There are many side effects following the induction of<unk> . These adverse effects are ventricular dysrhythmia, bradycardia, hypotension and shock. The adverse effects occur even more often if the daily doses are increased.<unk>  may also lead to drug fever and other allergic responses. There is also a chance that drug-induced lupus erythematosus occurs, which at the same time leads to arthralgia, myalgia and pleurisy. Most of these side effects may occur due to the acetylation of<unk> . Toxicity There is a close line between the plasma concentrations of the therapeutic and toxic effect, therefore a high risk for toxicity. Many symptoms resemble systemic lupus erythematosus because<unk>  reactivates hydroxylamine and nitroso metabolites, which bind to histone proteins and are toxic to lymphocytes. The hydroxylamine and nitroso metabolites are also toxic to bone marrow cells and can cause agranulocytosis. These metabolites are formed due to the activation of polymorphonuclear leukocytes. These leukocytes release myeloperoxidase and hydrogen peroxide, which oxidize the primary aromatic amine of<unk>  to form<unk>  hydroxylamine. The release of hydrogen peroxide is also called a respiratory burst, which occurs for<unk>  in monocytes but not in lymphocytes. Furthermore, the metabolites can be formed by activated neutrophils. These metabolites could then bind to their cell membranes and cause a release of autoantibodies which would react with the neutrophils.<unk>  hydroxylamine has more cytotoxicity by hindering the response of lymphocytes to T-cell and B-cell mitogens. Hydroxylamine can also generate methemoglobin, a protein that could hinder further oxygen exchange. It was also detected that the antiarrhythmic drug<unk>  interferes with<unk> cemakers. A toxic level of<unk>  leads to decrease in ventricular conduction velocity and increase of the ventricular refractory period. This results in a disturbance in the artificial membrane potential and leads to a supraventricular tachycardia which induces failure of the<unk> cemaker and death. Thus, it prolongs QT interval of action potential and increases the risk of torsade de pointes.<unk>  could initiate leukopenia and/or agranulocytosis, which are serious hematologic disorders, and is also known for causing gastrointestinal disturbances and aggravating pre-existing abnormalities in impulse initiation and propagation.
Procainamide
Tocainide
Flecainide
Acecainide
Setiptiline
Veratridine
Maprotiline
Verapamil