(2) The percentage and MFI of peripheral CD4(+) IL-17(+) cells in RA patients were significantly higher comparing to normal controls (1.64 ± 0.97% vs. 0.75 ± 0.20%, p < 0.01; and 29.8 ± 9.7 vs. 19.8 ± 4.6, p < 0.05, respectively), and positively correlated with ESR and DAS28.
While the gene encoding this enzyme has been implicated in the pathophysiology of rheumatoid arthritis (RA), little is known about its mechanism of catalysis, its in vivo role, or its role in the pathophysiology of RA; however, recent reports suggest that this enzyme can act as a transcriptional corepressor for the estrogen receptor.
The bone marrow (BM) mononuclear cells showed 2581 up-regulated and 649 down-regulated genes in RA patients relative to the OA group: Our analysis indicated that several differentially expressed genes might play crucial roles in RA development, including SP1, RARA, ETS1, ETS2, FOS and ESR1.
In multivariable logistic regression models, BMI ≤ 22 kg/m (odds ratio = 3.43, P = .043) and DAS28-ESR > 3.2 (odds ratio = 3.85, P = .032) were independent risk factors for osteoporosis at either site in male patients with RA.Our data demonstrate that male patients with RA had a 2.1 times higher risk for osteoporosis compared with healthy individuals.
Here we report that enhanced expression of ERα mRNA and protein in SLE and rheumatoid arthritis is associated with DNA demethylation within the proximal promoter region located between -232 and +81 base pair relative to transcription start site of human ERα gene (GenBank Accession no.AL356311.6).
PsA patients had significantly lower disease activity according to DAS28-ESR (p=0.006) but not according to DAS28-CRP (p=0.319), and lower serum levels of proinflammatory and angiogenic cytokines than RA patients in remission.
The results of the present study suggest that ESR1 gene polymorphisms in females with RA may be associated with the response to treatment with leflunomide.
In early (disease duration less than one year) RA patients (52F/29M; mean [SE] age 63 +/- 2 years) and in 39 controls (23F/16M; mean age 63 +/- 2 years) blood samples were taken between 8:00 and 10:00 a.m. GR expression (GR number), cortisol levels (fluorescence polarization immunoassay, FPIA), ESR, CRP, and the presence of swollen and painful knees were determined.
RA activity markers including rheumatoid factor, anti-cyclic citrullinated protein antibodies, C reactive protein, ESR in addition to disease activity score 28 (DAS28) of RA patients were also evaluated to explore their association with Toxoplasma seropositivity.
These results suggest that a genetic variation at the ER locus may be associated with other pathogenetic factors in patients with rheumatoid arthritis, but not with BMD and disease aggressiveness.
Twenty patients with highly active rheumatoid arthritis (mean DAS28-ESR 5.25±1.0) and thirteen healthy volunteers underwent clinical examination, FOI and contrast-enhanced 3T-MRI.
In the current investigation, the effects of the P2Y12 blocker ticagrelor, the sodium/glucose transporter-2-inhibitor empagliflozin, and the selective estrogen receptor modulator tamoxifen were examined against rheumatoid arthritis (RA)/diabetes mellitus (DM)-co-morbidity-induced defects in vascular reactivity.
The utility of pathway selective estrogen receptor ligands that inhibit nuclear factor-kappa B transcriptional activity in models of rheumatoid arthritis.
An increased IL-1 beta 2 carriage is associated with active rheumatoid disease as indicated by a higher CRP (P < 0.001), ESR (P < 0.001) and pain score (P = 0.001) and a higher BMD at the lumbar spine (P = 0.007), lower vit-D3 and.
Synthesis and activity of substituted 4-(indazol-3-yl)phenols as pathway-selective estrogen receptor ligands useful in the treatment of rheumatoid arthritis.
In RA patients, there was no statistically significant relationship between joint temperature and clinical assessment of disease activity including Health Assessment Questionnaire (coefficient estimate - 0.54, p = 0.056), swollen joints (coefficient estimate - 0.09, p = 0.238), or serologic markers of inflammation such as CRP (coefficient estimate - 0.006, p = 0.602) and ESR (coefficient estimate - 0.01, p = 0.503).