Rheumatoid Arthritis, Depression, and the Role of Celecoxib

Abstract Rheumatoid arthritis (RA) is a chronic autoimmune disease, causing joint destruction and associated physical, mental, and financial distress. Depression is not uncommonly found in patients with RA as both disorders share sociodemographic, functional, and biologic factors. There is growing evidence on the role of anti-inflammatory agents in managing depression, particularly celecoxib, which has been shown to significantly alleviate depressive symptoms as an augmenting agent. Compared with traditional nonsteroidal anti-inflammatory drugs (tNSAIDs), however, celecoxib offers modest improvement in clinical symptoms, with uncertain results for pain management, physical function, and adverse effects in patients with RA. Further research is needed to assess the effectiveness of celecoxib in the management of RA, particularly in patients suffering from comorbid depression.

Download Full-text

Anti-inflammatory drugs and tumor necrosis factor-α production from monocytes: role of transcription factor NF-κB and implication for rheumatoid arthritis therapy

European Journal of Pharmacology ◽

10.1016/j.ejphar.2004.07.101 ◽

2004 ◽

Vol 501 (1-3) ◽

pp. 199-208 ◽

Cited By ~ 28

Author(s):

Luisa Lavagno ◽

Gabriele Gunella ◽

Claudio Bardelli ◽

Simona Spina ◽

Luigia Grazia Fresu ◽

...

Keyword(s):

Rheumatoid Arthritis ◽

Transcription Factor ◽

Tumor Necrosis Factor ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Inflammatory Drugs ◽

Anti Inflammatory ◽

Factor Α ◽

Necrosis Factor

Download Full-text

Dysregulation of lncRNAs in Rheumatoid Arthritis: Biomarkers, Pathogenesis and Potential Therapeutic Targets

Frontiers in Pharmacology ◽

10.3389/fphar.2021.652751 ◽

2021 ◽

Vol 12 ◽

Author(s):

Chenggui Miao ◽

Liangliang Bai ◽

Yaru Yang ◽

Jinling Huang

Keyword(s):

Rheumatoid Arthritis ◽

Epigenetic Modification ◽

Joint Destruction ◽

Research Progress ◽

Unknown Etiology ◽

Signal Pathways ◽

Cartilage Erosion ◽

Chronic Autoimmune Disease ◽

Fibroblast Like Synoviocytes

Rheumatoid arthritis (RA) is a chronic autoimmune disease of unknown etiology, mainly manifested by persistent abnormal proliferation of fibroblast-like synoviocytes (FLSs), inflammation, synovial hyperplasia and cartilage erosion, accompanied by joint swelling and joint destruction. Abnormal expression or function of long noncoding RNAs (lncRNAs) are closely related to human diseases, including cancers, mental diseases, autoimmune diseases and others. The abnormal sequence and spatial structure of lncRNAs, the disorder expression and the abnormal interaction with the binding protein will lead to the change of gene expression in the way of epigenetic modification. Increasing evidence demonstrated that lncRNAs were involved in the activation of FLSs, which played a key role in the pathogenesis of RA. In this review, the research progress of lncRNAs in the pathogenesis of RA was systematically summarized, including the role of lncRNAs in the diagnosis of RA, the regulatory mechanism of lncRNAs in the pathogenesis of RA, and the intervention role of lncRNAs in the treatment of RA. Furthermore, the activated signal pathways, the role of DNA methylation and other mechanism have also been overview in this review.

Download Full-text

Arthritis and the role of endogenous glucocorticoids

Bone Research ◽

10.1038/s41413-020-00112-2 ◽

2020 ◽

Vol 8 (1) ◽

Cited By ~ 1

Author(s):

Eugenie Macfarlane ◽

Markus J. Seibel ◽

Hong Zhou

Keyword(s):

Rheumatoid Arthritis ◽

Joint Destruction ◽

Degenerative Joint Disease ◽

Joint Disease ◽

Current Evidence ◽

Inflammatory Microenvironment ◽

Glucocorticoid Signaling ◽

Anti Inflammatory ◽

Fibroblast Like Synoviocytes

Abstract Rheumatoid arthritis and osteoarthritis, the most common forms of arthritis, are chronic, painful, and disabling conditions. Although both diseases differ in etiology, they manifest in progressive joint destruction characterized by pathological changes in the articular cartilage, bone, and synovium. While the potent anti-inflammatory properties of therapeutic (i.e., exogenous) glucocorticoids have been heavily researched and are widely used in clinical practice, the role of endogenous glucocorticoids in arthritis susceptibility and disease progression remains poorly understood. Current evidence from mouse models suggests that local endogenous glucocorticoid signaling is upregulated by the pro-inflammatory microenvironment in rheumatoid arthritis and by aging-related mechanisms in osteoarthritis. Furthermore, these models indicate that endogenous glucocorticoid signaling in macrophages, mast cells, and chondrocytes has anti-inflammatory effects, while signaling in fibroblast-like synoviocytes, myocytes, osteoblasts, and osteocytes has pro-inflammatory actions in rheumatoid arthritis. Conversely, in osteoarthritis, endogenous glucocorticoid signaling in both osteoblasts and chondrocytes has destructive actions. Together these studies provide insights into the role of endogenous glucocorticoids in the pathogenesis of both inflammatory and degenerative joint disease.

Download Full-text

Role of antimalarials in rheumatoid arthritis – the British experience

Lupus ◽

10.1177/0961203396005001091 ◽

1996 ◽

Vol 5 (1_suppl) ◽

pp. 37-40

Author(s):

MJ Davis ◽

AD Woolf

Keyword(s):

Rheumatoid Arthritis ◽

Onset Of Action ◽

First Report ◽

Inflammatory Drugs ◽

British Experience ◽

Disease Modifying ◽

Anti Inflammatory ◽

Over 40 Years ◽

Established Treatment

Antimalarials have been used to treat rheumatoid arthritis (RA) for over 40 years, the first report of suggestive efficacy being published in 1951. Over the years they have become part of the established treatment of RA being one of a category of drugs referred to as disease modifying anti-rheumatic drugs (DMARDs). The onset of action with antimalarials is slow. Most patients use these drugs in combination with non-steroidal anti-inflammatory drugs (NSAIDs) and analgesics. This article reviews the evidence for the efficacy of antimalarials, their place in comparison to other DMARDs and comments on the current use in RA as perceived in British rheumatology.

Download Full-text