The effect of antirheumatic drugs on circulating immune complexes in rheumatoid arthritis

The relationship between antirheumatic drug treatment and levels of circulating immune complexes (125I-C1q binding activity) has been investigated in a prospective two-year study of patients with rheumatoid arthritis using the erythrocyte sedimentation rate (ESR) and serum C-reactive protein concentration as indices of disease activity. Twenty-eight patients were treated with non-steroid anti-inflammatory drugs, 14 patients had 'second line' drugs and 13 patients were treated with adrenal corticosteroids. Serum 125I-C1q binding activity did not change during non-steroid anti-inflammatory drug treatment; however, immune complex levels did fall during treatment with new (ICI 55,897, sulphasalazine) and established (gold, penicillamine) second line drugs. Serum 125I-C1q binding activity reflected the response to treatment shown by serum C-reactive protein and ESR. Serum C-reactive protein concentration and ESR fell with all doses of adrenal corticosteroids. In contrast, immune complex levels did not fall when doses of adrenal corticosteroids were below 20 mg/day prednisolone. 125I-C1q binding activity fell during high dose adrenal corticosteroid therapy (greater than 40 mg/day prednisolone; 1 g methylprednisolone infusions). Serial measurements of 125I-C1q binding activity correspond to ESR and the serum C-reactive protein concentration in distinguishing between anti-inflammatory drugs, which provide symptomatic relief only, and second line drugs which may retard disease progression. The fall in circulating immune complex levels during 'high' dose corticosteroid treatment, but not during 'low' dose treatment, suggests that corticosteroids have a dose-dependent effect on the immune system in addition to their anti-inflammatory properties.