Editing Procainamide (section)

===Metabolism===
Procainamide is metabolized via different pathways. The most common one is the [[acetylation]] of procainamide to the less-toxic [[N-acetylprocainamide]].<ref>{{cite journal | vauthors = Roden DM, Reele SB, Higgins SB, Wilkinson GR, Smith RF, Oates JA, Woosley RL | title = Antiarrhythmic efficacy, pharmacokinetics and safety of N-acetylprocainamide in human subjects: comparison with procainamide | journal = The American Journal of Cardiology | volume = 46 | issue = 3 | pages = 463–468 | date = September 1980 | pmid = 6158263 | doi = 10.1016/0002-9149(80)90016-8 }}</ref> The rate of acetylation is genetically determined. There are two phenotypes that result from the acetylation process, namely the slow and rapid acetylator. Procainamide can also be oxidized by the [[cytochrome P-450]] to a reactive oxide metabolite. But it seems that acetylation of the nitrogen group of procainamide decrease the amount of the chemical that would be available for the oxidative route.<ref name="Uetrecht, J. P. 1981">{{cite journal | vauthors = Uetrecht JP, Freeman RW, Woosley RL | title = The implications of procainamide metabolism to its induction of lupus | journal = Arthritis and Rheumatism | volume = 24 | issue = 8 | pages = 994–1003 | date = August 1981 | pmid = 6169352 | doi = 10.1002/art.1780240803 }}</ref> Other metabolites of procainamide include desethyl-N-acetylprocainamide, desethylprocainamide, p-aminobenzoic acid, which are excreted via the urine.  N-acetyl-4-aminobenzoic acid as well as N-acetyl-3-hydroxyprocainamide, N-acetylprocainamide-N-oxide and N-acetyl-4-aminohippuric acid are also metabolites of procainamide.<ref name="Uetrecht, J. P. 1981"/>