Update on the British Society for Rheumatology guidelines for prescribing TNF  blockers in adults with rheumatoid arthritis (update of previous guidelines of April 2001)

Ledingham, Joanna; Deighton, Chris

doi:10.1093/rheumatology/keh464

Cited by 324 publications

(233 citation statements)

References 59 publications

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“…31 Clinically, blockage of TNF-a with anti-TNF has been widely used in many immune-mediated diseases, including rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease, psoriasis and psoriatic arthritis. 21,[38][39][40] Several studies reported that elevated HBV viral load subsequently leads to active hepatitis. 24,25 A recent study analyzing patients with inflammatory arthritis also revealed an increased risk of HBV reactivation associated with anti-TNF therapy in patients with chronic HBV infection.…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor-alpha blockage therapy impairs hepatitis B viral clearance and enhances T-cell exhaustion in a mouse model

Chyuan

Tsai²,

Tzeng

et al. 2015

Cell Mol Immunol

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Hepatitis B virus (HBV) reactivation and recurrence are common in patients undergoing immunosuppression therapy. Tumor necrosis factor (TNF) blockage therapy is effective for the treatment of many autoimmune inflammatory diseases. However, the role of TNF-a blockage therapy in the innate and adaptive immune responses against HBV is still not clear. A detailed analysis of HBV infection under TNF-a blockage therapy is essential for the prophylaxis and therapy for HBV reactivation and recurrence. In this study, HBV clearance and T-cell responses were analyzed in a HBV-transfected mouse model under anti-TNF blockage therapy. Our results demonstrated that under TNF-a blockage therapy, HBV viral clearance was impaired with persistent elevated HBV viral load in a dose-and temporal-dependent manner. The impairment of HBV clearance under anti-TNF-a blockage therapy occurred at early time points after HBV infection. In addition, TNF-a blockade maintained a higher serum HBV viral load and increased the number of intrahepatic programmed cell death (PD)-1 high CD127 low exhausted T cells. Furthermore, TNF-a blockade abolished Toll-like receptor 9 (TLR9) ligand-induced facilitation of HBV viral clearance. Taken together, TNF-a blockade impairs HBV clearance and enhances viral load, and these effects depend on early administration after HBV infection. Our results here demonstrate that early TNF-a blockade reduces viral clearance and persistently maintains elevated HBV viral load in a mouse model, suggesting that HBV may reactivate during therapy with TNF-a-blocking agents.

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Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor-alpha blockage therapy impairs hepatitis B viral clearance and enhances T-cell exhaustion in a mouse model

Chyuan

Tsai²,

Tzeng

et al. 2015

Cell Mol Immunol

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“…The methods of this register have been described in detail elsewhere (21). Briefly, as part of UK national guidelines, all patients with RA starting a new anti-TNF␣ therapy are registered with the BSRBR, with the goal of recruiting a total of 12,000 biologically naive patients (4,000 in each treatment start group [etanercept, adalimumab, or infliximab]) (22). The present analysis was restricted to patients registered with the BSRBR with a diagnosis of RA (as determined by the treating rheumatologist) who had reached a minimum of 6 months of followup by the end of April 2005.…”

Section: Methodsmentioning

confidence: 99%

Outcomes after switching from one anti–tumor necrosis factor α agent to a second anti–tumor necrosis factor α agent in patients with rheumatoid arthritis: Results from a large UK national cohort study

Hyrich

Lunt

Watson

et al. 2007

Arthritis & Rheumatism

379

215

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Objective. Patients with rheumatoid arthritis (RA) who experience treatment failure with one antitumor necrosis factor (anti-TNF) agent, due to either inefficacy or toxicity, are frequently switched to a second anti-TNF agent, although the benefits of switching are unknown. The present study was undertaken to compare drug continuation rates between the first course and second course of anti-TNF therapy.Methods. The study involved a prospective cohort of RA patients from a UK national register of new anti-TNF treatment starts (n ‫؍‬ 6,739; 876 starting adalimumab, 2,826 starting etanercept, and starting 3,037 infliximab). Over a mean 15 months of followup, 841 patients stopped taking the first drug due to inefficacy and 1,023 stopped the first drug due to toxicity, of whom 503 and 353, respectively, were switched to a second anti-TNF agent. Kaplan-Meier survival curves were plotted to determine continuation rates for each course, and Cox regression was used to compare each course for the risk of stopping and the reason for stopping (inefficacy or toxicity).Results. Overall, 73% of patients who switched to a second anti-TNF agent remained on the new therapy by the end of followup. First drug discontinuation due to inefficacy was associated with an increased rate of second drug discontinuation due to inefficacy (hazard ratio [HR] 2.7, 95% confidence interval [95% CI] 2.1-3.4) but not toxicity (HR 1.1, 95% CI 0.9-1.5). Similarly, first drug discontinuation due to toxicity was associated with an increased rate of second drug discontinuation due to toxicity (HR 2.3, 95% CI 1.9-2.9) but not inefficacy (HR 1.2, 95% CI 0.8-1.6).Conclusion. RA patients who are switched to a second anti-TNF drug have high rates of continuation, although among those who must discontinue treatment, the reasons for stopping a second drug are related to the reasons for stopping the first drug. This large data set from the UK provides the first estimates of the magnitude of these effects in patients with long-standing severe RA.

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“…Common side effects, including rashes and constitutional symptoms, are usually mild and self-limiting, and generally do not lead to drug discontinuation. Because initial safety studies suggested no increase in adverse hematologic events, current guidelines do not recommend regular complete blood cell count (CBC) monitoring for anti-TNF therapy (2)(3)(4)(5). However, significant hematologic reactions, in particular neu-tropenia, have been reported in patients treated with all 3 TNF inhibitor agents (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

Neutropenia in patients receiving anti–tumor necrosis factor therapy

Hastings¹,

Ding²,

Butt³

et al. 2010

Arthritis Care & Research

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Objective. To examine the rates of and risk factors for neutropenia together with the dynamics of neutrophil and other white cell subset counts in a cohort of patients treated with a tumor necrosis factor (TNF) inhibitor for inflammatory arthritis. Methods. We performed a retrospective cohort study examining the association between baseline demographics, clinical features, medications used, and development of neutropenia, and behavior of neutrophil and other white cell subset counts during TNF inhibitor therapy. Results. In 367 patients (298 [81.2%] with rheumatoid arthritis, 38 [10.4%] with ankylosing spondylitis, and 31 [8.4%] with psoriatic arthritis), 69 (18.8%) had at least one episode of neutropenia (<2.0 ؋ 10 9 /liter) during TNF inhibitor therapy, and of these, 6% developed serious infections secondary to neutropenia. There was no significant difference in disease, demographic, or drug variables between patients with and without neutropenia. However, patients with neutropenia had significantly lower baseline neutrophil counts (4.2 ؋ 10 9 /liter; 95% confidence interval [95% CI] 3.8, 4.6 versus 6.2 ؋ 10 9 /liter; 95% CI 6.0, 6.5), and a previous history of neutropenia while receiving disease-modifying antirheumatic drugs increased the risk while receiving TNF inhibitors (hazard ratio 2.97; 95% CI 1.69, 5.25). A significant drop in mean neutrophil count (1.12 ؋ 10 9 /liter; 95% CI 0.92, 1.32) was observed after 2 weeks of TNF inhibitor therapy. Other white cell subsets tended to significantly increase. Conclusion. TNF inhibitor therapy is associated with a significant reduction in peripheral blood neutrophil count, leading to 19% of patients becoming neutropenic. Risk of neutropenia is significantly higher in patients with a low baseline neutrophil count or previous history of neutropenia. We suggest that patients receiving TNF inhibitor therapy would benefit from regular complete blood cell count monitoring.

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Update on the British Society for Rheumatology guidelines for prescribing TNF blockers in adults with rheumatoid arthritis (update of previous guidelines of April 2001)

Cited by 324 publications

References 59 publications

Tumor necrosis factor-alpha blockage therapy impairs hepatitis B viral clearance and enhances T-cell exhaustion in a mouse model

Tumor necrosis factor-alpha blockage therapy impairs hepatitis B viral clearance and enhances T-cell exhaustion in a mouse model

Outcomes after switching from one anti–tumor necrosis factor α agent to a second anti–tumor necrosis factor α agent in patients with rheumatoid arthritis: Results from a large UK national cohort study

Neutropenia in patients receiving anti–tumor necrosis factor therapy

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