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Purpose: To investigate a two‐compartment kinetic model applied to the dynamic time course of contrast enhancement as a method to differentiate between finger‐joint synovitis in established osteoarthritis (OA) and rheumatoid arthritis (RA).Material and Methods: Dynamic contrast‐enhanced magnetic resonance imaging (DCE‐MRI) of one hand in 19 patients and six healthy volunteers was undertaken. Eight patients had OA of the hand and eleven patients had RA. From the signal intensity curves, the three parameters Kps (endothelial transfer constant), Kep (elimination rate constant from extracellular space back to plasma) and Kel (elimination rate constant from plasma by renal excretion) were calculated.Results: The rate constant Kps showed the best separation between the groups with significantly higher values in the RA group compared to the OA group (P<0.005) and in the OA group compared to the control group (P<0.005). Significantly higher values of Kep were also found in the RA group compared with the OA group (P<0.005).Conclusion: DCE‐MRI may provide useful information that can help differentiate synovitis in OA from synovitis in RA. [ABSTRACT FROM AUTHOR]

We investigated the effects of acute starvation on mitogen-induced T-cell activation and Th1/Th2 cytokine responses in rheumatoid arthritis (RA) patients. Ten RA patients with active disease underwent a 7-day fast followed by a 2-week refeeding period. Immunological, hormonal, laboratory and clinical evaluations were carried out on days 0, 7 and 21. Using flow cytometry, mitogen-stimulated T-cell activation was assessed in fresh heparinised blood via analysis of CD69 expression. Production of Th1 (interferon-γ) and Th2 (interleukin-4, IL-4) cytokines was also assessed by ELISA. The 7-day fast significantly decreased the erythrocyte sedimentation rate, C-reactive protein level, joint count, morning stiffness, body weight, CD4+ and CD8+ counts and CD69+ expression on mitogen stimulated CD4+ lymphocytes. A significant increase in mitogen-induced IL-4 production after fasting was found. The fast markedly reduced serum leptin and insulin-like growth factor-1 concentrations. No significant differences occurred in serum cortisol or prolactin before and after fasting. Decreases in CD4+ lymphocyte activation during fasting correlated with decreases in body weight. Our results suggest that the clinical and laboratory improvements in fasting RA patients may be attributed to decreased CD4+ T-cell activation and an increase in the number and/or function of IL-4-producing Th2 cells. Factors associated with loss of body weight during acute starvation appear to have an inhibitory effect on CD4+ lymphocyte activation. [ABSTRACT FROM AUTHOR]

Using the anti-TcRγ/δ-l monoclonal antibody and flow cytometry, we examined the number of TcRγ/δ cells in paired samples of peripheral blood and synovial fluid or tissue from 24 children with juvenile rheumatoid arthrítís (JRA), five adult patients with JRA, and 14 patients with rheumatoid arthritis (RA). No significant difference was found in the synovial compartment Tγδ values compared with the blood in JRA, adult JRA, or RA patients. Nor was any significant difference found in the peripheral blood or synovial compartment Tγδ values in any of the three patient groups compared with the peripheral blood of normal controls. However, seven of the children with JRA had very high Tγδ values in the synovial compartment while none of the normal children had high T γδ values in the blood (P = 0.02, Fisher's exact lest). This may indicate a possible separate JRA patient group with high Tγδ levels in the synovial compartment. In six JRA patients further analysed for Tγδ subpopulation, a significant predominance of Vδ1+ cells was found in the synovial compartment compared with the corresponding peripheral blood samples (P <0-05, Mann-Wilcoxon's signed test) and with peripheral blood of child controls (P< 0-05, Mann Whitney U test). In these six patients, the Tγδ cell expression of the very early activation antigen CD69 were significantly higher (P <0.05, Wilcoxon's signed test) in the synovial compartment compared with the peripheral blood. Synovial Tγδ cells expressing HLA-DR and interleukin 2 receptors could also be detected, in contrast to the peripheral blood in which no Tγδ cells expressing these antigens could be found. These data suggest that the synovial Tγδ cells had been activated in vivo. [ABSTRACT FROM AUTHOR]

The stage of activation of synovial inflammatory T cells was studied in rheumatoid arthritis and compared with that of normal T cells stimulated in vitro by dendritic cells. Increased numbers of rheumatoid inflammatory T cells expressed activation antigens such as HLA-DR, interleukin 2 receptors (Tac), and transferrin receptors. These T cells also had high spontaneous proliferation. Peripheral blood T cells stimulated by autologous dendritic cells showed a similar expression of activation antigens and had high proliferation. Resting T cells and T cells cocultured with monocytes expressed much less activation markers. Exogenous interleukin 2 significantly increased the proliferation of the various T cells. All responses were inhibited by an antibody which blocks the interleukin 2 receptor, Supernatants from mitogen-stimulated rheumatoid inflammatory mononuclear cells and mitogen-stimulated T cells preactivated by dendritic cells usually contained less interleukin 2 than supernatants from mitogen-stimulated normal T cells. Furthermore, the various in vivo and in vitro-activated Tac-positive T cells, in contrast to nonactivated Tac-negative T cells from peripheral blood of patients and controls, significantly absorbed interleukin 2, The results indicate a turnover of interleukin 2 in rheumatoid inflammatory T cells comparable to that of T cells activated by dendritic cells, [ABSTRACT FROM AUTHOR]

Monoclonal antibodies with specificities for various human T-cell antigens were used in direct immunofluorescence to quantify the proportions of T lymphocytes with suppressor/cytotoxic-cell markers and with helper/inducer-cell markers and of T lymphocytes with HLA-D R antigens. Normal percentages of lymphocytes with suppressor/cytotoxic-cell markers were detected in the peripheral blood synovial fluid and synovial tissue lymphocytes from patients with juvenile rheumatoid arthritis (JRA) and rheumatoid arthritis (RA), respectively. Normal percentages of T lymphocytes with helper/inducer-cell markers were seen in the peripheral blood of RA and JRA patients and in the synovial tissues of RA patients. Slightly decreased percentages of cells with the helper/inducer-cell marker were detected in the synovial fluids of JRA patients. The proportions of HLA-DR-positive T lymphocytes were highly increased in the synovial fluid and synovial tissue, whereas the numbers of these cells in the peripheral blood were normal. No significant differences in Tγ cells were detected between peripheral blood, synovial fluid and synovial tissue of JRA patients or between peripheral blood and synovial tissue of RA patients. [ABSTRACT FROM AUTHOR]

: The aim of the study was to investigate the effects a 72-h fast upon serum total and free cortisol concentrations in RA patients not previously treated with glucocorticoids. Total serum cortisol and transcortin concentrations were measured in four RA patients with active disease at 4-h intervals during two 24-h periods (1200 h–1200 h), the first while eating a normal diet (fed state) and the second during the last 24 h of a 72-h water fast. Free cortisol concentrations were calculated from the total cortisol and transcortin values. The 3-day fast increased overall 24-h free and total cortisol concentrations by 50% and 35%, respectively. This was due largely to a marked increase in nocturnal serum cortisol concentrations during fasting, particularly at 0400 h, when mean total and free cortisol levels were increased by 170% and 260% compared to the fed state. Between 2000 and 0800 h overall total- and free cortisol concentrations were increased by 72% and 99%, respectively. These results suggest that an increase in nocturnal concentrations of cortisol occurs in response to fasting in RA patients not previously treated with glucocorticoids. These increases may mediate the beneficial clinical response previously found in studies of longer fasting periods in RA patients. [ABSTRACT FROM AUTHOR]