scholarly journals Incidence, Clinical Features, Management, and Prevention of Herpes Zoster in Patients Receiving Antitumor Necrosis Factor Therapy: A Clinical Review

2020 ◽  
Vol 24 (3) ◽  
pp. 278-284
Author(s):  
Byung-Soo Kim ◽  
Emanual Maverakis ◽  
Clarie Alexanian ◽  
Jenny Z. Wang ◽  
Siba P. Raychaudhuri
Keyword(s):  
Herpes Zoster ◽  
Clinical Features ◽  
Viral Infections ◽  
Therapeutic Option ◽  
Tnf Inhibitors ◽  
Tnf Inhibitor ◽  
Inflammatory Conditions ◽  
Increased Risk ◽  
Factor Therapy ◽  
Necrosis Factor

Tumor necrosis factor (TNF) inhibitors have been used as an excellent therapeutic option in a variety of chronic inflammatory conditions. However, a recognized significant adverse effect of TNF inhibitor therapy is the increased risk of infections. The influence of TNF inhibitors on the course of coexisting or newly developed viral infections has not been extensively investigated. Therefore, we reviewed the recent publications to highlight the incidence, clinical features, management, and prevention of herpes zoster in patients who are receiving TNF inhibitors.

scholarly journals Two Cases of Paradoxical Hidradenitis Suppurativa while on Adalimumab

2016 ◽  
Vol 10 (1) ◽  
pp. 92-98 ◽  
Author(s):  
Glenn Harvin ◽  
George Kasarala
Keyword(s):  
Tumor Necrosis Factor ◽  
Skin Disease ◽  
Hidradenitis Suppurativa ◽  
Tumor Necrosis ◽  
Tnf Inhibitors ◽  
Tnf Inhibitor ◽  
Inflammatory Skin Disease ◽  
Inflammatory Skin ◽  
Necrosis Factor ◽  
Inhibitor Treatment

Hidradenitis suppurativa (HS) is a chronic, inflammatory skin disease characterized by recurring abscesses, nodules, and fistulas predominantly in the groin and axillae. The association between HS and Crohn’s disease (CD) has been well documented. Tumor necrosis factor (TNF) inhibitors have shown to be effective in treating both HS and CD. We report 2 patients who developed HS while on TNF inhibitor treatment for CD.

scholarly journals Changing Patterns of Tumor Necrosis Factor Inhibitor Use in 9074 Patients with Rheumatoid Arthritis

2009 ◽  
Vol 36 (5) ◽  
pp. 907-913 ◽  
Author(s):  
YUSUF YAZICI ◽  
SVETLANA KRASNOKUTSKY ◽  
JAIME P. BARNES ◽  
PATRICIA L. HINES ◽  
JASON WANG ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Dose Escalation ◽  
Tumor Necrosis ◽  
Randomized Clinical Trials ◽  
Tnf Inhibitors ◽  
Tnf Inhibitor ◽  
Insurance Claims ◽  
Claims Database ◽  
Necrosis Factor

Objective.Patients with rheumatoid arthritis (RA) commonly switch between tumor necrosis factor (TNF) inhibitors after failing to control disease activity. Much of the clinical data that support switching to a second TNF agent when one agent fails to work has come from small, short-term studies. We utilized a US insurance claims database to determine patterns of use such as dose escalation, time to discontinuation, and switching between TNF inhibitors in patients with RA.Methods.A retrospective analysis was performed using an insurance claims database in the US from 2000 to 2005. TNF inhibitor use, time to switch, dose escalation, and continuation times were analyzed in patients with RA.Results.Nine thousand seventy-four patients with RA started TNF inhibitors during the period 2000 to 2005. Etanercept was the most commonly used TNF inhibitor; infliximab had the highest duration of continuation, about 50% at 2 years. In addition, infliximab showed higher rates of dose escalation compared to etanercept and adalimumab. For all TNF inhibitors, time to switching decreased from 2000 to 2005.Conclusion.TNF inhibitor use patterns changed from 2000 to 2005, with more frequent changes among the different TNF inhibitors and a shorter duration of treatment before the change. Only about 50% of TNF inhibitors are still continued at 2 years, reflecting the difference between randomized clinical trials and real-world experience.

scholarly journals Increased Risk of Vitiligo Following Anti-Tumor Necrosis Factor Therapy: A 10-Year Population-Based Cohort Study

2018 ◽  
Vol 138 (4) ◽  
pp. 768-774 ◽  
Author(s):  
Jung Min Bae ◽  
Miri Kim ◽  
Han Hee Lee ◽  
Ki-Jo Kim ◽  
Hyoseung Shin ◽  
...  
Keyword(s):  
Cohort Study ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Population Based ◽  
Increased Risk ◽  
Factor Therapy ◽  
Necrosis Factor

scholarly journals Tumour necrosis factor inhibitor-associated sinusitis

2014 ◽  
Vol 52 (3) ◽  
pp. 246-251
Author(s):  
S. Yoshihara ◽  
K. Kondo ◽  
K. Kanaya ◽  
K. Suzukawa ◽  
S. Baba ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Medical Records ◽  
Tumour Necrosis ◽  
Chronic Sinusitis ◽  
Tnf Inhibitors ◽  
Sinus Surgery ◽  
Tnf Inhibitor ◽  
Factor Inhibitor ◽  
Continuous Use ◽  
Necrosis Factor

Aim: To describe the features of chronic sinusitis associated with the use of tumour necrosis factor (TNF) inhibitors. Methodology: A retrospective review of the medical records between 2003 and 2011 revealed that five patients had developed chronic sinusitis after the start of TNF inhibitor administration and required rhinological evaluation and treatment. Results: The incidence of refractory sinusitis associated with TNF inhibitors was approximately 2%. Of the five patients identified, four patients were medicated with etanercept and one with infliximab. The maxillary sinus was most commonly involved and cultures of the sinus discharge revealed Pseudomonas aeruginosa in three cases. Two patients showed improvement of sinusitis with antibiotic medication, despite the continuous use of TNF inhibitor, while in two other patients, sinusitis was resistant to antibiotic medication. Another patient who had developed recurrence of sinusitis after complete remission of previous chronic sinusitis by endoscopic sinus surgery showed remission only after cessation of TNF inhibitor. Conclusion: Chronic sinusitis associated with TNF inhibitors is considered to be a new disease entity, and it will become more common due to the increasing use of TNF inhibitors.

Severe Extraarticular Manifestations in a Community-based Cohort of Patients with Rheumatoid Arthritis: Risk Factors and Incidence in Relation to Treatment with Tumor Necrosis Factor Inhibitors

2017 ◽  
Vol 44 (7) ◽  
pp. 981-987 ◽  
Author(s):  
Lisa Theander ◽  
Britt-Marie Nyhäll-Wåhlin ◽  
Jan-Åke Nilsson ◽  
Minna Willim ◽  
Lennart T.H. Jacobsson ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tnf Inhibitors ◽  
Time Dependent ◽  
Community Based ◽  
Rheumatoid Arthritis Risk ◽  
Increased Risk ◽  
Clinical Records ◽  
Necrosis Factor

Objective.The aims of this study were to evaluate whether treatment with tumor necrosis factor (TNF) inhibitors in patients with rheumatoid arthritis (RA) affects the risk of developing severe extraarticular rheumatoid arthritis (ExRA) manifestations and to investigate potential predictors for developing ExRA.Methods.A dynamic community-based cohort of patients with RA was studied (n = 1977). Clinical records were reviewed and cases of severe ExRA were identified. Information on exposure to TNF inhibitors was obtained from a regional register. Exposure to TNF inhibitors was analyzed in a time-dependent fashion and the incidence of severe ExRA in exposed patients was compared with the incidence in unexposed patients. Cox regression models were used to assess potential predictors of severe ExRA.Results.During treatment with TNF inhibitors, there were 17 patients with new onset of severe ExRA in 2400 person-years at risk (PY; 0.71/100 PY, 95% CI 0.41–1.13) compared with 104 in 15,599 PY (0.67/100 PY, 95% CI 0.54–0.81) in patients without TNF inhibitors. This corresponded to an incidence rate ratio of 1.06 (95% CI 0.60–1.78). The age- and sex-adjusted HR for ExRA in anti-TNF–treated patients was 1.21 (95% CI 1.02–1.43), with similar findings in models adjusted for time-dependent Health Assessment Questionnaire and propensity for anti-TNF treatment. Male sex, positive rheumatoid factor (RF), long disease duration, and greater disability were predictors for ExRA.Conclusion.This study suggests that patients treated with TNF inhibitors are at a slightly increased risk of developing severe ExRA. RF-positive patients with disabling disease of long duration were more likely to develop severe ExRA.

scholarly journals Risk of lymphoma in patients exposed to antitumour necrosis factor therapy: results from the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis

2016 ◽  
Vol 76 (3) ◽  
pp. 497-503 ◽  
Author(s):  
Louise K Mercer ◽  
James B Galloway ◽  
Mark Lunt ◽  
Rebecca Davies ◽  
Audrey L S Low ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Cox Regression ◽  
British Society ◽  
Increased Risk ◽  
Factor Therapy ◽  
Necrosis Factor ◽  
Biologics Register

ObjectivesPatients with rheumatoid arthritis (RA) are at increased risk of lymphoma compared with the general population. There are concerns that tumour necrosis factor inhibitors (TNFi) may exacerbate this risk. However, since the excess risk of lymphoma in RA is related to the cumulative burden of inflammation, TNFi may conversely reduce the risk of lymphoma by decreasing the burden of inflammation. The aim of this study was to compare the risk of lymphoma in subjects with RA treated with TNFi with those treated with non-biological therapy.MethodsSubjects diagnosed by a rheumatologist with RA enrolled in the British Society for Rheumatology Rheumatoid Arthritis Register (BSRBR-RA), a prospective cohort study, were followed until first lymphoma, death or until 30 November 2013. Rates of lymphoma in the TNFi and non-biological-treated cohorts were compared using Cox regression.Results11 931 TNFi-treated patients were compared with 3367 biological-naive patients. 84 lymphomas (88 (95% CI 70 to 109) per 100 000 person-years) were reported in the TNFi cohort and 30 lymphomas (154 (95% CI 104 to 220)) in the biological-naive cohort. After adjusting for differences in baseline characteristics, there was no difference in the risk of lymphoma for the TNFi versus the biological-naive group: HR 1.00 (95% CI 0.56 to 1.80). No risk differences were observed for individual TNFi.ConclusionsIn medium-term follow-up, there is no evidence that tumour necrosis factor inhibition influences the risk of lymphoma over the background risk in subjects with RA.

Rates of Serious Infections and Malignancies Among Patients with Rheumatoid Arthritis Receiving Either Tumor Necrosis Factor Inhibitor or Rituximab Therapy

2015 ◽  
Vol 42 (3) ◽  
pp. 372-378 ◽  
Author(s):  
Kalle Jyri Aaltonen ◽  
Jaana Tuulikki Joensuu ◽  
Liisa Virkki ◽  
Tuulikki Sokka ◽  
Pasi Aronen ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Inhibitor ◽  
Poisson Model ◽  
Tnf Inhibitor ◽  
Biologic Treatment ◽  
Increased Risk ◽  
Serious Infections ◽  
Necrosis Factor

Objective.Because of the role of tumor necrosis factor (TNF) in host defense, it was hypothesized that its inhibition might lead to an increased risk of malignancies and infections. The objective of our study was to assess the incidence of serious infections leading to hospitalization and malignancies among patients with rheumatoid arthritis (RA) receiving either TNF inhibitor or rituximab (RTX) therapy.Methods.The study population was identified from the National Register for Biologic Treatment in Finland and the hospital records of Central Finland Central Hospital for conventional disease-modifying antirheumatic drug (cDMARD) users. Data on infections and malignancies were acquired from national healthcare registers. A Poisson model was used to calculate the adjusted incidence rate ratios (aIRR) and was composed of age, sex, time from diagnosis, year of the beginning of the followup, rheumatoid factor status, Disease Activity Score at 28 joints, Health Assessment Questionnaire, prior malignancy, prior serious infection, prior biologic use, and time-updated use of methotrexate, sulfasalazine, hydroxychloroquine, and oral corticosteroids as confounders.Results.In total, during the followup of 10,994 patient-years, 92 malignancies and 341 serious infections were included in the analyses. The aIRR of infections compared to cDMARD users were 1.2 (95% CI 0.63–2.3), 0.84 (95% CI 0.53–1.3), 0.98 (95% CI 0.60–1.6), and 1.1 (95% CI 0.59–1.9) for the patients treated with infliximab (IFX), etanercept, adalimumab, and RTX, respectively. The crude rates of malignancies were highest among the users of cDMARD and RTX, and lowest among patients treated with IFX with no differences in aIRR.Conclusion.Our results provide some reassurance of the safety of biologic treatments in the treatment of RA.

scholarly journals Epigenetic DNA Methylation of EBI3 Modulates Human Interleukin-35 Formation via NFkB Signaling: A Promising Therapeutic Option in Ulcerative Colitis

2021 ◽  
Vol 22 (10) ◽  
pp. 5329
Author(s):  
Alexandra Wetzel ◽  
Bettina Scholtka ◽  
Fabian Schumacher ◽  
Harshadrai Rawel ◽  
Birte Geisendörfer ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Dna Methylation ◽  
Dna Methyltransferase ◽  
Therapeutic Option ◽  
Human Colon ◽  
Functional Protein ◽  
Barr Virus ◽  
Inflammatory Conditions ◽  
Increased Risk ◽  
Anti Inflammatory

Ulcerative colitis (UC), a severe chronic disease with unclear etiology that is associated with increased risk for colorectal cancer, is accompanied by dysregulation of cytokines. Epstein–Barr virus-induced gene 3 (EBI3) encodes a subunit in the unique heterodimeric IL-12 cytokine family of either pro- or anti-inflammatory function. After having recently demonstrated that upregulation of EBI3 by histone acetylation alleviates disease symptoms in a dextran sulfate sodium (DSS)-treated mouse model of chronic colitis, we now aimed to examine a possible further epigenetic regulation of EBI3 by DNA methylation under inflammatory conditions. Treatment with the DNA methyltransferase inhibitor (DNMTi) decitabine (DAC) and TNFα led to synergistic upregulation of EBI3 in human colon epithelial cells (HCEC). Use of different signaling pathway inhibitors indicated NFκB signaling was necessary and proportional to the synergistic EBI3 induction. MALDI-TOF/MS and HPLC-ESI-MS/MS analysis of DAC/TNFα-treated HCEC identified IL-12p35 as the most probable binding partner to form a functional protein. EBI3/IL-12p35 heterodimers (IL-35) induce their own gene upregulation, something that was indeed observed in HCEC cultured with media from previously DAC/TNFα-treated HCEC. These results suggest that under inflammatory and demethylating conditions the upregulation of EBI3 results in the formation of anti-inflammatory IL-35, which might be considered as a therapeutic target in colitis.

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