Adult rheumatoid arthritis (RA) is an autoimmune disorder affecting joints and frequently characterised by initial local and later systemic inflammation. Researchers have, for many years, traced its cause to diverse genetic, environmental and especially immunological responses that work against the body's own cells and tissues. Investigation into several of these biomarkers reveals interconnections that exist between multiple factors, which ultimately lead to specific pathologies. The goal of this paper is to highlight connections present between the major biological players long identified by researchers including more recently uncovered biomarkers in the RA repertoire and some of the pathophysiologies typically affiliated with the disease. Biomarkers reviewed, and becoming more clearly defined for RA include genetic, cytokines like tumor-necrosis factor-α (TNF-α), lymphocytes, nuclear antigens, antibodies to citrullinated peptides (anti-CPs), acute-phase proteins (APPs), microRNA, S100 proteins, platelets and erythrocytes. Some of the disease manifestations that have been connected are bone erosion, diabetes, metabolic syndrome, anemia, synovitis, felty's syndrome, extra-articular manifestations (EAMs) such as atherosclerosis, rheumatoid nodules and cardiovascular (CV) events. Several RA markers associated with malignancy have been identified in literature although there is insufficient evidence of cancer in patients. Due to the complex nature of the disease, the appearance of symptoms and markers vary amongst individuals and the connections may manifest only in part. This manuscript addresses defining factors relevant to rapid identification of pathological influences these biomolecules could exert and to the management of the disease. Each of these biological players may have its place in connecting to symptomatic pathologies and help to highlight potential targets for therapy.
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http://dx.doi.org/10.2174/1381612822666151209153535 | DOI Listing |
ACR Open Rheumatol
January 2025
Jefferson Einstein Philadelphia Hospital, Philadelphia, Pennsylvania.
Objective: Evaluate prevalence of new onset autoimmune conditions (ACs) after commencement of immune checkpoint inhibitors (ICIs).
Methods: This retrospective observational study was done using TriNetX. Patients with neoplasm for which ICIs were approved were stratified into two groups based on ICI use.
Clin Rheumatol
January 2025
Department of Rheumatology and Immunology, Peking University People's Hospital, 11 Xizhimen South Street, Beijing, 100044, China.
Objective: This study aimed to analyze and compare the proportion of patients with different types of inflammatory arthritis and investigate the clinical characteristics, including symptoms and signs, medication choices, and disease activity, in the daily clinical practice of China.
Methods: Patients with inflammatory arthritis were recruited from 16 Grade-A tertiary hospitals between August 2021 and April 2022. The medical profiles, encompassing sociodemographic characteristics, clinical and laboratory date, were collected.
Clin Rheumatol
January 2025
Department of Orthopedics, Wuxi No. 2 People's Hospital, Jiangnan University Medical Center, No. 68 Zhongshan Road, Wuxi, Jiangsu, 214001, China.
Objective: The purpose of this study was to examine the association of folate levels, including red blood cell (RBC) and serum folate with mortality (cardiovascular disease (CVD)-related, all-cause, and cancer-related) in patients with arthritis.
Methods: We integrated and analyzed the data from the 1999-2018 National Health and Nutrition Examination Survey to conduct this study. Weighted Cox proportional hazard regression, restricted cubic spline (RCS) model, and subgroup analysis were used to analyze the association of RBC and serum folate levels with all-cause, cancer-related, and CVD-related mortality.
Z Rheumatol
January 2025
Medizinische Klinik 2, Schwerpunkt Rheumatologie/Klinische Immunologie, Universitätsklinikum Würzburg, Oberdürrbacher Str. 6, 97080, Würzburg, Deutschland.
Neutropenia in rheumatoid arthritis (RA) is a problem that often needs to be addressed. Side effects of basic antirheumatic treatment, infections or substrate deficiencies are common causes; however, T‑cell large granular lymphocytic (T-LGL) leukemia, a mature T‑cell neoplasm, can also lead to autoimmune cytopenia. The T‑LGL leukemia can be associated not only with RA but also with other autoimmune diseases or neoplasms.
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