The aim of this study was to assess the association between the TNFR1 rs2234649 polymorphism and ankylosing spondylitis susceptibility in a Russian Caucasian population. A total of 41 ankylosing spondylitis patients and 43 healthy controls, matched according to age and sex, were enrolled, and polymerase chain reaction-restriction fragment length polymorphism analysis was used to genotype the rs2234649 variant. We evaluated genotype distributions in the patient and control groups with the chi-square test, and assessed the relationship between genotypes and ankylosing spondylitis using the odds ratio. Our analysis showed that the rs2234649 polymorphism does not increase ankylosing spondylitis risk. In conclusion, the TNFR1 gene polymorphism tested does not appear to be useful for assessing predisposition to this disease or for its diagnosis or prognosis.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.4238/gmr16019581 | DOI Listing |
Curr Rheumatol Rep
January 2025
Rheumatologisches Versorgungszentrum Steglitz, Ruhr Universität Bochum, Schloßstr.110, 12163, Berlin, Germany.
Purpose Of Review: Axial spondyloarthritis (axSpA) is a rather prevalent chronic inflammatory rheumatic disease that affects already relatively young patients. It has been known better since the end of the nineteenth century but quite a lot has been learned since the early 60ies when the first classification (diagnostic) criteria for ankylosing spondylitis (AS) were agreed on. I have been part of many developments in the last 30 years, and I'm happy to have been able to contribute to the scientific progress in terms of diagnosis, imaging, pathophysiology and therapy.
View Article and Find Full Text PDFReumatismo
January 2025
Unit of Dermatology, Department of Medicine and Aging Science, G. d'Annunzio University, Chieti.
Objective: Psoriatic arthritis (PsA) can be treated with biological drugs targeting IL-17A, such as secukinumab, with good responses and long-term positive outcomes in clinical studies.
Methods: An observational study was conducted on adult subjects with PsA and comorbidities, treated with secukinumab after prior therapy with conventional disease-modifying anti-rheumatic drugs or biological agents that were discontinued due to lack of efficacy or adverse drug reactions. Patients were followed up with clinical visits at 3, 6, 9, and 12 months and evaluated for disease activity, pain, and quality of life, with respect to values recorded at baseline.
We examine disease-specific and cross-disease functions of the human gut microbiome by colonizing germ-free mice, at risk for inflammatory arthritis, colitis, or neuroinflammation, with over 100 human fecal microbiomes from subjects with rheumatoid arthritis, ankylosing spondylitis, multiple sclerosis, ulcerative colitis, Crohn's disease, or colorectal cancer. We find common inflammatory phenotypes driven by microbiomes from individuals with intestinal inflammation or inflammatory arthritis, as well as distinct functions specific to microbiomes from multiple sclerosis patients. Inflammatory disease in mice colonized with human microbiomes correlated with systemic inflammation, measured by C-reactive protein, in the human donors.
View Article and Find Full Text PDFJ Inflamm Res
January 2025
Department of Rheumatism and Immunity, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, People's Republic of China.
Background: Ankylosing spondylitis (AS) is a chronic autoimmune disease characterized by inflammation of the sacroiliac joints and spine. Cuproptosis is a newly recognized copper-induced cell death mechanism. Our study explored the novel role of cuproptosis-related genes (CRGs) in AS, focusing on immune cell infiltration and molecular clustering.
View Article and Find Full Text PDFJ Transl Autoimmun
June 2025
Rheumatology Research Center, Tehran University of Medical Science, Tehran, Iran.
Iron is a crucial element for living organism in terms of oxygen transport, hematopoiesis, enzymatic activity, mitochondrial respiratory chain function and also immune system function. The human being has evolved a mechanism to regulate body iron. In some rheumatic diseases such as rheumatoid arthritis (RA), systemic lupus erythematous (SLE), systemic sclerosis (SSc), ankylosing spondylitis (AS), and gout, this balanced iron regulation is impaired.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!