Rheumatoid arthritis (RA) is characterized by low serum Zn and high serum Cu. In multiple linear regression both were explained by disease activity parameters. It is suggested that interleukin-1 causes both changes by 1) increasing the metallothionein-mediated hepatic uptake to serum Zn and 2) upregulating ceruloplasmin (acute phase reactant) gene and synthesis in liver and subsequently the level of ceruloplasmin-Cu complexes in the blood. Cu absorption was diminished by zinc intake. Cu- and Zn-dependent erythrocyte SOD was increased in RA. In contrast to plasma GSHPx serum selenium was low in RA and this was associated with disease activity parameters.