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The intensity of joint pain in relation to changes in serum TNFα during therapy with anti-TNFα inhibitors

INTRODUCTION: Tumor necrosis factor-alpha (TNFα) inhibitors have significantly improved the outcomes of treatment for rheumatoid arthritis (RA). In the present study, we aimed to determine whether serum levels of TNFα during therapy with TNFα inhibitors do really reflect the disease activity and cor...

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Autores principales: Sikorska, Dorota, Kawka, Edyta, Rutkowski, Rafał, Samborski, Włodzimierz, Witowski, Janusz
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer International Publishing 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6663924/
https://www.ncbi.nlm.nih.gov/pubmed/30675683
http://dx.doi.org/10.1007/s10787-019-00564-x
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author Sikorska, Dorota
Kawka, Edyta
Rutkowski, Rafał
Samborski, Włodzimierz
Witowski, Janusz
author_facet Sikorska, Dorota
Kawka, Edyta
Rutkowski, Rafał
Samborski, Włodzimierz
Witowski, Janusz
author_sort Sikorska, Dorota
collection PubMed
description INTRODUCTION: Tumor necrosis factor-alpha (TNFα) inhibitors have significantly improved the outcomes of treatment for rheumatoid arthritis (RA). In the present study, we aimed to determine whether serum levels of TNFα during therapy with TNFα inhibitors do really reflect the disease activity and correspond to the intensity of pain experienced. MATERIALS AND METHODS: Thirty RA patients were examined before and after 12 weeks of routine therapy with TNFα inhibitors. Serum levels of TNFα were measured with a high-sensitivity immunoassay and related to patients’ clinical and biochemical status. Disease activity was assessed by the modified disease activity score (DAS28). RESULTS: A median relative change in TNFα was 13%. The patients were stratified according to whether the relative change in serum TNFα after therapy was above or below this median value. The patients from both subgroups did not differ in baseline characteristics and response to therapy. However, the patients in whom serum TNFα increased after therapy above the median value had more tender joints after treatment than patients from the other group. Consequently, the number of tender joints after the treatment correlated with absolute TNFα concentrations at this time (r = 0.37; p = 0.049) and the magnitude of changes in serum TNFα correlated with a change in the number of tender joints (r = − 0.48; p = 0.008). CONCLUSIONS: Circulating TNFα levels did not decrease in RA patients treated with TNFα inhibitors, despite clinical and biochemical improvement. It is possible, that circulating TNFα is responsible for the persistence of joint pain in this group of patients.
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spelling pubmed-66639242019-08-12 The intensity of joint pain in relation to changes in serum TNFα during therapy with anti-TNFα inhibitors Sikorska, Dorota Kawka, Edyta Rutkowski, Rafał Samborski, Włodzimierz Witowski, Janusz Inflammopharmacology Original Article INTRODUCTION: Tumor necrosis factor-alpha (TNFα) inhibitors have significantly improved the outcomes of treatment for rheumatoid arthritis (RA). In the present study, we aimed to determine whether serum levels of TNFα during therapy with TNFα inhibitors do really reflect the disease activity and correspond to the intensity of pain experienced. MATERIALS AND METHODS: Thirty RA patients were examined before and after 12 weeks of routine therapy with TNFα inhibitors. Serum levels of TNFα were measured with a high-sensitivity immunoassay and related to patients’ clinical and biochemical status. Disease activity was assessed by the modified disease activity score (DAS28). RESULTS: A median relative change in TNFα was 13%. The patients were stratified according to whether the relative change in serum TNFα after therapy was above or below this median value. The patients from both subgroups did not differ in baseline characteristics and response to therapy. However, the patients in whom serum TNFα increased after therapy above the median value had more tender joints after treatment than patients from the other group. Consequently, the number of tender joints after the treatment correlated with absolute TNFα concentrations at this time (r = 0.37; p = 0.049) and the magnitude of changes in serum TNFα correlated with a change in the number of tender joints (r = − 0.48; p = 0.008). CONCLUSIONS: Circulating TNFα levels did not decrease in RA patients treated with TNFα inhibitors, despite clinical and biochemical improvement. It is possible, that circulating TNFα is responsible for the persistence of joint pain in this group of patients. Springer International Publishing 2019-01-24 2019 /pmc/articles/PMC6663924/ /pubmed/30675683 http://dx.doi.org/10.1007/s10787-019-00564-x Text en © The Author(s) 2019 OpenAccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Original Article
Sikorska, Dorota
Kawka, Edyta
Rutkowski, Rafał
Samborski, Włodzimierz
Witowski, Janusz
The intensity of joint pain in relation to changes in serum TNFα during therapy with anti-TNFα inhibitors
title The intensity of joint pain in relation to changes in serum TNFα during therapy with anti-TNFα inhibitors
title_full The intensity of joint pain in relation to changes in serum TNFα during therapy with anti-TNFα inhibitors
title_fullStr The intensity of joint pain in relation to changes in serum TNFα during therapy with anti-TNFα inhibitors
title_full_unstemmed The intensity of joint pain in relation to changes in serum TNFα during therapy with anti-TNFα inhibitors
title_short The intensity of joint pain in relation to changes in serum TNFα during therapy with anti-TNFα inhibitors
title_sort intensity of joint pain in relation to changes in serum tnfα during therapy with anti-tnfα inhibitors
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6663924/
https://www.ncbi.nlm.nih.gov/pubmed/30675683
http://dx.doi.org/10.1007/s10787-019-00564-x
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