scholarly journals Confirmation of administrative claims-identified opportunistic infections and other serious potential adverse events associated with tumor necrosis factor α antagonists and disease-modifying antirheumatic drugs

2007 ◽  
Vol 57 (2) ◽  
pp. 343-346 ◽  
Author(s):  
J. R. Curtis ◽  
C. Martin ◽  
K. G. Saag ◽  
N. M. Patkar ◽  
J. Kramer ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Opportunistic Infections ◽  
Administrative Claims ◽  
Disease Modifying Antirheumatic Drugs ◽  
Antirheumatic Drugs ◽  
Disease Modifying ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Biological disease-modifying antirheumatic drugs in the main monogenic autoinflammatory diseases treatment. Experience of application in rheumatological practice

2021 ◽  
Vol 15 (4) ◽  
pp. 24-30
Author(s):  
S. O. Salugina ◽  
E. S. Fedorov ◽  
M. I. Kaleda
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Periodic Fever ◽  
Interleukin 1 ◽  
Autoinflammatory Diseases ◽  
Response To Treatment ◽  
Disease Modifying Antirheumatic Drugs ◽  
Antirheumatic Drugs ◽  
Disease Modifying ◽  
Necrosis Factor

Objective: to assess the frequency of prescription, efficacy and tolerability of biological disease-modifying antirheumatic drugs (bDMARDs) therapy in patients with major monogenic autoinflammatory diseases (mAID) according to the Federal Rheumatology Center clinical practice. Patients and methods. From 2008 to 2020 years, 158 patients with mAID were included in the study, 53 of whom were prescribed bDMARDs: 12 patients had Familial Mediterranean Fever (FMF); 26 – Cryopyrin-Associated Periodic Syndromes (CAPS), including 21 patients with MuckleWells Syndrome (MWS) and 5 – with Chronic Infantile Onset Neurologic Cutaneous Articular / Neonatal Onset Multisystem Inflammatory Disease (CINCA/NOMID), 12 patients had Tumor necrosis factor (TNF) receptor-Associated Periodic Fever Syndrome (TRAPS) and 3 – Hyper-Immunoglobulinemia D-syndrome (HIDS/MKD). Among all these patients 25 were male and 28 female, aged 1.5 to 44 years, 45 were children (under 18) and 8 adults. Interleukin 1 inhibitors (iIL1) were prescribed in accordance with the following scheme: canakinumab – subcutaneously 2–5 mg/kg or 150 mg per injection, every 4–8 weeks; anakinra – subcutaneously 1–5 mg/kg or 100 mg/day, daily. Etanercept (ETC) was injected subcutaneously 0.4–0.8 mg/kg 1–2 times a week, and adalimumab (ADA) was injected subcutaneously 20–40 mg once every 2 weeks. Tocilizumab (TCZ) was administered intravenously, 8–12 mg/kg once every 2–4 weeks. The duration of the disease at the time of treatment initiation ranged from 1 to 44 years. The duration of bDMARDs therapy in patients with mAID ranged from 1 month to 12 years.Results and discussion. From 158 patients with mAID, in 53 (33.5%) bDMARDs were administered. They were used more often in patients with CAPS (56.6%), and less often – in TRAPS (26.4%), FMF (28.3%) and HIDS/MKD (5.7%). iIL1 were the most frequently prescribed bDMARDs (90.6%): canakinumab (in 38 patients) and anakinra (in 10), they were mainly used in patients with CAPS, in 2/3 of patients with TRAPS, HIDS/MKD and colchicine-resistant FMF. During the first days of iIL1 treatment, all patients with mAID showed a statistically significant clinical improvement: normalization of general condition, emotional recovery, relief of fever, disappearance of rash, decrease in the severity of lymphadenopathy and hepatosplenomegaly, relief or significant positive dynamics of eye symptoms, subjective improvement in hearing and audiogram (with dynamic control in patients with CAPS), decrease in the level of acute phase markers (in all cases). In 7 patients with CAPS, who received anakinra, after a positive response was achieved, switching to canakinumab was performed, which maintained the full effectiveness of therapy. TCZ (in 7 patients) and inhibitors of tumor necrosis factor α (iTNFα) – ADA (in 3) and ETC (in 4), – were used less frequently. iTNFα were more often prescribed to FMF patients with a complete response to treatment. Tolerability of bDMARD therapy was satisfactory in all patients. Conclusion. Currently, iIL1 are the first line of therapy among biological agents for mAID, especially in patients with CAPS. If they are ineffective or intolerant in certain situations, alternative bDMARDs (iTNFα and IL6 inhibitors) can also be used, but this issue needs further study.

Accelerated Atherosclerosis in Rheumatoid Arthritis: Mechanisms and Treatment

2019 ◽  
Vol 25 (9) ◽  
pp. 969-986 ◽  
Author(s):  
Allison B. Reiss ◽  
Andrew Silverman ◽  
Muhammed Khalfan ◽  
Nicholas A. Vernice ◽  
Lora J. Kasselman ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Cardiovascular Disease ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Cyclooxygenase Inhibitors ◽  
Disease Modifying ◽  
Factor Α ◽  
The Impact ◽  
Necrosis Factor

Background:Rheumatoid arthritis (RA) is a chronic systemic autoimmune inflammatory disorder that increases the risk of developing cardiovascular disease. There is accumulating evidence that the RA disease state accelerates the formation of atherosclerotic plaques. Treatments for RA improve joint symptomatology and may reduce inflammation, but consideration of their effects on the cardiovascular system is generally low priority.Objective:Since cardiovascular disease is the leading cause of mortality in RA patients, the impact of RA therapies on atherosclerosis is an area in need of attention and the focus of this review.Results:The drugs used to treat RA may be analgesics, conventional disease-modifying anti-rheumatic drugs, and/or biologics, including antibodies against the cytokine tumor necrosis factor-α. Pain relievers such as nonselective non-steroidal anti-inflammatory drugs and cyclooxygenase inhibitors may adversely affect lipid metabolism and cyclooxygenase inhibitors have been associated with increased adverse cardiovascular events, such as myocardial infarction and stroke. Methotrexate, the anchor disease-modifying anti-rheumatic drug in RA treatment has multiple atheroprotective advantages and is often combined with other therapies. Biologic inhibitors of tumor necrosis factor-α may be beneficial in preventing cardiovascular disease because tumor necrosis factor-α promotes the initiation and progression of atherosclerosis. However, some studies show a worsening of the lipid profile in RA with blockade of this cytokine, leading to higher total cholesterol and triglycerides.Conclusion:Greater understanding of the pharmacologic activity of RA treatments on the atherosclerotic process may lead to improved care, addressing both damages to the joints and heart.

scholarly journals Back to Basics: Prioritizing Communication as a Key Instrument in Managing Rheumatoid Arthritis

2021 ◽  
pp. jrheum.210984
Author(s):  
Paul Studenic ◽  
Helga Radner
Keyword(s):  
Rheumatoid Arthritis ◽  
Drug Therapy ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Inhibitors ◽  
Disease Modifying Antirheumatic Drugs ◽  
Antirheumatic Drugs ◽  
Synthetic Dmards ◽  
Disease Modifying ◽  
Necrosis Factor

Patients with rheumatoid arthritis (RA) have come to experience a tremendous increase in therapeutic options with disease-modifying antirheumatic drugs (DMARDs).1 After decades of dissatisfying drug therapy results with conventional synthetic DMARDs (csDMARDs) only, the introduction of the first tumor necrosis factor inhibitors in the late 1990s has revolutionized RA treatment.2

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