Abstract

In-vitro studies of superoxide (O-2) anion production by blood monocytes after stimulation with either serum treated zymosan (STZ), IgG treated zymosan (IgGTZ), or fluoride ion (F-) were performed on cells from normal controls (n = 22) and patients with classical or definite rheumatoid arthritis (RA) (n = 35). Twenty-two of the patients were on nonsteroidal anti-inflammatory drugs (NSAID) alone and 13 were on either sodium aurothiomalate, penicillamine, corticosteroids, or a combination. Monocytes from RA patients on 'second-line therapy' showed significantly increased rates of O-2 release in response to STZ compared with normal controls, but no increase was seen in monocytes from patients on NSAID alone. With IgGTZ as the stimulus, rates of O-2 release were increased in monocytes from patients on NSAID alone compared with normal controls (p less than 0.02), but were increased to a greater extent in monocytes from patients on second-line therapy (p less than 0.01). There were no differences in basal unstimulated O-2 production and no differences after stimulation with F-. The enhanced release of O-2 by monocytes from patients on second-line therapy could not be attributed to increased disease activity and may be an effect of therapy.