Efficacy Of TNF Inhibitors Research Articles

Behçet's syndrome: one year in review 2024.

The aim of this review is to provide a critical summary of studies published during 2023 that contribute to our understanding of Behçet's syndrome. An increase in the incidence of BS was reported in Northern Spain after 2014.Studies on patient perspectives showed the impact of Behçet's syndrome on quality of life, daily activities, education, work, and relationships. Differences in genetics among Behçet's syndrome patients with different types of organ involvement were reported and an association between HLA-B/MICA and SLCO4A1 polymorphisms and eye involvement and between DDX60L polymorphisms and nervous system involvement were observed. It was suggested that Integrin α9β1 plays a crucial role in the neutrophil-mediated inflammatory pathways underlying this syndrome and the dysfunction of the PDL1/PD-1 pathway may be associated with the hyperactivity of the Th-1/Th-17 axis. Vein wall thickness seems to be increased in patients with Behçet's syndrome, but its pathogenetic and clinical implications are not clear. There is growing evidence regarding the efficacy of TNF inhibitors in different types of organ involvement. A number of small case series point out to the potential role of TCZ and JAK inhibitors.

The safety and efficacy of TNF inhibitors in patients with Behçet's disease: Retrospective study from eastern Turkey

ObjectiveWe aimed to evaluate the clinical features, disease course, and associated factors for outcome in severe/refractory BD patients receiving TNF-i treatment. Material and methodsThis retrospective study was conducted by reviewing medical records from a tertiary referral center in Van province in Eastern Turkey. Data were obtained from patients' charts followed up between June 2019 and June 2022. ResultsWe included 469 BD patients (59.3% male) whose 80 patients (17%) received TNF-i treatment in the study. The mean ± standard deviation of the patient age was 36.7 ± 10.1 years and the median (IQR) disease duration was 12 (12) years. IFX and ADAwere initiated in 67.5% (n = 54) and 32.5% (n = 26) patients, respectively. Overall and first-line retention rates of TNF-i were 84.7% and 92.6% for IFX and 83.3% and 80.8% for ADA, respectively. IFX was discontinued in 9 patients which were in 2 patients due to allergic reaction and tuberculosis, 3 patients for inefficacy, one patient for heart failure, and one patient for orbital zona. Although no serious adverse event was observed with ADA, 5 patients switched to IFX due to inefficacy. Overall, 72 patients (90%) resumed TNF-i at the end of the study; TNF-i was discontinued in 3 patients (3.8%) due to severe adverse events and in 5 patients (6.2%) with prolonged remission. ConclusionIn our study, no case of death was observed in TNF-i receiving patients. Most patients achieved attack-free and CS-free disease and retained TNF-i treatment. TNF inhibitors appear to be safe and effective in patients with severe/refractory Behçet's disease.

P266 The impact of vedolizumab and ustekinumab on arthropathy and arthralgia in IBD patients: a real-life multicentric cohort study

Abstract Background Extra-intestinal manifestations (EIM) are frequently reported in inflammatory bowel diseases (IBD). Although the efficacy of TNF inhibitors is well documented, data regarding the effect of vedolizumab (VDZ) and ustekinumab (UST) are limited. Theoretically, the advantage of VDZ, i.e. gut-selectivity, may reduce the efficacy on EIM while the systemic effect of UST may be of benefit. Therefore, we evaluated the differences in new onset and evolution of EIM during both treatments. Methods An international multicentric retrospective study was performed on IBD patients who started VDZ or UST between May 2010 and December 2020. EIM were assessed at baseline and during follow-up. Arthropathy was defined as joint inflammation (arthritis/sacroiliitis) and arthralgia as articular pain without confirmed inflammation. Skin EIM included erythema nodosum (EN), pyoderma gangrenosum (PG) and Sweet syndrome. Ocular EIM included (epi)scleritis and uveitis. Uni- and multivariate analyses were performed. Results In total 856 patients were included: 528 treated with VDZ and 328 with UST. At baseline, arthropathy was more prevalent in UST treated patients (12.2% vs 7.2%; p=0.037; Table 1). No differences in rates of new onset (Fig 1) or evolution of pre-existing arthropathies could be identified between VDZ and UST. In multivariate analyses new onset arthropathy was not associated with smoking, IBD type, sex nor studied biological. In 5 out of 48 (10.4%) VDZ patients and 2 of 46 (4.3%) UST patients with either pre-existing or new arthropathy, treatment was stopped due to articular disease (difference not significant). In contrast, new arthralgia onset within 1 year of follow-up was significantly associated with VDZ treatment (OR 2.1 (1.1–4.0); p=0.022; Fig 1). Arthralgia was the reason to stop treatment in 2 of 87 (2.3%) VDZ patients and never in UST patients. Beside joint EIM, 2 patients developed EN, 1 PG and 1 episcleritis during VDZ treatment. Under UST treatment 1 patient developed EN. No patients developed new Sweet syndrome, scleritis nor uveitis. Conclusion No differences in the rate of new arthropathy onset were observed between VDZ and UST. In contrast, VDZ treatment did increase the risk of new onset arthralgia.

Efficacy of TNF inhibitors in advanced ankylosing spondylitis with total spinal fusion: case report and review of literature.

Ankylosing spondylitis (AS) is a chronic and progressive inflammatory disorder that primarily affects the axial skeleton. Unfortunately, diagnosis of AS is often delayed compared to other rheumatologic conditions. It is not uncommon for patients to already have an advanced disease when the correct diagnosis is eventually made. TNF inhibitors are well-known and effective treatment options in patients with AS. However, many clinical trials have excluded patients with advanced AS. This paper reports a 45-year-old male with newly diagnosed AS with already fused sacroiliac joints, lumbar spine, and cervical spine. Due to persistent and severe pain despite having taken multiple NSAIDs, etanercept was prescribed. After 4 years of treatment, the patient continues to experience marked improvement of his AS symptoms without any significant adverse effects. This case illustrates etanercept can be an effective treatment in patients with advanced AS and is well tolerated. An extensive literature review is also carried out regarding this topic.

Anti-TNF Therapy in Spondyloarthritis and Related Diseases, Impact on the Immune System and Prediction of Treatment Responses.

Immune-mediated inflammatory diseases (IMIDs), such as spondyloarthritis (SpA), psoriasis, Crohn's disease (CD), and rheumatoid arthritis (RA) remain challenging illnesses. They often strike at a young age and cause lifelong morbidity, representing a considerable burden for the affected individuals and society. Pioneering studies have revealed the presence of a TNF-dependent proinflammatory cytokine cascade in several IMIDs, and the introduction of anti-TNF therapy 20 years ago has proven effective to reduce inflammation and clinical symptoms in RA, SpA, and other IMID, providing unprecedented clinical benefits and a valid alternative in case of failure or intolerable adverse effects of conventional disease-modifying antirheumatic drugs (DMARDs, for RA) or non-steroidal anti-inflammatory drugs (NSAIDs, for SpA). However, our understanding of how TNF inhibitors (TNFi) affect the immune system in patients is limited. This question is relevant because anti-TNF therapy has been associated with infectious complications. Furthermore, clinical efficacy of TNFi is limited by a high rate of non-responsiveness (30–40%) in RA, SpA, and other IMID, exposing a substantial fraction of patients to side-effects without clinical benefit. Despite the extensive use of TNFi, it is still not possible to determine which patients will respond to TNFi before treatment initiation. The recent introduction of antibodies blocking IL-17 has expanded the therapeutic options for SpA, as well as psoriasis and psoriatic arthritis. It is therefore essential to develop tools to guide treatment decisions for patients affected by SpA and other IMID, both to optimize clinical care and contain health care costs. After a brief overview of the biology of TNF, its receptors and currently used TNFi in the clinics, we summarize the progress that has been made to increase our understanding of the action of TNFi on the immune system in patients. We then summarize efforts dedicated to identify biomarkers that can predict treatment responses to TNFi and we conclude with a section dedicated to the recently introduced inhibitors of IL-17A and IL-23 in SpA and related diseases. The focus of this review is on SpA, however, we also refer to RA on topics for which only limited information is available on SpA in the literature.

Crosstalk between tumor necrosis factor-alpha signaling and aryl hydrocarbon receptor signaling in nuclear factor –kappa B activation: A possible molecular mechanism underlying the reduced efficacy of TNF-inhibitors in rheumatoid arthritis by smoking

ObjectivesTo examine the influence of smoking on biologics treatment against different therapeutic targets, such as TNFα, IL-6, and T cell, in rheumatoid arthritis (RA) and elucidate the underlying molecular mechanism. MethodsThe association between drug-discontinuation due to poor therapeutic response and smoking status was analyzed individually in biologics against different therapeutic targets by a multivariable logistic regression analysis using the “NinJa” Registry, one of the largest cohorts of Japanese RA patients. In vitro enhancement of TNFα-induced NF-κB activation and subsequent proinflammatory cytokine production by cigarette chemical components was examined by RT-PCR, qPCR, ELISA, and western blotting using an immortalized rheumatoid synovial cell line, MH7A. ResultsThe rate of drug-discontinuation due to poor therapeutic response was higher in the current smoking group than in the never- or ever-smoking groups (the odds ratio of current/never smoking: 2.189, 95%CI; 1.305–3.672,P = 0.003; current/ever: 1.580, 95%CI; 0.879–2.839,P = 0.126) in the TNF inhibitor (TNFi) treatment group. However, this tendency was not observed in either the IL-6 or T cell inhibitor treatment groups. Cigarette smoke chemical components, such as benzo[α]pyrene, known as aryl hydrocarbon receptor (AhR) ligands, themselves activated NF-κB and induced proinflammatory cytokines, IL-1β and IL-6. Furthermore, they also significantly enhanced TNFα-induced NF-κB activation and proinflammatory cytokine production. This enhancement was dominantly inhibited by Bay 11-7082, an NF-κB inhibitor. ConclusionsThese results suggest a crosstalk between TNFα signaling and AhR signaling in NF-κB activation which may constitute one of the molecular mechanisms underlying the higher incidence of drug-discontinuation in RA patients undergoing TNFi treatment with smoking habits.

The influence of comorbidities on the efficacy of tumour necrosis factor inhibitors, and the effect of tumour necrosis factor inhibitors on comorbidities in rheumatoid arthritis: report from a National Consensus Conference.

To define the safety and efficacy of TNF inhibitors (TNFi) in RA patients with comorbidities. A National Consensus Conference adopted a five-step process to better address the place of TNFi in the treatment of RA. Here we report the work focused on the influence of comorbidities on TNFi efficacy and the effect of TNFi on comorbidities using a Population Intervention Comparison Outcome-based strategy from 8 April 2013 to 15 January 2016. A total of 4453 hits were analysed, of which 10 were eligible for full review. Data show that the presence of comorbidities influences the treatment strategy and several clinical outcomes. The risk of solid cancer is similar in RA patients treated with TNFi or with conventional synthetic DMARDs, and the risk of recurrent breast cancer is not higher in RA patients treated with TNFi. The risk of developing serious infections is higher in RA patients receiving TNFi than conventional synthetic DMARDs. Patients with previous serious infections before starting TNFi are not at increased risk of subsequent serious infection. The hazard rate of hospitalization due to infections is not different among patients remaining on the same TNFi, or switching to a different TNFi or to an agent with another mechanism of action. Longer exposure to TNFi is associated with a reduction in the risk of cardiovascular events. Comorbidities affect RA treatment strategies and the efficacy of TNFi. TNFi treatment may decrease the risk of cardiovascular diseases and their use in patients with previous infection is not associated with a higher risk of recurrences.

Comparison of efficacy of TNF inhibitors and abatacept in patients with rheumatoid arthritis; Adjusted with propensity score matching

The aim of this study was to compare the clinical outcome of patients with rheumatoid arthritis seen in routine clinical practice treated with either TNF inhibitors or abatacept. To overcome potential bias, both propensity score matching and Inverse Probability of Treatment Weighting were used for patient selection. The propensity score matching procedure selected 315 matched pairs of patients who were treated with TNF inhibitors or abatacept. At week 52, SDAI in TNF inhibitors was lower than abatacept. In contrast, analysis of biologics-naive patients using the propensity-score matching (n = 150; in each group) showed comparable clinical efficacy. Consistent results were obtained by the use of Inverse Probability of Treatment Weighting (581 patients treated with TNF inhibitors and 353 patients treated with abatacept). The predictors of response to each treatment were different; abatacept appeared to benefit patients with high baseline RF titers while TNF inhibitors appeared to benefit patients with low baseline HAQ-DI.

Influence of NKG2D Genetic Variants on Response to Anti-TNF Agents in Patients with Rheumatoid Arthritis.

A natural killer group 2 member D (NKG2D) acts as a powerful activating and co-stimulatory receptor on immune effector cells including NK and T cells. Disruptions within the NKG2D signalling pathway may trigger an exacerbated immune response and promote autoimmune reactions. The objective of the study was to evaluate a plausible role of polymorphisms within the NKG2D gene as a predictor of how effective anti-tumor necrosis factor (TNF) therapy is in rheumatoid arthritis (RA) patients. A total of 280 RA patients receiving anti-TNF therapy were genotyped for NKG2D rs2255336 (A > G), rs1049174 (C > G), and rs1154831 (C > A). Clinical response was evaluated according to the European League against Rheumatism (EULAR) criteria at the 12th and 24th week. Both the NKG2D rs225336 and rs1049174 polymorphisms were significantly associated with efficacy of TNF inhibitors. Inefficient therapy was more frequently observed in patients with rs2255336 GG or rs1049174 CC genotype as compared to other genotypes (p-value = 0.003 and p-value = 0.004, respectively). The presence of the rs2255336 G or the rs1049174 C allele correlated with a worse EULAR response (p-value = 0.002, p-value = 0.031, respectively). Moreover, patients carrying the rs2255336 or rs1049174 heterozygous genotype achieved better EULAR responses than patients with homozygous genotypes (p-value = 0.010 and p-value = 0.002, respectively). Data from the present study provides evidence that NKG2D polymorphisms may affect response to anti-TNF inhibitors in RA patients.

Poor efficacy of TNF inhibitors in non-radiographic axial spondyloarthritis in the absence of objective signs: A bicentric retrospective study

ObjectiveTo compare BASDAI 50 response rate to TNFi in axial spondyloarthritis (axSpA) depending on the presence or not of objective signs of axSpA and to look for predictive factors of TNFi efficacy. MethodsPatients diagnosed with axSpA according to ASAS criteria “clinical arm” and treated between January 2001 and September 2015 with TNFi were included. First group included patients with at least one objective sign such as arthritis, dactylitis, enthesitis, uveitis, inflammatory bowel disease, elevated C-reactive protein or radiological sacroiliitis, and second group included non-radiographic axSpA (nr-axSpA) patients without any objective sign corresponding to patients with inflammatory back pain and either a good response to NSAID or a SpA family history. The primary outcome was the TNFi efficacy, defined as an achievement of BASDAI 50 at 3 months. The secondary outcomes were BASDAI 50 achievement over 1 year and analysis of predictive factors of TNFi response. ResultsWe included 84 nr-axSpA patients without any objective signs and 84 axSpA patients with objective signs (48.2% r-axSpA and 52.8% nr-axSpA). BASDAI 50 achievement rates were significantly higher in patients with objective signs than in patients without, at 3 months (45.1% versus 13.7%, P<0.0001) and at any of the visit-time points over the first year (61.9% versus 21.4%, P<0.0001). In multivariate analysis, overweight/obesity and sacroiliitis on MRI were respectively negative and positive predictive factors of TNFi efficacy in the total population at 3 months (OR=0.32, 95%CI [0.11, 0.96], P=0.041 and OR=6.92, 95% CI (2.41, 19.8), P<0.0001, respectively). ConclusionTNFi should be used with caution in axSpA when objective signs are absent as only 13.7% of these patients were BASDAI 50 responders at 3 months.

Periodontal Disease in Patients with Ankylosing Spondylitis: myth or reality?

Although the relation between periodontitis (PD) and systemic disorders (e.g. cardiovascular diseases, diabetes and rheumatoid arthritis) is widely accepted, the association with ankylosing spondylitis (AS) is inconsistently mentioned. We prospectively examined the relationship between periodontal disease and AS, focusing on the rate and course of PD, factors associated with severity and the impact of anti-TNF-a treatment on inflammatory status. Standard assessments performed twice (week 0, week 24) included an extensive dental evaluation (plaque index, gingival index, bleeding on probing, periodontal pocket depth, clinical attachment loss), inflammatory parameters and AS activity scores (BASDAI, ASDAS-CRP). More than half of AS presented with impaired periodontal health at baseline (mild to moderate PD) meaning increased sites with dental plaque, abnormal bleeding, increased periodontal pocket depth and clinical attachment loss. Significant positive correlation between presence and severity of PD, AS activity and systemic inflammation (CRP) was reported at baseline (p[0.05). A final analysis performed at 24 weeks revealed significant improvement in periodontal status, inflammatory parameters and AS activity, suggesting efficacy of TNF inhibitors directed not only against systemic, but also on local (articular, periodontal) inflammation (p[0.05). Patients with AS are at risk to develop periodontal disease, particularly those with high levels of systemic inflammation. Benefits of anti-TNFa therapy in the particular settings of AS patient and concomitant periodontal disease should be validated through further studies in larger cohorts.

Therapies of Early, Advanced, and Late Onset Forms of Axial Spondyloarthritis, and the Need for Treat to Target Strategies.

This study aims to provide an update on current status of pharmacological therapies in early and advanced stages of axial spondyloarthritis (axSpA), as well as its late onset forms, and to discuss the need for treat to target strategies in this entity. Efficacy of TNF inhibitors has been assessed in randomized controlled trials in axSpA, which included patients who had non-radiographic axSpA according to the ASAS classification criteria. The role of IL17/23 pathway as a therapeutic target in ankylosing spondylitis (AS) has been the focus of phase III studies of secukinumab (named MEASURE 1 and MEASURE 2) and a proof-of-concept study of ustekinumab. Potential efficacy of novel small molecules such as apremilast and tofacitinib has been explored in recent phase II trials. All the trials of TNF inhibitors in non-radiographic axSpA have achieved their primary endpoints, which resulted in their approval for this indication in Europe, but not in USA. The phase III trials of secukinumab have demonstrated significant therapeutic benefit as compared to placebo, resulting in its approval as the first non-TNF biologic for the treatment of AS, both by the US Food and Drug Administration and the European Medicines Agency.

Effects of targeted therapies on the bone in arthritides.

Inflammatory arthritides, such as rheumatoid arthritis (RA) and spondyloarthritides (SpA) have been associated with both localized bone resorption and/or formation, and generalized osteoporosis. Systemic inflammation may be the major driver for bone loss in arthritis. In RA and peripheral SpA the RANK-RANKL-OPG network is involved in bone resorption, while in axial SpA the Wnt-β-catenin axis and its inhibitors (DKK-1, sclerostin) are the most relevant. Targeted therapies including biologics and small molecule tyrosine kinase inhibitors may interfere with inflammatory bone metabolism. Most of these compounds are able to slow down radiographic progression and osteoporosis in arthritides. In very early cases of non-radiological SpA, there may be a window of opportunity allowing to prevent syndesmophyte formation. The inability of targeted therapies to increase the production of DKK-1 and sclerostin may explain the lack of efficacy of TNF inhibitors to halt syndesmophyte formation in SpA. Further clinical trials are needed to better understand the bone effects of targeted therapies.

Association of Fcgamma receptor type 2A and 3A genotypes with rheumatoid arthritis in Chinese population.

SNPs of FcγRs were implicated in pathogenesis of rheumatoid arthritis (RA) and treatment efficacy of TNF inhibitors (TNFi). This study aims to investigate the associations of FcγRIIa and FcγRIIIa genotypes with autoantibody production and treatment response to TNFi in Chinese patients with RA. FcγRIIa and FcγRIIIa polymorphisms were genotyped in 158 RA patients. Response to TNFi was evaluated in 18 patients at 3 and 6 months after treatment. FcγRIIa-131H allele was significantly increased in autoantibody-negative RA patients. FcγRIIa-131H/H+H/R was closely associated with differences in 28-joint disease activity score in patients at months 3 and 6 of TNFi treatment. FcγRIIa-131H allele may have a protective role in autoantibody production and might be a biomarker for predicting good response to TNFi in Chinese RA patients.

Efficacy and effectiveness of tumour necrosis factor inhibitors in the treatment of rheumatoid arthritis in randomized controlled trials and routine clinical practice.

Efficacy of TNF inhibitors in the treatment of RA assessed in randomized controlled trials (RCTs) may not be fully comparable to routine care owing to the stringent inclusion criteria. The objective of this study was to observe the effectiveness of TNF inhibitors in real-world patients and assess the patients' potential eligibility for the RCTs. RA patients starting a TNF-inhibitor treatment between 2004 and 2014 were identified from the National Register for Biologic Treatment in Finland, which is a longitudinal observational cohort study. Effectiveness was measured using the ACR and EULAR response criteria and by studying the proportion of patients reaching DAS28 remission. The patients' baseline characteristics were compared against the inclusion criteria of 27 RCTs. EULAR moderate and good treatment responses at 6 months were achieved by 69 and 40% of the users of the first TNF inhibitor, respectively. ACR20, ACR50 and ACR70 responses were reached by 48, 27 and 13%, respectively. DAS28 remission was reached by 47%. Only 7.6-44% of the patients would have been potentially eligible for the RCTs. The eligible patients had better treatment responses compared with the non-eligible patients. Different TNF inhibitors were mostly equipotent, but the usage of MTX co-therapy had a major influence on treatment response. Only a small proportion of patients would have been eligible for RCTs, and the efficacy of TNF inhibitors assessed in them cannot be generalized directly into Finnish routine health care.

In vitro response pattern of monocytes after tmTNF reverse signaling predicts response to anti-TNF therapy in rheumatoid arthritis.

BackgroundTreatment with TNF inhibitors is very efficient in the majority of the patients with rheumatoid arthritis (RA), but it does not achieve a sufficient treatment response in 40–50% of the cases. Goal of the study was to assess functional ex vivo-tests of RA monocytes as prognostic parameters of the subsequent treatment response.Methods20 anti-TNF naïve RA patients were enrolled in a prospective, open-label trial, and Etanercept therapy was initiated. Prior to treatment, reverse signaling was induced in peripheral blood monocytes by tmTNF crosslinking via TNFR2:Ig construct Etanercept in a standardized ex vivo-assay. Released cytokine and cytokine receptor concentrations were determined as parameters of the monocyte response.ResultsCrosslinking of tmTNF and consecutive reverse signaling led to production of pro- and anti-inflammatory cytokines and of soluble cytokine decoy receptors such as sTNFR1 and sIL-1R2. Several of the measured concentrations were found to correlate with the treatment response according to the EULAR criteria. The correlation was most pronounced in sTNFR1 concentrations (r = −0.657, p = 0.0031), which also predicted a good clinical response with the highest sensitivity and specificity according to EULAR criteria.ConclusionsHerein we propose that the tmTNF crosslinking-triggered shedding of soluble decoy receptors and production of anti-inflammatory cytokines could contribute to the clinical efficacy of TNF inhibitors, and that in vitro quantification of this secretion by RA monocytes prior to treatment can be used to predict the clinical response. Further development of such standardized tests could be a step towards personalized medicine by providing rheumatologists with a rational choice for first line biological therapy in patients with RA.

Effects of mud-bath therapy in psoriatic arthritis patients treated with TNF inhibitors. Clinical evaluation and assessment of synovial inflammation by contrast-enhanced ultrasound (CEUS)

ObjectivesDespite the efficacy of TNF inhibitors, most patients with psoriatic arthritis maintain a residual synovial inflammation. The main aim of the study was to evaluate the effects of mud-bath therapy on clinical picture of PsA patients treated with TNF inhibitors. The secondary outcome was to assess synovial inflammation in hand joints detected by contrast-enhanced ultrasound. Other aims were to verify the risk of arthritis flare and to evaluate the effects of spa treatment on functional ability and on quality of life. MethodsThirty-six patients with psoriatic arthritis, treated in the last 6 months with TNF inhibitors, were enrolled. After 1:1 randomisation, 18 patients (group A) underwent mud-bath therapy (12 mudpacks and 12 thermal baths), maintaining treatment with TNF inhibitors; 18 patients (group B) continued pharmacological therapy alone. CRP, PASI, DAS28, swollen and tender joint count, VAS pain, HAQ and SF-36 were evaluated at baseline (T0) and after 45 days (T1). Synovial inflammation detected by contrast-enhanced ultrasound, analysed by a software system, was also assessed. ResultsA significant improvement in PASI (P<0.005), DAS28 (P<0.05), swollen joint count and tender joint count (P<0.001), and HAQ (P<0.001) between T0 and T1 was observed in group A. No patient underwent a flare-up of arthritis. Ultrasound videos demonstrated a significant appearance delay (P<0.05) and faster washout (P<0.02) of contrast dye in group A patients with respect to group B. ConclusionsThese data suggest a decrease of residual synovial inflammation and a beneficial clinical effect of spa therapy in psoriatic arthritis patients treated with TNF inhibitors.

SAT0358 Impact of Methotrexate on Anti-TNF Treatment in Psoriatic Arthritis? an In-Depth Analysis of A Large Prospective Observational Study with Adalimumab

BackgroundIn active psoriatic arthritis (PsA) the efficacy of TNF-inhibitors (TNFi) has been proven in randomized clinical trials (RCT). Methotrexate (MTX) co-medication can improve the therapeutic benefit of TNFi in rheumatoid...

SAT0361 Short Term Efficacy of Tumor Necrosis Factor Inhibitors in Patients with Non–Radiographic Axial Spondylarthritis and Ankylosing Spondylitis; Results from TURKBIO Registry

BackgroundAxial spondylarthritis (AxSpA) has been proposed as an umbrella term for ankylosing spondylitis (AS) and non-radiographic (nr) AxSpA. This new concept makes diagnosis of AS possible at an early stage...

AB0451 The efficacy of anti-tumor necrosis factor therapy and the factors which contribute to fatigue in rheumatoid arthritis

BackgroundFatigue is an important domain in the assessment of disease impact but has rarely been evaluated consistently after initiation of treatment in Rheumatoid Arthritis (RA) patients. Due tothe known efficacy...