Synovial fluid and plasma selenium, copper, zinc, and iron concentrations in patients with rheumatoid arthritis and osteoarthritis

YAZAR M., SARBAN S., Kocyigit A. , ISIKAN U.

BIOLOGICAL TRACE ELEMENT RESEARCH, vol.106, no.2, pp.123-132, 2005 (Journal Indexed in SCI) identifier identifier

  • Publication Type: Article / Article
  • Volume: 106 Issue: 2
  • Publication Date: 2005
  • Doi Number: 10.1385/bter:106:2:123
  • Page Numbers: pp.123-132
  • Keywords: rheumatoid arthritis, osteoarthritis, selenium, zinc, copper, iron, SERUM SELENIUM, BLOOD, DISEASE, VARIABLES


In recent years, a great number of studies have investigated the possible role of trace elements in the etiology and pathogenesis of rheumatoid arthritis (RA) and osteoartritis (OA). We studied synovial fluid and plasma concentrations of selenium (Se), zinc (Zn), copper (Cu), and iron (Fe) in patients with RA and OA and compared them with sex- and age-matched healthy subjects. Plasma albumin levels were measured as an index of nutritional status. Plasma Se, Cu, and Zn concentrations were determined by atomic absorption spectrophotometry and Fe concentrations were determined by the colorimetric method. Although plasma and synovial fluid Se concentration were found to be significantly lower (p < 0.05, and p < 0.05, respectively), Cu concentrations were significantly higher in patients with RA than those of healthy subjects and OA (p < 0.05 and p < 0.05, respectively). There were no significant differences in plasma and synovial fluid Zn concentrations and albumin levels among three groups (p > 0.05). On the other hand, synovial fluid Cu and Fe concentrations were significantly higher in patients with OA than those of healthy subjects (p < 0.05). There was a significantly positive correlation between synovial fluid Se-Cu values and Zn-Fe values in patients with RA. Our results showed that synovial fluid and plasma trace element concentrations, excluding Zn, change in inflammatory RA, but not in OA. These alterations in trace element concentrations in inflammatory RA might be a result of the changes of the immunoregulatory cytokines.