We observed a patient with lepromatous leprosy and a circulating anticoagulant. Intrinsic pathway inhibition was demonstrated by prolongation of the activated partial thromboplastin time. Extrinsic pathway inhibition was demonstrated by prolongation of the prothrombin time when performed with diluted thromboplastin. A plasma co-factor was required for inhibition. Immunoadsorption with specific antisera and Sephadex G-200 fractionation suggested that the anticoagulant was an IgM immunoglobulin. The similarities between this patient's anticoagulant and those associated with other disease states are discussed.