procainamideinduced

Procainamide-induced refers to adverse effects associated with the antiarrhythmic drug procainamide, most notably a drug-induced lupus erythematosus (DILE) syndrome. It can also be linked to hematologic toxicity, hepatotoxicity, and rhythm disturbances such as QT prolongation.

The risk of procainamide-induced DILE is higher in slow acetylators, due to genetic variation in N-acetyltransferase 2. Metabolism produces the active metabolite N-acetylprocainamide (NAPA), which can contribute to immune sensitization and autoantibody formation. Immunologically, DILE is characterized by anti-histone antibodies and typical lupus-like symptoms, while anti-dsDNA antibodies are usually absent. The syndrome resembles systemic lupus erythematosus clinically but lacks some organ involvement seen in idiopathic lupus. Symptoms often appear after months of therapy and improve after drug withdrawal.

Clinical features of procainamide-induced DILE include arthralgia or arthritis, fever, pleuritis or pericarditis, and a malar or other nonerosive rash. Musculoskeletal and serologic findings are common, and ANA is frequently positive with anti-histone antibodies. Resolution typically occurs within weeks to months after stopping the drug, though longer courses may be needed in some cases.

Other adverse effects of procainamide can include agranulocytosis or neutropenia, hepatotoxicity, and QT interval prolongation with potential for torsades de pointes, especially in patients with electrolyte disturbances or concomitant QT-prolonging drugs.

Diagnosis relies on clinical history (procainamide exposure) plus serologic testing and symptom pattern; management centers on discontinuation of the drug and supportive therapy, with consideration of alternative antiarrhythmic treatment if needed.