THE EFFECT OF METHYLDOPA AND PROCAINAMIDE ON SUPPRESSOR-CELL ACTIVITYIN RELATION TO RED-CELL AUTOANTIBODY PRODUCTION

Kirtland et al (1980) suggested that methyldopa caused the production of red cell (RBC) autoantibodies by causing a persistent increase in l ymphocyte cyclic AMP, which inhibited suppressor T cell function, lead ing to unregulated autoantibody production in some patients. They show ed that significantly higher lymphocyte cyclic AMP concentrations were generated by lymphocytes from healthy donors after adding methyldopa, and by lymphocytes from patients who were receiving methyldopa compar ed to lymphocytes from healthy donors without methyldopa present. They also showed that methyldopa affected suppressor cell activity. We mea sured the effect of methyldopa and procainamide on suppressor cell act ivity, using a similar approach to Kirtland et al (1980). Suppressor c ell activity was measured by measuring the amount of IgG, produced in vitro, by B cells following mitogen stimulation preceded by a 24 h inc ubation period. We found no significant increase in the amount of IgG generated by normal donor lymphocytes, when methyldopa or procainamide was present during the preincubation period. This is in contrast to t he findings of Kirtland et al (1980). We also measured the amount of I gG generated in vitro by mitogen-stimulated lymphocytes from patients (with and without positive direct antiglobulin tests) taking methyldop a and compared this to the amount of IgG generated by lymphocytes from normal donors and patients (with and without positive direct antiglob ulin tests). The results were similar for each group. This does not ag ree with the findings of Kirtland et al (1980) who found that lymphocy tes from patients taking methyldopa produced more IgG in vitro than ly mphocytes from normal donors. Our results do not support the hypothesi s that methyldopa and procainamide induce autoantibodies by affecting suppressor cell function.