Background Rheumatoid arthritis (RA) is a chronic polyarticular disease manifesting as painful inflammation of the synovial tissue with progressive joints destruction. The colony-stimulating factors (CSFs) are a family of four cytokine growth factors originally identified by their ability to support the proliferation and differentiation of hemopoietic progenitor stem cells into mature monocytes/macrophages and granulocytes. The CSF family comprises the lineage-specific members, macrophage CSF (M-CSF or CSF-1) and granulocyte CSF (G-CSF), and the nonlineage-specific members, granulocyte-macrophage CSF (GM-CSF) and multi-CSF [also called interleukin (IL)-3
Objectives to determine serum and synovial levels of the granulocyte colony stimulating factor (G-CSF) in order to evaluate their utility as biomarkers of disease activity and/or severity in rheumatoid arthritis (RA) patients.
Methods Thirty patients with established RA as well as a control group of 20 apparently healthy individuals matched for age and sex to our patients were included and thoroughly examined. RA disease activity was assessed using the modified disease activity score of 28 joint count (DAS28)while, disease severity was evaluated using the clinical spread severity Index (SSI).Plain radiography was done for both knees as well as affected joints with evaluation according to Laresn scores. Serum and synovial levels of (G-CSF) were measured by the ELISA technique
Results Both serum and synovial G-CSF levels of RA patients were higher than their levels in the controls (mean±SD 1.36± 0.69pg), (0.875±0.531pg)versus (mean±SD 0.47±0.07 pg), (0.47±0.04 pg) with a significant difference between both groups (p<0.05). The serum and synovial G-CSF levels were also higher in patients with a positive rheumatoid factor (p<0.05) and those with subcutaneous nodules (p<0.01) compared to other RA patients and the difference were statistically significant. Investigating the correlations of serum and synovial G-CSF levels with different clinical and laboratory parameters of RA showed that both levels of G-CSF significantly correlated positivey with morning stiffness durations (p<0.01),VAS values (p<0.05), spread severity index scores (p<0.01), DAS scores (p<0.01), ESR values (p<0.01), inversely with HB concentrations (p<0.01) but they were not correlated with either disease durations or radiographic larsen scores
Conclusions Our results reveal that G-CSF has a potential role in driving joint inflammation and also underscore that G-CSF would likely be a therapeutic target in RA.
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Disclosure of Interest None declared