Plasma concentrations of complement split product C3d and immune complexes after procainamide induced production of antinuclear antibodies.
Seventeen patients treated with procainamide for cardiac ventricular arrhythmias were followed for up to 40 weeks. Immunological data as a clue to developing the systemic lupus erythematosus (SLE)-like syndrome was emphasized. Ten patients developed antinuclear antibodies (IgG or IgM), but no increase in the plasma concentration of the complement split product C3d or immune complexes, measured by two different methods, was demonstrated. This finding is in contrast to the high levels of both C3d and immune complexes in SLE. The discrepancy may be caused by a lack of immune complex mediated complement activation by the procainamide induced antibodies, or may be due to a difference in severity of disease. The acetylator phenotype of the patients was determined but due to the low frequency of fast acetylators no comparison of the immunological response of the two phenotypes could be done.
D000368:Aged; D000906:Antibodies / Q000032:analysis* / Q000235:genetics; D000974:Antibodies, Antinuclear / Q000032:analysis; D000936:Antigen-Antibody Complex / Q000032:analysis* / Q000235:genetics; D001145:Arrhythmias, Cardiac / Q000188:drug therapy / Q000276:immunology; D003176:Complement C3 / Q000032:analysis*; D015933:Complement C3d; D006801:Humans; D007074:Immunoglobulin G / Q000032:analysis; D007075:Immunoglobulin M / Q000032:analysis; D008875:Middle Aged; D010641:Phenotype; D011342:Procainamide / Q000494:pharmacology*
D000906:Antibodies; D000974:Antibodies, Antinuclear; D000936:Antigen-Antibody Complex; D003176:Complement C3; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D015933:Complement C3d; D011342:Procainamide