Incidence of Tuberculosis Among Korean Patients with Ankylosing Spondylitis Who Are Taking Tumor Necrosis Factor Blockers

2011 ◽  
Vol 38 (10) ◽  
pp. 2218-2223 ◽  
Author(s):  
EUN-MI KIM ◽  
WAN-SIK UHM ◽  
SANG-CHEOL BAE ◽  
DAE-HYUN YOO ◽  
TAE-HWAN KIM
Keyword(s):  
Ankylosing Spondylitis ◽  
Tumor Necrosis Factor ◽  
General Population ◽  
Incidence Rate ◽  
Tumor Necrosis ◽  
Tnf Blockers ◽  
Korean Patients ◽  
Tnf Blocker ◽  
Significant Difference ◽  
Necrosis Factor

Objective.To assess the incidence and relative risk of new tuberculosis (TB) infections in Korean patients with ankylosing spondylitis (AS) and patients with AS who are undergoing treatment with tumor necrosis factor (TNF) blockers.Methods.New cases of TB were identified by reviewing the medical records of 919 patients with AS not treated with TNF blockers and those of 354 patients with AS treated with adalimumab (n = 66), infliximab (n = 78), or etanercept (n = 210) between 2002 and 2009. Reference data were obtained from the Korean National Tuberculosis Association.Results.The mean incidence rate of TB was 69.8 per 100,000 person-years (PY) in the general population, 308 per 100,000 PY in the TNF blocker-naive AS cohort, and 561 per 100,000 PY in the TNF blocker-exposed AS cohort. The incidence rate of TB in the infliximab-treated AS cohort (540 per 100,000 PY) was higher than that in the adalimumab-treated AS cohort (490 per 100,000 PY). No cases of TB occurred in the etanercept-treated AS cohort. Comparing the relative risks of TB infections between the TNF blocker-exposed AS cohort and the TNF blocker-naive AS cohort, no statistically significant difference was identified (risk ratio 0.53; 95% CI 0.144–1.913).Conclusion.The risk of TB was higher in the TNF blocker-naive AS cohort than it was in the general population. However, the risk of TB was not increased in the TNF blocker-exposed AS cohort compared with the TNF blocker-naive AS cohort. Among patients with AS, etanercept is associated with a lower risk of TB compared with monoclonal antibodies.

scholarly journals Tumor necrosis factor alpha and alpha-1 antitrypsin gene variants in Serbian pediatric arterial ischemic stroke patients

Genetika ◽  
2013 ◽  
Vol 45 (3) ◽  
pp. 621-628 ◽  
Author(s):  
Valentina Djordjevic ◽  
Aleksandra Divac-Rankov ◽  
Marija Stankovic ◽  
Vesna Brankovic-Sreckovic ◽  
Dragica Radojkovic
Keyword(s):  
Ischemic Stroke ◽  
Tumor Necrosis Factor ◽  
General Population ◽  
Tumor Necrosis ◽  
Protective Role ◽  
Arterial Ischemic Stroke ◽  
Significant Difference ◽  
Alpha 1 Antitrypsin ◽  
Necrosis Factor

The etiology of arterial ischemic stroke (AIS) in children is complex, and different from that in adults. Although rare, stroke in children is an important cause of mortality and morbidity. There is increasing evidence that genetic factors, including inflammation mediators, have a role in occurrence and outcome of stroke. We have chosen to assess the role of polymorphism -308G/A in the promoter of tumor necrosis factor ? (TNF?) gene and S and Z mutations in alpha 1-antitrypsin (AAT) gene in the etiology of stroke in children. TNF? polymorphism affects plasma levels of this proinflamatory cytokine, and this could contribute to stroke pathology. It has been shown that increased AAT concentration may present a risk for AIS in children. Since S and Z mutations in AAT gene reduce its levels in plasma they could have a protective role in pediatric stroke. In this study twenty six children with AIS and 100 unrelated individuals from Serbian general population were investigated by PCR/RFLP for these gene variations. No statistically significant difference was observed between patients and general population in distribution of genotypes for -308G/A TNF? polymorphism, so its contributory role in the etiology of stroke was not evident in our group of patients. None of the tested AAT gene mutations were found in patients, which is in concordance with the proposed protective role of deficient AAT variants. AIS is a multifactorial disease, with many genes having a modest role in its pathophysiology, so further analyses of their combined effect are needed to elucidate genetic risk factors in the etiology and outcome of stroke in pediatric patients.

scholarly journals Risk and characteristics of tuberculosis after anti-tumor necrosis factor therapy for inflammatory bowel disease: a hospital-based cohort study from Korea

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jae Yong Lee ◽  
Kyunghwan Oh ◽  
Hee Seung Hong ◽  
Kyuwon Kim ◽  
Seung Wook Hong ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Tumor Necrosis Factor ◽  
Incidence Rate ◽  
Bowel Disease ◽  
Clinical Characteristics ◽  
Tumor Necrosis ◽  
Medical Center ◽  
Significant Difference ◽  
Inflammatory Bowel ◽  
Necrosis Factor

Abstract Background Anti-tumor necrosis factor (TNF) treatment for inflammatory bowel disease (IBD) increases the risk of tuberculosis (TB) infection. In the present study, we analyzed the clinical characteristics and risks of TB in Korean patients with IBD who received anti-TNF treatment. Methods The study included patients with IBD who were treated using anti-TNF agents between January 2001 and June 2018 at the Asan Medical Center. Overall, 1434 patients with ulcerative colitis or Crohn’s disease were enrolled. We calculated the incidence of active TB infection after anti-TNF treatment and compared the clinical characteristics of the TB group with those of the non-TB group. Results Twenty-one patients (1.46%) developed active TB infection, and the incidence rate of active TB was 366.73 per 100,000 person-years. In total, 198 patients (14.9%) were positive for latent tuberculosis infection (LTBI), of whom only eight (4%) did not complete LTBI treatment. The age at which the anti-TNF therapy was started was significantly higher in the TB group than in the non-TB group (HR 1.041, 95% CI 1.014–1.069, p = 0.002), and as age increased, so did the incidence rate of active TB infection (linearity p < 0.001). There was no significant difference in the incidence rate of LTBI between the TB and non-TB groups (HR 0.896, 95% CI 0.262–3.066, p = 0.862). Conclusions In patients with IBD, the incidence rate of TB increased with age at anti-TNF therapy initiation. Active treatment of LTBI may lower the incidence of TB in patients with IBD who are to undergo anti-TNF therapy.

scholarly journals Low BASDAI score alone is not a good predictor of anti-tumor necrosis factor treatment efficacy in ankylosing spondylitis: a retrospective cohort study

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Bora Nam ◽  
Bon San Koo ◽  
Tae-Han Lee ◽  
Ji-Hui Shin ◽  
Jin-Ju Kim ◽  
...  
Keyword(s):  
Cohort Study ◽  
Ankylosing Spondylitis ◽  
Tumor Necrosis Factor ◽  
Disease Activity ◽  
Retrospective Cohort Study ◽  
Retrospective Cohort ◽  
Tumor Necrosis ◽  
Activity Index ◽  
Rank Test ◽  
Necrosis Factor

Abstract Background The purpose of this study was to determine the prevalence of high disease activity as measured using the Ankylosing Spondylitis Disease Activity Score (ASDAS) in ankylosing spondylitis (AS) patients who nonetheless have low Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) scores after anti-tumor necrosis factor (TNF) treatment. Its clinical impact on anti-TNF survival was also investigated. Methods We conducted a single-centre retrospective cohort study of AS patients having low BASDAI scores (< 4) and available ASDAS-C-reactive protein (CRP) data after 3 months of first-line anti-TNF treatment. Patients were grouped into high-ASDAS (≥ 2.1) and low-ASDAS (< 2.1) groups according to the ASDAS-CRP after 3 months of anti-TNF treatment. Their characteristics were compared. And survival analyses were carried out using Kaplan–Meier curves and log-rank test with the event being discontinuation of anti-TNF treatment due to lack/loss of efficacy. Results Among 116 AS patients with low BASDAI scores after 3 months of anti-TNF treatment, 38.8% were grouped into the high-ASDAS group. The high-ASDAS group tended to have greater disease activity after 9 months of treatment (BASDAI 2.9 ± 1.1 vs. 2.3 ± 1.4, p=0.007; ASDAS-CRP 1.8 ± 0.6 vs. 1.5 ± 0.7, p=0.079; proportion of high ASDAS-CRP 27.8% vs. 13.8%, p=0.094) and greater risk of discontinuing anti-TNF treatment due to lack/loss of efficacy than the low-ASDAS group (p=0.011). Conclusions A relatively high proportion of AS patients with low BASDAI scores had high ASDAS-CRP. These low-BASDAI/high-ASDAS-CRP patients also had a greater risk for discontinuation of anti-TNF treatment due to low/lack of efficacy than the low-ASDAS group. The use of the ASDAS-CRP alone or in addition to the BASDAI may improve the assessment of AS patients treated with anti-TNF agents.

Polymorphism within the tumor necrosis factor α (TNF) promoter region in patients with ankylosing spondylitis

1999 ◽  
Vol 60 (2) ◽  
pp. 140-144 ◽  
Author(s):  
Eric L Kaijzel ◽  
Brigitta M.N Brinkman ◽  
Michiel V van Krugten ◽  
Louise Smith ◽  
Tom W.J Huizinga ◽  
...  
Keyword(s):  
Ankylosing Spondylitis ◽  
Tumor Necrosis Factor ◽  
Promoter Region ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Tumor necrosis factor-α (TNFα) inhibitors in the treatment of nonradiographic axial spondyloarthritis: current evidence and place in therapy

2017 ◽  
Vol 9 (8) ◽  
pp. 197-210 ◽  
Author(s):  
Valeria Rios Rodriguez ◽  
Denis Poddubnyy
Keyword(s):  
Ankylosing Spondylitis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Axial Spondyloarthritis ◽  
Efficacy And Safety ◽  
Tnfα Inhibitors ◽  
Factor Α ◽  
Nonradiographic Axial Spondyloarthritis ◽  
Necrosis Factor

Nonradiographic axial spondyloarthritis (SpA) and radiographic SpA (also known as ankylosing spondylitis) are currently considered as two stages or forms of one disease (axial SpA). The treatment with tumor necrosis factor-α (TNFα) inhibitors has been authorized for years for ankylosing spondylitis. In recent years, most of the anti-TNFα agents have also been approved for the treatment of nonradiographic axial SpA by the European Medicines Agency (EMA) and similar authorities in many countries around the world (but not in the US), increasing the number of possible therapies for this indication. Data from several clinical trials have demonstrated the good efficacy and safety profiles from those anti-TNFα agents. Presently, a large number of patients achieve a satisfactory clinical control with the current therapies, however, there remains a percentage refractory to nonsteroidal anti-inflammatory drugs (NSAIDs) and TNFα inhibitors; therefore, several new drugs are currently under investigation. In 2015, the first representative of a new class of biologics [an interleukin (IL)-17 inhibitor] secukinumab, was approved for the treatment of ankylosing spondylitis; a clinical trial in nonradiographic axial SpA is currently underway. In this review, we discuss the recent data on efficacy and safety of TNFα-inhibitors focusing on the treatment of nonradiographic axial SpA.

scholarly journals Tumor Necrosis Factor Receptor 1 Expression Is Upregulated in Dendritic Cells in Patients with Chronic HCV Who Respond to Therapy

2010 ◽  
Vol 2010 ◽  
pp. 1-10
Author(s):  
Raul Cubillas ◽  
Katherine Kintner ◽  
Frances Phillips ◽  
Nitin J. Karandikar ◽  
Dwain L. Thiele ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Mononuclear Cells ◽  
Tumor Necrosis Factor Receptor ◽  
Mrna Levels ◽  
Specific Subset ◽  
Significant Difference ◽  
Chronic Hcv ◽  
Necrosis Factor

The present studies assessed the level of tumor necrosis factor receptor (TNFR) expression in peripheral blood mononuclear cells (PBMCs) subsets from patients with chronic HCV undergoing interferon /ribavirin-based therapy (Ifn/R). Methods. TNFR family member mRNA expression was determined using quantitative real-time PCR assays (RTPCRs) in PBMC from 39 HCV+ patients and 21 control HCV patients. Further subset analysis of HCV + patients (untreated (U), sustained virological responders (SVR), and nonresponders (NR)/relapsers (Rel)) PBMC was performed via staining with anti-CD123, anti-CD33, anti-TNFR1 or via RTPCR for TNFR1 mRNA. Results. A similar level of TNFR1 mRNA in PBMC from untreated HCV+ genotype 1 patients and controls was noted. TNFR1 and TNFR2 mRNA levels in PBMC from HCV+ patients with SVR were statistically different than levels in HCV() patients. A significant difference was noted between the peak values of TNFR1 of the CD123+ PBMC isolated from SVR and the NR/Rel. Conclusion. Upregulation of TNFR1 expression, occurring in a specific subset of CD123+ dendritic cells, appeared in HCV+ patients with SVR.

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