Abstract
Circulating anticoagulants are unusual in drug-induced syndromes. The prolonged thrombin time of plasma from a patient with a procainamide-induced syndrome was evaluated. This defect apparently was due to a circulating anticoagulant that was not of fibrin or fibrinogen origin and that prolonged thrombin and reptilase clotting times of plasma. Subclinical doses of heparin sodium induced hemorrhagic manifestations in this patient. Following cessation of heparin therapy, the circulating anticoagulant persisted, but the bleeding tendency abated. All clinical and laboratory manifestations of this syndrome abated gradually following cessation of procainamide therapy.