Objective – to investigate clinical and diagnostic significance of IL-31 and IL-33 determination in patients with rheumatoid arthritis (RA).Material and methods. 154 patients with a reliable diagnosis of RA were examined. Serum levels of IL-31 and IL-33 were studied using multiplex xMAP technology on Bio-PlexTM 200 System analyzer (BIO-RAD, USA). The upper limit of the norm in the study of 20 healthy donor sera was (M+3σ): IL-31 – 15.08 pg/ml, IL-33 – 3.40 pg/ml.Results. IL-31 (Me (25th; 75th percentile) – 13.75 (5.63; 308.52) and 6.10 (2.87; 8.62) pg/ml (p<0.001), IL-33 – 18.86 (7.45; 65.95) and 0.52 (0.17; 0.78) pg/ml (p><0.001) levels were observed in RA patients in comparison with the control group. An increase in IL-33 concentration (more than 3.40 pg/ml) was observed in 87.0% of patients, and IL-31 (more than 15.08 pg/ml) in 48.1% of patients with RA. An increase in IL-33 alone was observed in 42.2% (65 of 154 patients) with RA, while an isolated increase in IL-31 concentration was observed in only 2 (1.3%) patients. Simultaneous hyperproduction of IL-33 and IL-31 occurred in 69 (44.9%) patients. We revealed positive correlation of clinical and laboratory parameters of RA with cytokine concentration: SDAI correlated with IL-33 (r=0.36; p><0.05); CRP – with IL-31 (r=0.49; p><0,05) and IL-33 (r=0.40; p><0.05). Conclusion. Concentrations of IL-31 and IL-33 are elevated in RA patients and correlate with the indices of inflammatory activity of the disease.>< 0.001), IL-33 – 18.86 (7.45; 65.95) and 0.52 (0.17; 0.78) pg/ml (p<0.001) levels were observed in RA patients in comparison with the control group. An increase in IL-33 concentration (more than 3.40 pg/ml) was observed in 87.0% of patients, and IL-31 (more than 15.08 pg/ml) in 48.1% of patients with RA. An increase in IL-33 alone was observed in 42.2% (65 of 154 patients) with RA, while an isolated increase in IL-31 concentration was observed in only 2 (1.3%) patients. Simultaneous hyperproduction of IL-33 and IL-31 occurred in 69 (44.9%) patients. We revealed positive correlation of clinical and laboratory parameters of RA with cytokine concentration: SDAI correlated with IL-33 (r=0.36; p><0.05); CRP – with IL-31 (r=0.49; p><0,05) and IL-33 (r=0.40; p><0.05). Conclusion. Concentrations of IL-31 and IL-33 are elevated in RA patients and correlate with the indices of inflammatory activity of the disease.>< 0.001) levels were observed in RA patients in comparison with the control group. An increase in IL-33 concentration (more than 3.40 pg/ml) was observed in 87.0% of patients, and IL-31 (more than 15.08 pg/ml) in 48.1% of patients with RA. An increase in IL-33 alone was observed in 42.2% (65 of 154 patients) with RA, while an isolated increase in IL-31 concentration was observed in only 2 (1.3%) patients. Simultaneous hyperproduction of IL-33 and IL-31 occurred in 69 (44.9%) patients. We revealed positive correlation of clinical and laboratory parameters of RA with cytokine concentration: SDAI correlated with IL-33 (r=0.36; p<0.05); CRP – with IL-31 (r=0.49; p><0,05) and IL-33 (r=0.40; p><0.05). Conclusion. Concentrations of IL-31 and IL-33 are elevated in RA patients and correlate with the indices of inflammatory activity of the disease.>< 0.05); CRP – with IL-31 (r=0.49; p< ,05) and IL-33 (r=0.40; p<0.05)Conclusion. Concentrations of IL-31 and IL-33 are elevated in RA patients and correlate with the indices of inflammatory activity of the disease.
Conclusion Discussion: The case suggests that hypertension and renal failure should be recognised as a complication of APS, the aetiology being primary intrarenal vascular disease with nephroangiosclerosis. It illustrates also how primary APS presenting with renal manifestation can result in a fatal form of CAPS.
Objective - to study the dynamics of clinical and laboratory parameters of inflammatory activity of the disease and cytokines in rheumatoid arthritis (RA) patients on a background of tofacitinib (TOFA) treatment.Material and methods. Ten patients with a reliable diagnosis of RA have been examined: patients' age was 51.0 (48.0; 62.0) years, duration of disease was 7.0 (3.0; 20.0) years. All patients had high disease activity: DAS28 -5.88 (5.53; 5.94), CDAI - 33.0 (29.0; 36.0), SDAI - 33.72 (30.75; 36.85). All patients were treated with TOFA at a dose of 5 mg 2 times a day on a background of methotrexate therapy, non-steroidal anti-inflammatory drugs, and glucocorticoids. Observations were performed before treatment and after 3 and 6 months of therapy. Serum levels of 15 cytokines (IL-1β, IL-4, IL-6, TNF-α, INF-γ, IL-10, IL-17A, IL-17F, IL-21, IL-22, IL-23, IL-25, IL-31, IL-33, sCD40L) were examined using multiplex xMAP technology.After 3 and 6 months of TOFA therapy, there was a significant decrease in DAS28 of 4.55 (3.47; 5.16) and 3.92 (3.80; 4.60); CDAI - 16.5 (11.0; 23.0) and 18.0 (15.0; 19.0); SDAI - 16.6 (11.23; 23.06) and 18.07 (15.06; 19.10); ESR - 19.0 (11.0; 26.0) and 7.0 (4.0; 18.0); CRP - 0.56 (0.50; 1.99) and 0.71 (0.51; 1.1) respectively. IL-6 levels decreased after 3 and 6 months of therapy (p<0.05). The concentration of INF-γ significantly decreased after 3 months (p<0.05), but remained unchanged thereafter. Concentrations of IL-25 and IL-31 decreased after 3 months (p<0.05), and by the 6th month of treatment there was an increase, however, not reaching the initial values.Conclusion. The results of the study show the efficacy of TOFA in RA and create prerequisites for further study of the cytokine-dependent mechanisms of inflammation in this disease.
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