Effects of long‐term procainamide therapy on immunoglobulin synthesis

Procainamide is a potent inducer of autoantibodies. In order to evaluate the immunologic effects of this drug in vivo, 23 cardiac disease patients who had received procainamide for at least 6 months and an equal number of matched cardiac disease control subjects were studied, and percentage of circulating T cell subsets, concanavalin A‐induced suppressor cell activity, and pokeweed mitogen‐stimulated generation of immunoglobulin‐secreting cells was quantitated. There was no significant difference between patient and control groups in the percentage of T cell subsets defined by OKT4 and OKT8 monoclonal antibodies or in concanavalin A‐induced suppressor cell activity. The numbers of pokeweed mitogen‐induced immunoglobulinsecreting cells were markedly decreased in the patient group, as measured by the protein A‐augmented reverse hemolytic plaque assay (3,000 ± 644, mean ± SEM in patients versus 10,826 ± 1,529, mean ± SEM in control subjects, P < 0.005). Removal of the adherent cell fraction did not improve the hyporesponsiveness. When B and T cell fractions of 6 patients were mixed with normal T and B cell fractions, all of the patients demonstrated diminished B cell responses, and one‐half also had diminished T cell responses. Addition of patient adherent cells to a co‐culture of normal B cells with deficient patient T cells restored plaque formation to normal levels, suggesting that the T cell defect was correctable by a macrophage‐derived factor. The data obtained suggest that procainamide exerts an immunosuppressive action on both B and T cell function in patients receiving this drug.