scholarly journals FRI0381 TROUGH SERUM DRUG LEVELS AND DISEASE ACTIVITY IN AXIAL SPONDYLOARTHRITIS PATIENTS ON LONG-TERM TREATMENT WITH TNF-α INHIBITORS

2019 ◽  
Author(s):  
Liseth de Wolff ◽  
Suzanne Arends ◽  
Freke Wink ◽  
Elisabeth Brouwer ◽  
Anneke Spoorenberg
Keyword(s):  
Disease Activity ◽  
Axial Spondyloarthritis ◽  
Term Treatment ◽  
Drug Levels ◽  
Trough Serum ◽  
Tnf Α ◽  
Long Term Treatment

scholarly journals Sustained Low Disease Activity Measured By ASDAS Slow Radiographic Spinal Progression in Axial Spondyloarthritis Patients Treated With TNF-inhibitors. Data from REGISPONSERBIO

2021 ◽  
Author(s):  
Maria Llop ◽  
Mireia Moreno ◽  
Victoria Navarro-Compán ◽  
Xavier Juanola ◽  
Eugenio de Miguel ◽  
...  
Keyword(s):  
Ankylosing Spondylitis ◽  
Disease Activity ◽  
Radiographic Progression ◽  
Axial Spondyloarthritis ◽  
Term Treatment ◽  
Tnf Inhibitors ◽  
Low Disease Activity ◽  
Long Term Treatment

Abstract Background: To evaluate the influence of the disease activity on radiographic progression in axial spondyloarthritis (axSpA) patients treated with TNF inhibitors (TNFi).Methods: The study included 101 axSpA patients from the Spanish Register of Biological Therapy in Spondyloarthritides (REGISPONSERBIO), which had clinical data and radiographic assessment available. Patients were classified into 2 groups based on the duration of TNFi treatment at baseline: i) long-term treatment (≥4 years) and ii) no long-term treatment (< 4 years). Radiographs were scored by two readers according to the modified Stoke Ankylosing Spondylitis Spine Score (mSASSS) with known chronology. Disease activity differences between patients’ groups at each time point were assessed using a linear mixed-effect model.Results: Radiographic progression was defined as an increase in ≥2 mSASSS units. At inclusion, approximately half of the patients (45.5%) were receiving long-term treatment with TNFi (≥4 years). In this group of subjects, a significant difference in averaged Ankylosing Spondylitis disease Activity Score (ASDAS) across follow-up was found between progressors and non-progressors (2.33 vs 1.76, p=0.027, respectively). In patients not under long-term TNFi treatment (54.5%) though, no significant ASDAS differences were observed between progressors and non-progressors until the third year of follow-up. Furthermore, no significant differences were found in progression status, when disease activity was measured by Bath Ankylosing spondylitis Disease Activity Index (BASDAI) and C reactive protein (CRP).Conclusions: Patients on long-term TNFi treatment with a mean sustained low disease activity measures by ASDAS presented lower radiographic progression than those with active disease.

Glatiramer acetate antibodies, gene expression and disease activity in multiple sclerosis

2011 ◽  
Vol 18 (3) ◽  
pp. 305-313 ◽  
Author(s):  
F Sellebjerg ◽  
CJ Hedegaard ◽  
M Krakauer ◽  
D Hesse ◽  
H Lund ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Transcription Factors ◽  
Disease Activity ◽  
Glatiramer Acetate ◽  
Immunological Response ◽  
Term Treatment ◽  
Pcr Analysis ◽  
Enhanced Mri ◽  
Long Term Treatment

Background: Glatiramer acetate (GA) treatment suppresses disease activity in multiple sclerosis (MS). The immunological response to treatment may differ in patients who are stable on GA therapy and patients with breakthrough disease activity, but the results of previous studies are inconsistent. Objectives: We studied the immunological response to GA and its relationship with disease activity. Methods: Anti-GA antibodies in plasma and the expression of genes encoding cytokines and T-cell-polarizing transcription factors in blood cells were analysed by flow cytometric bead array and polymerase chain reaction (PCR) analysis in 39 untreated and 29 GA-treated relapsing–remitting MS patients. Definition of breakthrough disease was based on the occurrence of relapses, disability progression, or gadolinium (Gd)-enhanced MRI. Results: The expression of T helper type 1 (Th1) and Th17 cytokines and transcription factors was reduced during long-term treatment, but there was no relationship between the expression of cytokines and transcription factors and anti-GA antibodies. High expression of mRNA encoding GATA3 and lymphotoxin-β (LT-β) was associated with low disease activity in Gd-enhanced MRI studies. None of the variables studied were associated with clinical disease activity. GA treatment resulted in the development of IgG and IgG4 anti-GA antibodies during the first months of treatment, persisting during long-term treatment. Conclusions: The observed relationship between the expression of mRNA encoding GATA3 and LT-β expression and MRI disease activity deserves further analysis in future studies. The development of anti-GA antibodies was observed in all patients treated with GA, but this was not related with measures of cellular immunity, clinical or MRI disease activity.

scholarly journals Long-Term Treatment of Cuban Policosanol Attenuates Abnormal Oxidative Stress and Inflammatory Response via Amyloid Plaques Reduction in 5xFAD Mice

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1321
Author(s):  
Jin-Ho Kim ◽  
Dong-Kyun Lim ◽  
Yoo-Hun Suh ◽  
Keun-A Chang
Keyword(s):  
Neurodegenerative Disorder ◽  
Lipid Peroxide ◽  
Amyloid Plaques ◽  
Term Treatment ◽  
Number Of Patients ◽  
Tnf Α ◽  
Long Term Treatment ◽  
5Xfad Mice ◽  
The Brain

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder resulting in cognitive decline or dementia, the number of patients with AD is continuously increasing. Although a lot of great progress has been made in research and development of AD therapeutics, there is no fundamental cure for this disease yet. This study demonstrated the memory-improving effects of Cuban policosanol (PCO) in 5xFAD mice, which is an animal model of AD. Following 4-months of treatment with PCO in 5xFAD mice, we found that the number of amyloid plaques decreased in the brain compared to the vehicle-treated 5xFAD mice. Long-term PCO treatment in 5xFAD mice resulted in the reduction of gliosis and abnormal inflammatory cytokines level (interleukin [IL]-1β, IL-6, and tumor necrosis factor [TNF]-α) in the cortex and hippocampus. Levels of lipid peroxide (4-hydroxynonenal [4-HNE]) and superoxide dismutase (SOD1 and SOD2) levels were also recoverd in the brains of PCO-treated 5xFAD mice. Notably, PCO administration reduced memory deficits in the passive avoidance test, as well as synaptic loss (PSD-95, synaptophysin) in 5xFAD mice. Collectively, we identified the potential effects of PCO as a useful supplement to delay or prevent AD progression by inhibiting the formation of Aβ plaques in the brain.

Invasive Trichophyton Rubrum Infection Occurring with Infliximab and Long-Term Prednisone Treatment

2007 ◽  
Vol 11 (2) ◽  
pp. 84-88 ◽  
Author(s):  
Abigail L. Lowther ◽  
Ally-Khan Somani ◽  
Melissa Camouse ◽  
Frances T. Florentino ◽  
Stephen C. Somach
Keyword(s):  
Trichophyton Rubrum ◽  
Fungal Spores ◽  
Giant Cells ◽  
Invasive Disease ◽  
Term Treatment ◽  
Systemic Steroids ◽  
Tnf Α ◽  
Long Term Treatment ◽  
Factor Α

Background: A 64-year-old woman presented with erythematous plaques, tender nodules, and pustules of the dorsal right hand and both legs following long-term treatment with systemic steroids and infliximab. Skin biopsy demonstrated dermal inflammation with foci of necrosis and multinucleated giant cells containing fungal spores. Tissue culture grew Trichophyton rubrum. Objective: To report a case that demonstrates the pathophysiology of invasive T. rubrum infection, the mechanisms of action and uses of tumor necrosis factor α (TNF-α)-inhibiting drugs, and how these drugs may increase patients' risk of invasive dermatophytosis. Conclusion: Dermatophytes such as T. rubrum rarely cause invasive disease. This unusual presentation of invasive T. rubrum occurred with immunosuppression by infliximab and systemic steroids. Patients should have a thorough examination for signs of latent infection before TNF-α inhibitors are prescribed, including inspection of the skin and nails for signs of dermatophytosis.

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