We report three cases from girls with Graves disease who developed serious rheumatic manifestations. One patient had systemic lupus erythematosus with articular, renal, neurological and cardiac afectation with fatal outcome. Other patient presented clinical features of scleroderma with skin thickness, myopathy, arthritis, Raynaud's phenomenon and findings of pulmonary fibrosis. A lupus-like syndrome associated to methimazole therapy (polyarthritis, rash and hemolytic anemia) with positive Cel-LE preparations but negative antinuclear-antibodies was observed in a third patient. A careful history and the recognition of these manifestations will help in the identification of these syndromes.
Download full-text PDF |
Source |
---|
Rheumatology (Oxford)
January 2025
Research Center for Genome & Medical Sciences, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Objectives: GCA is a granulomatous vasculitis affecting large vessels, leading to intimal occlusion accompanied by the accumulation of myofibroblasts. Histopathologically, GCA is characterized by destruction of the tunica media and hypertrophy of the intima with invasion of activated CD4+ T cells, macrophages and multinucleated giant cells (MNGCs). Despite these well-defined histopathological features, the molecular pathology of GCA has largely remained elusive.
View Article and Find Full Text PDFImmun Inflamm Dis
January 2025
Department of Rheumatology, Guanghua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Objective: To assess CXC chemokine receptor 5 (CXCR5) circulating DNA methylation differences in autoimmune rheumatic diseases and their relation with clinical features.
Methods: Targeted methylation sequencing was performed using peripheral blood from 164 rheumatoid arthritis (RA), 30 systemic lupus erythematosus (SLE), 30 ankylosing spondylitis (AS), 30 psoriatic arthritis (PsA), 24 Sjögren's syndrome (SS) patients, and 30 healthy controls (HC).
Results: Significant differences in CXCR5 cg19599951 methylation were found between RA and HC, as well as AS and SLE.
Int J Rheum Dis
January 2025
Third Hospital of Shanxi Medical University, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Taiyuan, China.
Objective: Since COVID-19 infections are more common in systemic lupus erythematosus (SLE) patients, most recent research has focused on the outcome of COVID-19, with fewer studies on disease activity in SLE. This research aims to evaluate flares in SLE with COVID-19 infection while investigating predictive factors.
Methods: A questionnaire survey was conducted to collect information on patients with previously diagnosed SLE from multi-center.
Front Immunol
January 2025
Rheumatology Unit, Department of Clinical Internal, Anesthesiologic and Cardiovascular Sciences, "Sapienza" University of Rome, Rome, Italy.
Introduction: Lupus nephritis (LN), caused by immune complexes produced or deposited from the bloodstream, is one of the most severe features of Systemic Lupus Erythematosus (SLE) leading to an increased morbidity and mortality. Toll like receptors (TLRs), such as TLR3, TLR7 and TLR9, may play a key role in its pathogenesis. Interleukin-32 (IL-32), a cytokine involved in both innate and adaptive immune responses, has been widely considered in autoimmune-inflammatory rheumatic diseases.
View Article and Find Full Text PDFMedicine (Baltimore)
January 2025
Department of Minimally Invasive Spinal Surgery, The Affiliated Hospital of Putian University, Putian, China.
Observational epidemiological studies indicate a higher fracture incidence in rheumatoid arthritis (RA) patients compared to the general population. However, the causal relationship between RA and fracture risk, particularly traumatic and osteoporotic fractures, is not well established. We performed Mendelian randomization (MR) analysis to evaluate the causal relationship between RA and fracture risk.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!