 0.8mg/kg per week with a six mouths’ period of treatment. The group included 17 oligoarticular cases (27.4 2%), 15 polyarticular cases (24.19%) and 30 SO-JIA cases (48.38%). The ACR Ped - 30, 50, 70 were used to assess the clinical efﬁcacy. The occurrence of adverse reactions are monitored and recorded at the same time. Results: The remission rate of different cases in treatment group was different at each time point (P1.5 μg/ml). Sonography of ﬁngers and wrist joint of each hand was performed. Synovial hypertrophy (SH) and power Doppler signal (PD) for synovitis was evaluated at 0 and 12 months. SH plus PD signal was considered as SAS and a total synovitis score was calculated. We present the results at study entry (visit 0). Results: Of 165 patients included, 100 (46 RA, 54 PsA) underwent US examination: 62% female, mean age 57±13 years, mean DAS28-ESR 2±0.5, 77% CR and 23% with LDA, 51% on monotherapy (26% RA, 72.2% PSA), 46% receiving low dosage of biologic (32.6% RA, 57.4% PsA), and taking ADA (35), ETN (50) and IFX (15). SAS was found in 45 patients (31 RA and 14 PsA), representing 42,8% of patients treated with ADA, 46% ETN, and 46,6% IFX. Total subclinical synovitis score was 8±6.3. No signiﬁcant differences were observed in mean SDAI, ESR, CRP, DAS28-ESR, drug serum trough levels or percentage of suboptimal trough anti-TNF serum levels between patients with or without US SAS. After using a logistic regression model, only diagnosis of RA, but not drug serum levels was signiﬁcantly associated with the presence SAS. No signiﬁcant correlation between total synovitis score and drug levels were found.
ADA serum trough levels (mean±SD) (n=35) ADA suboptimal serum trough levels (1.274 μg/ml) (n=30) ETN serum trough levels (mean±SD) (n=50) ETN suboptimal serum trough levels (1.242 μg/ml) (n=32) IFX serum trough levels (mean±SD) (n=15) IFX suboptimal serum trough levels (1.5 μg/ml) (n=10)
US activesynovitis negative (PD+GS) (n=55)
US activesynovitis positive (PD+GS) (n=45)
6.9±4 3 17 1.8±1 10 17 4.1±4 3 5
7.2±4 2 13 1.8±1 8 15 3±2 2 5
0.836 0.619 0.419 0.994 1.00 0.552 0.570 1.00 0.573
SERUM RANKL ACTIVITY IS SUPPRESSED BY TNF ALPHA INHIBITION BUT NOT WITH MTX ALONE
J. Nedovic 1 , B. Stamenkovic 1,2 , S. Stojanovic 2 . 1 Rheumatology; 2 Institute for rheumatology, Nis, Serbia
Conclusions: Subclinical synovitis by US is frequent in patients with RA or PsA receiving TNF who achieve good disease control. Drug serum levels of TNF antagonists do not correlate with subclinical synovitis in these patients. References:  Chen D-Y, et al. Ann Rheum Dis 2014;0:1-9 Disclosure of Interest: J. Inciarte-Mundo Grant/research support: Grant from Hospital Clinic of Barcelona (Premi Emili Letang 2013), J. Ramirez Garcia: None declared, P. Estrada Alarcón: None declared, M. Garcia Manrique: None declared, A. Gonzalez Navarro: None declared, C. Saura: None declared, J. Narvaez Grant/research support: Unrestricted grant from Pﬁzer, J. Rodríguez-Moreno Grant/research support: Unrestricted grant from Pﬁzer, A. Gómez-Centeno Grant/research support: Unrestricted grant from Pﬁzer, J. Yagüe Grant/research support: Unrestricted grant from Pﬁzer, J. Cañete Grant/research support: Unrestricted grant from Pﬁzer, R. Sanmarti Grant/research support: Unrestricted grant from Pﬁzer DOI: 10.1136/annrheumdis-2014-eular.3604
(63% of tests). The average time of treatment for the whole population was 14±13 years; but lower in AR/PsA patients respect to AS patients (9.5 vs 17 years; p=0.08). In patients with RA/PsA, the mean DAS28 and SDAI was 2.03±1 and 4.2±5.8 respectively; in AS patients the mean BASDAI and ASDAS was 6.7 and 3.5, respectively. The mean time on treatment with GLM was 12±9 months (range: 1-28). 65% of patients was treated with some DMARD (100% of patients with RA/PsA) and 65% have treated before with some anti-TNF drugs: adalimumab: 40%, etanercept: 35%, inﬂiximab: 25% (1 anti-TNF: 18%; 2 anti-TNF: 31%; 3 anti-TNF: 16%). The mean serum level of GLM was 1.006 ng/mL (RA/PsA: 889 ng/mL vs AS: 986 ng/mL). Three (11%) patients had developed anti-TNF antibodies previously: 2 patients against inﬂiximab and 1 patient against adalimumab. One patient with AS on GLM treatment as the third anti-TNF (adalimumab and etanercept), and with previously ant-adalimumab antibodies, developed anti-GLMAb (773 UA/mL), in the sixth month of treatment, losing efﬁcacy (prevalence of anti-GLM-Ab in the total patients: 4%). In the group of patients who had been developed anti-adalimumab antibodies, 20% of them developed anti-GLM-Ab. Conclusions: 1. Immunogenicity induced by GLM is scarce. The prevalence of anti-GLM-Ab was of 4% of patients in this study. 2. In 20% of patients with previous anti-adalimumab antibodies, developed anti-GLM-Ab. Disclosure of Interest: None declared DOI: 10.1136/annrheumdis-2014-eular.3862
EVALUATION OF SERUM LEVEL OF GOLIMUMAB AND ANTIBODIES ANTI-GOLIMUMAB IN PATIENTS WITH RHEUMATIC DISEASES: RESULTS FROM A LOCAL REGISTRY
J. Rosas 1 , F. Llinares-Tello 2 , S. Martín 3 , J.M. Senabre 1 , E. Salas 1 , S. Oliver 3 , G. Santos Soler 1 , C. Santos Ramírez 4 , X. Barber 5 , A. Pons 1 , C. Cano 1 , M. Lorente 1 , on behalf of AIRE-MB Group. 1 Rheumatology Dept.; 2 Laboratory Department, Hospital Marina Baixa, Villajoyosa (Alicante); 3 Proteomika, S.L., Derio (Vizcaya); 4 Rheumatology Dept., Hospital Marina Alta, Denia (Alicante); 5 CIO, Universidad Miguel Hernández, Elche (Alicante), Spain Objectives: To assess the clinical relevance of serum levels of Golimumab (GLM) and the prevalence of antibodies anti-Golimumab (anti-GLM-Ab), in patients with rheumatic diseases. Methods: We included 49 test of serum level of GLM and anti-GLM-Ab in 27 consecutives patients, on treatment with GLM at least 6 months, diagnosed of rheumatoid arthritis (RA), peripheral psoriatic arthritis (PsA) (18 test in 9 patients), or ankylosing spondylitis (AS) (31 test in 18 patients). Clinical characteristics, clinical activity index (DAS in 28 joints or SDAI, for RA and PsA; BASFI, BASDAI for AS, were recorded. Serum levels of GLM and anti-GLM-Ab was evaluated by a new ELISA kit developing: Promonitor® -GLM y Promonitor® -anti-GLM-Ab (Proteomika, Derio. Vizcaya. Spain). Cut-off level for serum level of GLM was >32 ng/mL and for anti-GLM-Ab was >20 UA/mL. Serum samples were collected before injection of GLM, and stored frozen −80°C, until analysis. Results: We enrolled 27 patients, 56% were women; mean age 50±12 years. The diagnosis of patients was: RA/PsA in 33% (37% of total test) and AS in 67%
Background: Bone is, together with cartilage a central target of rheumatoid arthritis (RA). Chronic synovitis attacks the juxtaarticular bone, where it causes bone erosions. Formation of bone erosions is a consequence of osteoclasts activity. Osteoclasts are generated from mononuclear precursor cells mediated by the receptor activator of NF-kappaB ligand (RANKL). Tumor necrosis factor alpha (TNF) is considered as a most important proinﬂammatory cytokine and also, a mediator of structural damage in RA. TNF is an important inducer of osteoclast formation by increasing production of RANKL and is thus a key molecular link between inﬂammation and bone damage. Objectives: The aim of our study was to investigate whether the serum concentration of RANKL is inﬂuenced by therapy with and without TNF inhibitors or by disease activity itself. Methods: 45 RA patients (86,7% female, mean age 55,09±11,61 years) who fulﬁlled 1987. ACR criteria for RA and 20 age-matched controls with osteoarthritis were enrolled in the study. Group of RA patients consisted from 25 patients treated with Methotrexate (MTX group), mean disease duration 6,83±4,78 years and from 20 patients treated with Methotrexte and Etanercept (TNF group), mean disease duration 9,8±5,59 years. The serum levels of RANKL was determined by commercially available ELISA kit, values expressed in pg/ml. Disease activity was measured by Erythrocyte Sedimentation Rate (ESR) in mm, concentration of hsCRP in mg/L and wit composite index DAS28. Results: The mean values of serum concentrations of RANKL in MTX group, TNF group and in control group were: 246,81±226,06; 134,53±86,85 and 122,85±138,89 respectively. Patients in MTX group had statistically signiﬁcantly higher values of RANKL compared with patients in TNF group and in control group, p