The rate of formation of tissue fluid for a given increase of venous pressure and for a known volume of tissue has been measured in the forearm. There is a significant increase in this figure in rheumatoid arthritis and a still greater increase in patients who develop recurrent oedema. This increase could not be attributed to steroid or phenylbutazone therapy, nor to a fall in the serum albumin. The results imply that there is some generalized abnormality in capillary function in rheumatoid disease and that this change is not limited to the joints.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1795866 | PMC |
| http://dx.doi.org/10.1136/bmj.2.5761.555 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Letter to the Editor Regarding: "Incidence of Malignancies and the Association with Biological Disease-Modifying Antirheumatic Drugs in Japanese Patients with Rheumatoid Arthritis: A Time-Dependent Analysis from the IORRA Patient Registry".
Rheumatol Ther
January 2025
Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China.
Molecular mechanism of osteoclast differentiation of PBMC in patients with rheumatoid arthritis.
Clin Rheumatol
January 2025
Guizhou University of Traditional Chinese Medicine, Guiyang, Guizhou Province, China.
Objective: Rheumatoid arthritis (RA) is an autoimmune condition that causes severe joint deformities and impaired functionality, affecting the well-being and daily life of individuals. Consequently, there is a pressing demand for identifying viable therapeutic targets for treating RA. This study aimed to explore the molecular mechanisms of osteoclast differentiation in PBMC from patients with RA through transcriptome sequencing and bioinformatics analysis.
View Article and Find Full Text PDFInterleukin 1 receptor associated kinase 1 gene polymorphism association with risk of rheumatological diseases in Egyptian population.
Mol Biol Rep
January 2025
Pediatric Rheumatology Department, Faculty of Medicine, Cairo University, Cairo, Egypt.
Background: Interleukin-1 receptor-associated kinase1 (IRAK1) plays a considerable role in the inflammatory signaling pathway. The current study aimed to identify any association between (rs1059703) single nucleotide polymorphism (SNP) and vulnerability to rheumatological diseases in the pediatric and adult Egyptian population.
Patients And Methods: The current study included four patient groups: adult Systemic lupus erythematosus (SLE), Rheumatoid arthritis (RA), juvenile systemic lupus erythematosus (JSLE), and juvenile idiopathic arthritis (JIA).
Ritlecitinib, a JAK3 /TEC inhibitor, modulates the markers of celiac autoimmunity in alopecia areata and vitiligo patients.
Arch Dermatol Res
January 2025
Division of Gastroenterology and Hepatology, 200 1st Street SW, Rochester, MN, 55905, USA.
Background: Celiac disease (CeD) has shown an association with autoimmune disorders including vitiligo and alopecia areata (AA). Ritlecitinib, a JAK3 and TEC kinase family inhibitor, has been approved for treatment of patients with AA and is in late-stage development for vitiligo. Ritlecitinib inhibits cytotoxic T cells, NK cells, and B cells which play a role in the pathogenesis of CeD.
View Article and Find Full Text PDFThe global prevalence of interstitial lung disease in patients with rheumatoid arthritis: a systematic review and meta-analysis.
Rheumatol Int
January 2025
School of Medicine, The University of Western Australia, 35 Stirling Highway, Perth, WA, 6009, Australia.
This study aims to review the literature and estimate the global pooled prevalence of interstitial lung disease among patients with rheumatoid arthritis (RA-ILD). The influence of risk factors like geography, socioeconomic status, smoking and DMARD use will be explored. A systematic review was performed according to the PRISMA and JBI guidelines.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!