scholarly journals Biological Agents in the Treatment of Rheumatoid Arthritis

1970 ◽  
Vol 29 (1) ◽  
pp. 27-31
Author(s):  
SM Kamal ◽  
MA Bakar
Keyword(s):  
Rheumatoid Arthritis ◽  
Interleukin 1 ◽  
Cartilage Damage ◽  
Key Words Rheumatoid Arthritis ◽  
Biological Agents ◽  
Joint Disease ◽  
Onset Of Action ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Considerable Morbidity

Rheumatoid arthritis (RA) is the commonest joint disease with considerable morbidity and mortality. Conventional disease modifying antirheumatic drugs like methotrexate form the cornerstone of therapy. These drugs have several limitations in terms of slow onset of action, adverse effects and modest remission rates. Several cytokines are involved in the pathogenesis of RA. Biological agents that specifically inhibit the effects of tumour necrosis factor-alpha (TNF-a) or interleukin-1 (IL-1) represent a major advancement in the treatment of RA. By targeting mediators that are directly involved in the pathogenesis of RA, these agents slow the radiological progression of bone and cartilage damage in joints, prevent or delay the onset of disability. These are highly specific and better tolerated. The use of these biological agents needs careful monitoring for side effects, including the development of infection. Additional anti-cytokine agents for the treatment of RA are under further development. Key words: Rheumatoid arthritis; biological agents; inflammatory cytokine. DOI: 10.3329/jbsp.v29i1.7168J Bangladesh Coll Phys Surg 2011; 29:27-31

scholarly journals Painful Rheumatoid Arthritis

2011 ◽  
Vol 5;14 (5;9) ◽  
pp. E427-E458
Author(s):  
Pya Seidner
Keyword(s):  
Rheumatoid Arthritis ◽  
Severe Pain ◽  
Interleukin 1 ◽  
Certolizumab Pegol ◽  
Key Words Rheumatoid Arthritis ◽  
Biologic Agents ◽  
Interdisciplinary Teams ◽  
Necrosis Factor Alpha ◽  
Clinical Indicators ◽  
The Past

Rheumatoid arthritis is a crippling disease that is often associated with severe pain, suffering, and diminished function, thereby detracting from an optimal quality of life. Over the past decade a greater appreciation of the pathophysiology of rheumatoid arthritis has been gained. In the past “decade of pain research,” biologic agents which may modify rheumatoid arthritis have emerged as potent therapeutic antirheumatic drugs. Biologic agents include 5 tumor necrosis factor alpha inhibitors (etanercept, infliximab, adalimumab, golimumab, certolizumab pegol), interleukin-1 blockers (anakinra), monocloncal antibodies against B cells (rituximab), T cell costimulation blocker (abatacept), and interleukin-6 inhibitors (tocilizumab). Currently, utilizing therapy aimed at targeting various abnormalities of rheumatoid arthritis may be possible. It appears that the combined use of etanercept and methotrexate may improve the imbalance of Th1/Th2 and Th17/regulatory T cells (Treg) (and related cytokines) often seen in rheumatoid arthritis. Furthermore, this improvement in Tcell ratios/cytokines is also associated with improvement in clinical indicators of rheumatoid arthritis severity. Although rheumatologists are generally the specialists “called on” to manage complex patients with rheumatoid arthritis, pain specialists may be asked to join interdisciplinary teams managing patients with advanced refractory rheumatoid arthritis with severe pain since one of the most common and debilitating symptoms of rheumatoid arthritis is pain. Thus, pain specialists should have some appreciation of the current thoughts regarding rheumatoid arthritis pathophysiology and treatment. This narrative review of rheumatoid arthritis is intended to familiarize the interventional pain specialist with current concepts surrounding rheumatoid arthritis. Key words: Rheumatoid Arthritis, Pain, DMARDs, biological agengs, TNF inhibitors

Pancreatic beta-cell-selective production of tumor necrosis factor-alpha induced by interleukin-1

Diabetes ◽  
1993 ◽  
Vol 42 (7) ◽  
pp. 1026-1031 ◽  
Author(s):  
K. Yamada ◽  
N. Takane ◽  
S. Otabe ◽  
C. Inada ◽  
M. Inoue ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Beta Cell ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Pancreatic Beta Cell ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Differential effects of cytokines on thermosensitive neurons in guinea pig preoptic area slices

1991 ◽  
Vol 261 (5) ◽  
pp. R1096-R1103 ◽  
Author(s):  
M. Shibata ◽  
C. M. Blatteis
Keyword(s):  
Guinea Pig ◽  
Preoptic Area ◽  
Interleukin 1 ◽  
Interleukin 1 Beta ◽  
Necrosis Factor Alpha ◽  
Firing Rates ◽  
Artificial Cerebrospinal Fluid ◽  
Cold Sensitive ◽  
Factor Alpha ◽  
Necrosis Factor

This study was undertaken to determine whether the reported different courses of the febrile responses to the cytokines interleukin-1 beta (IL-1), interferon-alpha 2 (IFN), and tumor necrosis factor-alpha (TNF) might have neuroelectrophysiological correlates. The reactions of individual thermosensitive neurons in the preoptic area (POA) were evaluated by recording their extracellular single-unit firing rates (FR) in slices of guinea pig POA perfused with artificial cerebrospinal fluid (aCSF), human recombinant IL-1 (50-500 ng), IFN (1,000-8,000 U), and TNF (400-5,000 ng) (all doses per min/ml aCSF); thermosensitivity was assessed by FR responses to changes of perfusate temperature (32-42 degrees C). Overall, these cytokines depressed the FR of warm-sensitive units and excited those of cold-sensitive units, in agreement with expectations. However, the responses of individual neurons treated with two or all three cytokines were dissimilar: 61% of the units tested reacted differentially to two or three cytokines, 32% exhibited identical responses, and 7% had no response to any cytokine. These results support the possibility that IL-1, IFN, and TNF may affect not the same but rather distinct neurons functionally connected to common pyrogenic effectors. Thus they suggest that differential neuronal substrates may be utilized by each cytokine to exert its pyrogenic effect.

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