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Smoking (but not nicotine) is associated with increased activity of CYP1A2. After giving up smoking, clearance of certain medications which are metabolized via CYP1A2 may be reduced. This may lead to increased plasma levels of certain medications. The increase may be of clinical significance for products with narrow therapeutic windows, e.g. theophylline, tacrine, clozapine or ropinirole.
Plasma level of other medications which are in part metabolized via CYP1A2, e.g. imipramine, olanzapine, clomipramine and fluvoxamine, might also rise after stopping smoking. There are no data supporting this, however, and the possible clinical significance of this effect on these medications is unknown.
Limited data indicates that the metabolism of flecainide and pentazocine might also be capable of being induced by smoking.
No clinically relevant interactions between nicotine replacement therapy and other drugs has definitely been established. However, nicotine may possibly enhance the haemodynamic effects of adenosine i.e. increase in blood pressure and heart rate and also increased pain response (angina-pectoris type chest pain) provoked by adenosine administration.
