scholarly journals Tuberculosis and targeted synthetic or biologic DMARDs, beyond tumor necrosis factor inhibitors

2020 ◽  
Vol 12 ◽  
pp. 1759720X2093011 ◽  
Author(s):  
Gerasimos Evangelatos ◽  
Vasiliki Koulouri ◽  
Alexios Iliopoulos ◽  
George E Fragoulis
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Real Life ◽  
Janus Kinase ◽  
Current Evidence ◽  
Tumor Necrosis Factor Inhibitors ◽  
Jak Inhibitors ◽  
Latent Tb ◽  
Endemic Areas ◽  
Necrosis Factor

Patients with autoimmune rheumatic diseases (ARD) have an increased risk for tuberculosis (TB). The use of tumor necrosis factor inhibitors (TNFi) and glucocorticoids in these patients has been associated with an increased prevalence of latent TB reactivation. Over the last few years, several biologic disease-modifying anti-rheumatic drugs (bDMARDs), other than TNFi (e.g. rituximab, abatacept, tocilizumab, secukinumab) and targeted synthetic DMARDs (tsDMARDs) [e.g. apremilast, Janus kinase (JAK) inhibitors] have been used for the treatment of patients with ARD. For many of these drugs, especially the newer ones like JAK inhibitors or antibodies against interleukin (IL)-23, most data stem from randomized clinical trials and few are available from real life clinical experience. We sought to review the current evidence for TB risk in patients with ARD treated with tsDMARDs or bDMARDs, other than TNFi. It seems that some of these drugs are associated with a lower TB risk, indirectly compared with TNFi treatment. In fact, it appears that rituximab, apremilast and inhibitors of IL-17 and IL-23 might be safer, while more data are needed for JAK inhibitors. As seen in TNFi, risk for TB is more pronounced in TB-endemic areas. Screening for latent TB must precede initiation of any tsDMARDs or bDMARDs. The growing use of non-TNFi agents has raised the need for more real-life studies that would compare the risk for TB between TNFi and other treatment modalities for ARD. Knowledge about the TB-safety profile of these drugs could help in the decision of drug choice in patients with confirmed latent TB infection or in TB endemic areas.

scholarly journals Twelve-Year Retention Rate of First-Line Tumor Necrosis Factor Inhibitors in Rheumatoid Arthritis: Real-Life Data From a Local Registry

2016 ◽  
Vol 68 (4) ◽  
pp. 432-439 ◽  
Author(s):  
Ennio Giulio Favalli ◽  
Francesca Pregnolato ◽  
Martina Biggioggero ◽  
Andrea Becciolini ◽  
Alessandra Emiliana Penatti ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Retention Rate ◽  
Real Life ◽  
Tumor Necrosis Factor Inhibitors ◽  
First Line ◽  
Life Data ◽  
Real Life Data ◽  
Necrosis Factor

scholarly journals Rheumatoid arthritis and myasthenia gravis: a case-based review of the therapeutic options

2022 ◽  
Author(s):  
Riccardo Bixio ◽  
Davide Bertelle ◽  
Francesca Pistillo ◽  
Elisa Pedrollo ◽  
Antonio Carletto ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Myasthenia Gravis ◽  
Tumor Necrosis ◽  
Kinase Inhibitors ◽  
Case Reports ◽  
Janus Kinase ◽  
Therapeutic Options ◽  
Tumor Necrosis Factor Inhibitors ◽  
Necrosis Factor

Abstract Introduction Myasthenia gravis is an autoimmune disease affecting the neuromuscular junction, often associated with other autoimmune diseases, including rheumatoid arthritis. Patients with rheumatoid arthritis present an increased prevalence of myasthenia gravis compared to the general population. While these two diseases share some therapeutic options, such as glucocorticoids, methotrexate, and rituximab, there are no guidelines for treating concomitant disease. We aim to review the available evidence and to discuss the efficacy and safety of the therapeutic options in patients with rheumatoid arthritis associated with myasthenia gravis. Method We described three patients with rheumatoid arthritis associated with myasthenia gravis and we performed a systematic review of the associated literature. Results A 48-year-old man and two women (48 and 55 years old) with concomitant diagnoses of active rheumatoid arthritis and well-controlled myasthenia gravis are described. They were treated with methotrexate, leflunomide, upadacitinib, and adalimumab. None of them experienced changes in their myasthenic symptoms. We found 9 additional cases from our literature review. Methotrexate, rituximab, upadacitinib, diphenyl sulfone, auranofin, and loxoprofen sodium did not show an impact on the seven patients with previously well-controlled myasthenia. Glucocorticoids, methotrexate, and rituximab proved effective in active myasthenia gravis and arthritis. Conflicting data emerged for Tumor-necrosis factor inhibitors. Conclusions Although the available evidence remains scarce, we consider glucocorticoids, methotrexate, and rituximab as safe and effective options. The role of tumor-necrosis factor inhibitors remains uncertain. Eventually, Janus Kinase inhibitors are a novel interesting option for these patients. Key Points• To date, the only evidence on the treatment of patients with rheumatoid arthritis and concomitant myasthenia gravis derives from case reports.• Based on the review of the available case reports and on the cases we described, we consider glucocorticoids, methotrexate, and rituximab as safe and effective options, while the role of Tumor-necrosis factor inhibitors remains uncertain.• Based on the cases we described, Janus Kinase inhibitors are a novel interesting option for patients with concomitant rheumatoid arthritis and myasthenia gravis.

scholarly journals AB0199 PLACEBO AND NOCEBO RESPONSES IN RANDOMIZED CONTROLLED TRIALS OF NON-TUMOR NECROSIS FACTOR BIOLOGICS AND JANUS KINASE INHIBITORS IN PATIENTS WITH ACTIVE RHEUMATOID ARTHRITIS SHOWING INSUFFICIENT RESPONSE TO TUMOR NECROSIS FACTOR INHIBITORS: A META-ANALYSIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1124.1-1124
Author(s):  
Y. H. Lee ◽  
G. G. Song
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Meta Analysis ◽  
Placebo Response ◽  
Tnf Inhibitors ◽  
Janus Kinase ◽  
Jak Inhibitors ◽  
Acr20 Response ◽  
Insufficient Response ◽  
Necrosis Factor

Background:Placebo and nocebo responses have important consequences for the development of pharmaceutical drugs and the design of randomized controlled trials (RCTs). They can lead to the incorrect measurement of treatment-related efficacy and adverse effects (AEs).Objectives:The goal of this study was to evaluate the frequency and magnitude of placebo and nocebo responses in placebo-controlled RCTs of non-tumor necrosis factor (TNF) biologics and Janus kinase (JAK) inhibitors in patients with rheumatoid arthritis (RA) showing an insufficient response to TNF inhibitors.Methods:We performed a meta-analysis on the rates of placebo response, AEs, severe AEs (SAEs), and withdrawal owing to AEs in placebo-controlled randomized clinical trials (RCTs) of non-TNF biologics and JAK inhibitors in patients with RA showing an insufficient response to TNF inhibitors.Results:Nine RCTs contained a total of 3,442 patients (1,840 experimental subjects and 1,602 controls). The pooled incidence of an ACR20 response rate in placebo-treated patients was 22.1% (95% CI 16.4–29.1%) and 27.9% (95% CI 24.5–31.6%) in RCTs of non-TNF inhibitors and JAK inhibitors, respectively. A strong negative correlation was observed between drug efficacies (ACR20 response) and AE rates in the placebo arm, indicating that the greater the placebo response, the weaker the nocebo response (r = -0.762, P = 0.017). A strong positive correlation was observed between drug efficacies (ACR20 response) in the placebo and active comparator, indicating that the greater the placebo response, the greater the treatment response (r = 0.737, P = 0.003). The pooled estimate in placebo-treated patients with at least one AE was 71.8% (95% CI 57.4–82.7%) and 58.7% (95% CI 52.8–64.3%) in RCTs of non-TNF inhibitors and JAK inhibitors, respectively. The pooled estimate in placebo-treated patients who withdrew from treatment owing to an AE was 3.8% (95% CI 2.7–5.3%) and 4.0% (95% CI 2.7–6.0%) in RCTs of non-TNF inhibitors and JAK inhibitors, respectively. A strong positive correlation was observed between AE rates in the placebo and active arms, indicating that the greater the nocebo response, the stronger the AE rate in the active arm (r = 0.855, P = 0.003).Conclusion:The frequency of the placebo and nocebo responses was 22.1% vs. 27.9% and 71.8% vs. 58.7% in placebo-controlled RCTs of non-TNF inhibitors and JAK inhibitors for RA, respectively, and the greater the placebo response, the weaker the nocebo response and the greater the efficacy.References:[1]Mitsikostas DD, Chalarakis NG, Mantonakis LI, Delicha EM, Sfikakis PP. Nocebo in fibromyalgia: meta-analysis of placebo-controlled clinical trials and implications for practice. Eur J Neurol 2012;19:672-80.[2]Kravvariti E, Kitas GD, Mitsikostas DD, Sfikakis PP. Nocebos in rheumatology: emerging concepts and their implications for clinical practice. Nat Rev Rheumatol 2018;14:727-40.[3]Colloca L, Barsky AJ. Placebo and Nocebo Effects. N Engl J Med 2020;382:554-61.Disclosure of Interests:None declared

The Effects of Tumor Necrosis Factor Inhibitors on Cardiovascular Risk in Rheumatoid Arthritis

2012 ◽  
Vol 18 (11) ◽  
pp. 1502-1511 ◽  
Author(s):  
Mike J.L. Peters ◽  
Alper M. van Sijl ◽  
Alexandre E. Voskuyl ◽  
Naveed Sattar ◽  
Yvo M. Smulders ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Cardiovascular Risk ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Inhibitors ◽  
Necrosis Factor

scholarly journals Recent Trends in Medication Usage for the Treatment of Juvenile Idiopathic Arthritis and the Influence of Tumor Necrosis Factor Inhibitors

2014 ◽  
Vol 41 (10) ◽  
pp. 2078-2084 ◽  
Author(s):  
Melissa L. Mannion ◽  
Fenglong Xie ◽  
Jeffrey R. Curtis ◽  
Timothy Beukelman
Keyword(s):  
Juvenile Idiopathic Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Temporal Trends ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Tumor Necrosis Factor Inhibitors ◽  
Antiinflammatory Drugs ◽  
Medication Usage ◽  
The Mean ◽  
Necrosis Factor

Objective.Using administrative data from a large commercial US health insurer, we investigated temporal trends in medication use among children diagnosed with juvenile idiopathic arthritis (JIA).Methods.Children with ≥ 1 physician diagnosis code for JIA in the calendar years 2005 through 2012 were included. Use of tumor necrosis factor inhibitors (TNFi), methotrexate (MTX), nonsteroidal antiinflammatory drugs (NSAID), and oral glucocorticoids (GC) was determined. Temporal changes in medication usage were evaluated with the Cochran-Armitage test for trend. We used paired t-tests to evaluate the use of NSAID and GC in the 6 months before and after new TNFi use.Results.We identified 4261 unique individuals with JIA. The proportion of patients receiving TNFi increased from 8.7% in 2005 to 22.4% in 2012 (p < 0.0001). MTX use increased from 18.4% to 23.2% (p = 0.02). NSAID use decreased from 49% to 40% (p = 0.02). GC use was relatively unchanged. Following new TNFi use, the mean number of NSAID prescriptions (among prevalent users) decreased from 2.8 to 2.0 (p < 0.0001), and the mean daily GC dose (among prevalent users) decreased from 7.3 mg/day to 3.9 mg/day (p < 0.0001). Many new TNFi users (57%) had not used MTX in the previous 6 months, and only 37% had any concurrent MTX use in the 6 months following new TNFi use.Conclusion.TNFi use in the treatment of JIA increased 2- to 3-fold over the last 8 years. New TNFi use was associated with decreased NSAID and GC use. TNFi may be replacing, rather than complementing, MTX in the treatment of many patients.

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