SLE: idiopathic or drug-induced?
Procainamide has become the most frequent cause of the drug-induced lupus syndrome. Like other drugs that produce this syndrome, procainamide induces disease that closely resembles idiopathic SLE but differs from it in race and sex distribution, in rare involvement of the kidneys and central nervous system, and in the absence of antibody to native DNA. Although complete remission of the signs and symptoms of the disease occurs in most patients following discontinuation of the drug, some patients continue to be symptomatic and require treatment with corticosteroids. With prolonged procainamide therapy, antinuclear antibody develops in at least 50% of patients, and the lupus syndrome develops in approximately 20%. At present, it does not appear that a cumulative or daily dose of procainamide can be exclusively implicated in the appearance of antinuclear antibody or symptoms. Acetylation status may be one of the determining factors in the development of the SLE syndrome.
D000328:Adult; D000368:Aged; D000974:Antibodies, Antinuclear / Q000032:analysis; D001323:Autoantibodies / Q000032:analysis; D002493:Central Nervous System Diseases / Q000209:etiology; D004247:DNA / Q000276:immunology; D064420:Drug-Related Side Effects and Adverse Reactions; D005260:Female; D006801:Humans; D007592:Joint Diseases / Q000209:etiology; D007674:Kidney Diseases / Q000209:etiology; D008171:Lung Diseases / Q000209:etiology; D008180:Lupus Erythematosus, Systemic / Q000139:chemically induced* / Q000150:complications; D008297:Male; D008875:Middle Aged; D010496:Pericardium; D011342:Procainamide / Q000009:adverse effects*
D000974:Antibodies, Antinuclear; D001323:Autoantibodies; D004247:DNA; D011342:Procainamide