OBJECTIVE: 38 untreated patients suffering from rheumatoid arthritis (RA) were studied to evaluate the relationship between serum sIL-2R levels and laboratory and clinical indexes of disease activity and circulating lymphocyte subpopulations. Furthermore, we serially analyzed the correlation between the clinical response to oral gold (Auranofin) treatment and serum sIL-2R levels in 28 RA patients. METHODS: Patients received a complete rheumatological examination at entry and every 3 months during the study. A complete biochemical analysis was executed every month. Serum sIL-2R levels were evaluated before entering and at the 3rd and 6th month by ELISA: Phenotype analysis of peripheral blood mononuclear cells was performed by a two-color technique using the association of specific monoclonal antibodies. Samples were analyzed by a FACS-scan 440 cytofluorimeter with a single Argonion laser. RESULTS: Serum sIL-2R were significantly higher in RA patients than in controls and had a significant negative correlation with disease duration and a positive correlation with serum IgG and C3 levels. A significant positive correlation was found between serum sIL-2R levels and circulating CD3 + HLADR+, CD3-HLADR+ and CD20 + CD5-cells. After 6 months of auranofin therapy no differences in serum sIL-2R in comparison with basal levels were found in either responders or in non-responders. CONCLUSION: Serum sIL-2R level is not a good index of activity in RA patients and is not a useful marker of response to AU therapy.
OBJECTIVE: 38 untreated patients suffering from rheumatoid arthritis (RA) were studied to evaluate the relationship between serum sIL-2R levels and laboratory and clinical indexes of disease activity and circulating lymphocyte subpopulations. Furthermore, we serially analyzed the correlation between the clinical response to oral gold (Auranofin) treatment and serum sIL-2R levels in 28 RApatients. METHODS:Patients received a complete rheumatological examination at entry and every 3 months during the study. A complete biochemical analysis was executed every month. Serum sIL-2R levels were evaluated before entering and at the 3rd and 6th month by ELISA: Phenotype analysis of peripheral blood mononuclear cells was performed by a two-color technique using the association of specific monoclonal antibodies. Samples were analyzed by a FACS-scan 440 cytofluorimeter with a single Argonion laser. RESULTS: Serum sIL-2R were significantly higher in RApatients than in controls and had a significant negative correlation with disease duration and a positive correlation with serum IgG and C3 levels. A significant positive correlation was found between serum sIL-2R levels and circulating CD3 + HLADR+, CD3-HLADR+ and CD20 + CD5-cells. After 6 months of auranofin therapy no differences in serum sIL-2R in comparison with basal levels were found in either responders or in non-responders. CONCLUSION: Serum sIL-2R level is not a good index of activity in RApatients and is not a useful marker of response to AU therapy.