2012
DOI: 10.5114/reum.2012.31407
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Tumor necrosis factor α antagonists in the treatment of the patients with rheumatoid arthritis

Abstract: Reumatoidalne zapalenie stawów (RZS) jest przewlekłą, układową zapalną chorobą tkanki łącznej o podłożu autoimmunologicznym, charakteryzującą się symetrycznym zapaleniem stawów, które prowadzi do rozległych uszkodzeń i zniekształceń aparatu ruchu. Coraz większa wiedza na temat mechanizmów prowadzących do rozwoju RZS przebiegającego z aktywacją prozapalnej odpowiedzi immunologicznej przyczyniła się do powstania nowej grupy leków biologicznych, do których należą antagoniści czynnika martwicy nowotworów α (tumor … Show more

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Cited by 5 publications
(5 citation statements)
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“…However, regarding the changes observed in our study, it can be concluded that anti-TNF therapy affects the genes associated with the TNF signal pathway by altering the expression of receptors for this cytokine. Moreover, the profile of changes in receptors expression depends on the type of anti-TNF drug and the observed TNFR1/TNFR2 ratio may result from a different structure and mechanism of action of adalimumab and etanercept [4,9,10,27]. However, given the fact that we noted a higher transcriptional activity of TNFR1 than TNFR2 in the control group, etanercept does not appear to be toxic.…”
Section: Discussionmentioning
confidence: 65%
See 1 more Smart Citation
“…However, regarding the changes observed in our study, it can be concluded that anti-TNF therapy affects the genes associated with the TNF signal pathway by altering the expression of receptors for this cytokine. Moreover, the profile of changes in receptors expression depends on the type of anti-TNF drug and the observed TNFR1/TNFR2 ratio may result from a different structure and mechanism of action of adalimumab and etanercept [4,9,10,27]. However, given the fact that we noted a higher transcriptional activity of TNFR1 than TNFR2 in the control group, etanercept does not appear to be toxic.…”
Section: Discussionmentioning
confidence: 65%
“…The increase in TNF-α expression observed in the first monitorings after the inclusion of etanercept may result from the extension of the inflammatory process to peripheral joints. TNF-α stimulates the secretion of extracellular matrix metalloproteinases (MMPs), responsible for the remodelling of extracellular matrix of the articular cartilage, from infiltrating inflammatory cells [27]. In addition, previous reports confirming an elevated concentration of TNF-α during etanercept therapy associated with its long halflife in serum should be taken into account [28].…”
Section: Discussionmentioning
confidence: 99%
“…Persisting relatively high level of cytokine expression when the drug was changed may explain the body compensation mechanism aiming at homeostasis. Or perhaps the lack of efficacy of the primary treatment was connected with an intensified TNF-α secretion that was not neutralized [17].…”
Section: Omówieniementioning
confidence: 99%
“…Utrzymujący się stosunkowo wysoki poziom ekspresji cytokiny przy zmianie leku można tłumaczyć mechanizmem kompensacyjnym organizmu i dążeniem do osiągnięcia homeostazy. Niewykluczone również, że brak skuteczności pierwotnego leczenia wiązał się z nasilającą się sekrecją TNF-α, który nie ulegał neutralizacji [17].…”
Section: Omówienieunclassified
“…The introduction of biologic drugs which neutralize TNF-α activity was a breakthrough in RA treatment. The results of clinical trials revealed a significant reduction of disease activity and inhibition of radiological progression, as well as improvement in the quality of life and physical function in RA patients treated with TNF-α inhibitors (TNFαI) [ 16 18 ]. However, the effect of anti-TNF therapy on PG/GAG metabolism in RA is still unknown.…”
Section: Introductionmentioning
confidence: 99%