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It is well known that some patients develop a syndrome resembling systemic lupus erythematosus in response to therapy with hydrazines or aromatic amines—notably with procainamide for arrhythmias, hydralazine for hypertension, and isoniazid for tuberculosis. New work suggests that minor molecular modifications of the offending agents might make it possible to use them without causing the lupus-like disease.
Most patients in whom drug-induced lupus develops are genetically slow acetylators, that is, in the course of metabolizing the drug in question, their livers add an acetyl group to the molecule at a relatively leisurely pace. With this finding in mind, Marcus A. Reidenberg, MD, professor of pharmacology and medicine and head, division of clinical pharmacology, Cornell University Medical College, and associates gave the acetylated version of procainamide—acecainide hydrochloride, also called N-acetylprocainamide—to 11 patients with ventricular arrhythmias and histories of procainamide lupus. In seven of these patients acecainide caused no recurrence of lupus;
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