Procainamide, N-acetylprocainamide, antinuclear antibody and systemic lupus erythematosus.

Abstract

Long-term therapy with procainamide (PA) leads to the systemic lupus erythematosus syndrome (SLE) in about 30% of patients and 80% develop antinuclear antibodies. Acetylation of procainamide results in the formation of N-acetylprocainamide (NAPA) the propensity of which to induce SLE and to increase antinuclear antibodies is negligible while its antiarrhythmic properties remain. Slow acetylators of PA have a greater tendency to induce SLE consistent with the observation that it is the level of PA that is responsible for the observed immunologically-mediated side effects of the compound. This is also suggested by the remission of PA-induced SLE when PA is replaced with NAPA for the control of cardiac arrhythmias. Thus, NAPA, compared to the parent compound, has little tendency to induce SLE.