Biological Treatment for Rheumatic Diseases

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Biopharmaceuticals".

Deadline for manuscript submissions: closed (25 May 2025) | Viewed by 2312

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Guest Editor
Department of Clinical Chemistry and Laboratory Diagnostics, Faculty of Pharmaceutical Sciences in Sosnowiec, Medical University of Silesia, Katowice, Poland
Interests: connective tissue diseases; pathology of the extracellular matrix; growth factors; systemic sclerosis; juvenile idiopathic arthritis
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Special Issue Information

Dear Colleagues,

The implementation of biological drugs into the treatment of rheumatic diseases has opened new possibilities in the management of diseases such as rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and juvenile idiopathic arthritis. The development of "targeted" therapies that are more effective at inhibiting bone and joint destruction has significantly improved the life quality of patients. Some of these therapies lead to both the inhibition of locally ongoing lesions in the vicinity of the joints and the inhibition of generalized disease processes. However, not all patients respond positively to biological therapy. Moreover, the long-term use of biological drugs may be associated with a decrease in their efficacy as well as the occurrence of side effects related to the potential immunogenicity of these medicines. This is because biological drugs can induce an immune response and the synthesis of anti-drug antibodies (ADA, anti-drug antibodies). Therefore, it is important to understand the detailed mechanisms through which metabolic changes occur when using biological drugs. In this Special Issue, our goal is to bring together the results of expert research in this field, allowing us to better understand the effects of biological drugs on metabolic processes occurring in the body and provide an opportunity for medicines to be used more effectively in treating rheumatic diseases.

Dr. Kornelia Kuźnik-Trocha
Guest Editor

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Keywords

  • biological drugs
  • new treatment strategies
  • antirheumatic agents
  • arthritis
  • rheumatic diseases

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Published Papers (2 papers)

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Research

14 pages, 848 KB  
Article
The Impact of 24-Month Etanercept Therapy on Changes in Adiponectin, Leptin and Tenascin C Levels in the Blood of Children with Juvenile Idiopathic Arthritis
by Jan Siwiec, Kornelia Kuźnik-Trocha, Katarzyna Winsz-Szczotka, Katarzyna Komosińska-Vassev, Andrzej Siwiec and Krystyna Olczyk
Pharmaceuticals 2025, 18(9), 1423; https://doi.org/10.3390/ph18091423 - 22 Sep 2025
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Abstract
Background/Objectives: The most commonly diagnosed group of rheumatic diseases in children is juvenile idiopathic arthritis. It is characterized by a chronic inflammatory process that leads to the degradation of the bone and joint system and increased secretion of pro-inflammatory cytokines such as [...] Read more.
Background/Objectives: The most commonly diagnosed group of rheumatic diseases in children is juvenile idiopathic arthritis. It is characterized by a chronic inflammatory process that leads to the degradation of the bone and joint system and increased secretion of pro-inflammatory cytokines such as TNF-α, IL-1, and IL-6. These cytokines contribute to the dysregulation of adipocytokine metabolism, including adiponectin and leptin, as well as extracellular matrix components, such as tenascin C. While it is known that children with JIA exhibit TNF-α-stimulated degradation of most ECM cartilage components, the effect of TNF-α antagonists, such as etanercept, on these processes has not yet been evaluated. Therefore, the aim of our study was to assess the dynamics of changes in tenascin C, adiponectin, and leptin levels in the blood of children with JIA, both before and during therapy. Methods: The study material consisted of blood samples collected from 66 children of both sexes, including 40 girls and 26 boys diagnosed with juvenile idiopathic arthritis and treated with etanercept, as well as from 40 healthy children (22 girls and 18 boys). The quantitative assessment of adiponectin, leptin, and tenascin C levels was performed using commercial ELISA tests. Results: The conducted study revealed that untreated children with JIA exhibit altered plasma levels of all examined parameters—adiponectin, leptin, and tenascin C. Specifically, there was an increase in adiponectin concentration and a decrease in leptin as well as TNC levels compared to healthy children. The results demonstrated the beneficial effects of the TNF-α antagonist, i.e., etanercept, which not only improved the clinical condition of children with JIA but also positively influenced the metabolism of both adipokines and tenascin C. Conclusions: The obtained results suggest the potential use of adiponectin, leptin, and tenascin C as biochemical markers of the effectiveness of etanercept therapy in inhibiting the progression of degenerative joint changes in children with JIA treated with TNF-α inhibitors. Full article
(This article belongs to the Special Issue Biological Treatment for Rheumatic Diseases)
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14 pages, 3818 KB  
Article
Plasma Sclerostin Levels in Rheumatoid Arthritis Women on TNF-α Inhibitor Therapy
by Anna Szeremeta, Agnieszka Jura-Półtorak, Aleksandra Zoń-Giebel, Krystyna Olczyk and Katarzyna Komosińska-Vassev
Pharmaceuticals 2024, 17(6), 666; https://doi.org/10.3390/ph17060666 - 22 May 2024
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Abstract
Rheumatoid arthritis (RA) is associated with significant systemic and local bone loss. The aim of this study was to assess whether or not 15-month tumor necrosis factor α inhibitor (TNFαI) therapy in combination with methotrexate (MTX) affects circulating levels of sclerostin (SOST) in [...] Read more.
Rheumatoid arthritis (RA) is associated with significant systemic and local bone loss. The aim of this study was to assess whether or not 15-month tumor necrosis factor α inhibitor (TNFαI) therapy in combination with methotrexate (MTX) affects circulating levels of sclerostin (SOST) in female RA patients. Plasma levels of SOST were measured using immunoassays kits. Baseline SOST levels showed no significant differences between RA patients and control participants. Postmenopausal women with RA tended to have higher sclerostin levels than premenopausal woman with RA. After 15 months of treatment with TNFαI, plasma levels of SOST were decreased. Before starting biological therapy, circulating levels of SOST significantly correlated with the patient’s age (p < 0.05) and the marker of inflammation, such as ESR (p < 0.05). Multivariate regression analysis showed that age was the only significant predictor for baseline SOST levels in women with RA (β = 0.008, p = 0.028, R2 model = 0.293). Moreover, a positive correlation between SOST levels and the 28 joint disease activity score value based on the erythrocyte sedimentation rate (DAS28-ESR) was found at baseline (p < 0.05), as well as after 15 months of biological therapy (p < 0.05). Thus, plasma SOST levels may be helpful for monitoring the efficacy of TNFαI treatment in RA patients. According to our results, TNFαI, in combination with MTX, has a beneficial effect on bone turnover with a significant reduction in bone metabolism marker SOST. Full article
(This article belongs to the Special Issue Biological Treatment for Rheumatic Diseases)
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