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1.
Pediatr Rheumatol Online J ; 21(1): 35, 2023 Apr 14.
Article in English | MEDLINE | ID: mdl-37060076

ABSTRACT

BACKGROUND: The ten-joint juvenile arthritis disease activity score (JADAS10) is designed to measure the level of disease activity in non-systemic juvenile idiopathic arthritis by providing a single numeric score. The clinical JADAS10 (cJADAS10) is a modification of the JADAS10 that excludes erythrocyte sedimentation rate (ESR). Three different sets of JADAS10/cJADAS10 cut-offs for disease activity states have been published, i.e., the Backström, Consolaro, and Trincianti cut-offs. The objective of this study was to investigate the performance of existing JADAS10 cut-offs in real-life settings using patient data from The Finnish Rheumatology Quality Register (FinRheuma). METHODS: Data were collected from the FinRheuma register. The proportion of patients with an active joint count (AJC) above zero when classified as being in clinically inactive disease (CID) or low disease activity (LDA) groups according to existing JADAS10/cJADAS10 cut-off levels were analyzed. RESULTS: A significantly larger proportion of the patients classified as being in CID had an AJC > 0 when using the JADAS10/cJADAS10 cut-offs by Trincianti et al. compared to those for the other cut-offs. In the LDA group, a significantly larger proportion of the polyarticular patients (35%/29%) had an AJC of two when Trincianti JADAS10/cJADAS10 cut-offs were used compared with when Backström (11%/10%) and Consolaro (7%/3%) JADAS10/cJADAS10 cut-offs were used. CONCLUSIONS: We found the cut-offs proposed by Consolaro et al. to be the most feasible, since these cut-off levels for CID do not result in the misclassification of active disease as remission, and the proportion of patients with AJC > 1 in the LDA group is lowest using these cut-offs.


Subject(s)
Antirheumatic Agents , Arthritis, Juvenile , Rheumatology , Humans , Arthritis, Juvenile/diagnosis , Arthritis, Juvenile/drug therapy , Antirheumatic Agents/therapeutic use , Finland , Feasibility Studies
2.
Scand J Rheumatol ; 37(1): 6-12, 2008.
Article in English | MEDLINE | ID: mdl-18189188

ABSTRACT

OBJECTIVE: To determine from single-centre data the treatment continuation, discontinuation, and reasons for discontinuation among the patients with active rheumatoid arthritis (RA) or spondyloarthropathies (SpA) who were treated with infliximab as their first biological anti-rheumatic drug. METHODS: All (n = 104) RA and SpA patients who were treated with infliximab as their first biological treatment according to the national guidelines in the Centre for Rheumatic Diseases, Tampere University Hospital during 1999-2005 were analysed at baseline and after 6 months of treatment. The treatment was regarded as ineffective if the response was lower than American College of Rheumatology (ACR) response criteria ACR50 in RA or the reduction of the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) was lower than 50% or 2 cm in SpA. RESULTS: After 6 months, 71% of the patients continued infliximab treatment and the prednisolone dose was diminished by 40%. Infliximab was discontinued in 30 patients and seven of them discontinued due to remission. Eight patients were regarded as poor responders. Thirteen patients discontinued because of adverse events, mainly infections and hypersensitivity reactions. One patient discontinued the treatment because of drug-related leucopaenia and one because of elevated aminotransferases. CONCLUSION: In this study, infliximab treatment was started in patients who had active disease despite ongoing treatment with combinations of disease-modifying anti-rheumatic drugs (DMARDs). Seventy-eight per cent achieved at least 50% response when infliximab was added to their DMARD treatment. Adverse events, mainly infections and hypersensitivity reactions, were in line with previous reports. Two rare adverse events were reported, one patient with leucopaenia and one with elevated aminotransferases.


Subject(s)
Antibodies, Monoclonal/therapeutic use , Antirheumatic Agents/therapeutic use , Arthritis, Rheumatoid/drug therapy , Spondylarthritis/drug therapy , Treatment Refusal/statistics & numerical data , Adolescent , Adult , Aged , Antibodies, Monoclonal/adverse effects , Antirheumatic Agents/adverse effects , Female , Glucocorticoids/metabolism , Humans , Hypersensitivity , Infliximab , Male , Middle Aged , Treatment Outcome
3.
Scand J Rheumatol ; 36(3): 189-93, 2007.
Article in English | MEDLINE | ID: mdl-17657672

ABSTRACT

OBJECTIVE: Infliximab is effective and well tolerated in the treatment of juvenile idiopathic arthritis (JIA). The aim of the present study was to measure circulating levels of inflammatory mediators in patients with JIA during treatment with infliximab. METHODS: Eight patients with active JIA refractory to standard treatments were treated with infliximab (3-4 mg/kg) at weeks 0, 2 and 6 and thereafter at approximately 6-week intervals up to 24 weeks. RESULTS: All patients (n = 8) responded to the treatment. By 6 weeks of treatment the number of active joints had reduced from 16+/-4 (mean+/-SEM) to 4+/-1 (p<0.01) and C-reactive protein (CRP) levels had fallen from 31+/-8 to 8+/-3 (p<0.001). Infliximab treatment also reduced the serum concentrations of interleukin-6 (IL-6), myeloperoxidase (MPO), and soluble adhesion molecules ICAM-1 (intercellular adhesion molecule-1), and E-selectin. Tumour necrosis factor-alpha (TNFalpha) levels tended to increase while the concentrations of endogenous TNF antagonists (sTNF-RI and sTNF-RII) reduced in most patients during treatment. CONCLUSIONS: Infliximab reduced serum levels of IL-6, MPO and soluble adhesion molecules in JIA patients, producing a good clinical response to the treatment.


Subject(s)
Antibodies, Monoclonal/therapeutic use , Arthritis, Juvenile/drug therapy , Cytokines/blood , E-Selectin/blood , Intercellular Adhesion Molecule-1/blood , Peroxidase/blood , Tumor Necrosis Factor-alpha/antagonists & inhibitors , Adolescent , Arthritis, Juvenile/blood , Child , Child, Preschool , Female , Humans , Infliximab , Male , Tumor Necrosis Factor-alpha/blood , Tumor Necrosis Factor-alpha/physiology
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