DRUG INTERACTIONS WITH SMOKING
Many interactions between tobacco smoke and medications have been identified. Note that it is the tobacco smoke—not the nicotine—that causes these drug interactions. Tobacco smoke may interact with medications through pharmacokinetic or pharmacodynamic mechanisms. Pharmacokinetic interactions affect the absorption, distribution, metabolism, or elimination of other drugs, potentially causing an altered pharmacologic response. The majority of pharmacokinetic interactions with smoking are the result of induction of hepatic cytochrome P450 enzymes (primarily CYP1A2). Pharmacodynamic interactions alter the expected response or actions of other drugs. The amount of tobacco smoking needed to have an effect has not been established and the assumption is that any smoker is susceptible to the same degree of interaction. The most clinically significant interactions are depicted in the shaded rows.
DRUG/CLASS MECHANISM OF INTERACTION AND EFFECTS Pharmacokinetic Interactions
Conflicting data on significance of an interaction. Possible È plasma concentrations (up to
Ç Metabolism (induction of CYP1A2); Ç clearance (56%). Likely
È Area under the curve (AUC) (36%) and serum concentrations (24%).
È Sedation and hypotension possible in smokers; smokers may need Ç dosages.
Ç Metabolism (induction of CYP1A2); È plasma concentrations (28%).
Ç Clearance (61%); È trough serum concentrations (25%). Smokers
Ç Metabolism (induction of CYP1A2); Ç clearance (24%); È AUC (31%); È plasma
Dosage modifications not routinely recommended but smokers may need Ç dosages.
Ç Clearance (44%); È serum concentrations (70%).
Ç clearance and È half-life are observed.
È insulin absorption secondary to peripheral vasoconstriction; smoking may cause
release of endogenous substances that antagonize insulin’s effects.
Interactions likely not clinically significant; smokers may need Ç dosages.
Ç Clearance (25%; via oxidation and glucuronidation); È half-life (36%).
Ç Metabolism (induction of CYP1A2); Ç clearance (98%); È serum concentrations (12%). Dosage modifications not routinely recommended but smokers may require Ç dosages.
Ç Clearance (77%; via side chain oxidation and glucuronidation)
Ç Metabolism (induction of CYP1A2); È half-life (50%); serum concentrations three-fold lower. Smokers
Ç Metabolism (induction of CYP1A2); Ç clearance (58–100%); È half-life (63%).
Levels should be monitored if smoking is initiated, discontinued, or changed. Ç Clearance with second-hand smoke exposure. Maintenance doses are considerably higher in smokers.
Possible interaction with tricyclic antidepressants in the direction of È blood levels, but the
È Sedation and drowsiness, possibly caused by nicotine stimulation of central nervous system.
Less effective antihypertensive and heart rate control effects; might be caused by nicotine-
È Analgesic effect; smoking may Ç the metabolism of propoxyphene (15–20%) and
Ç Risk of cardiovascular adverse effects (e.g., stroke, myocardial infarction, thromboembolism)
in women who smoke and use oral contraceptives.
Ç Risk with age and with heavy smoking (15 or more cigarettes per day) and is quite marked in
Adapted from Zevin S, Benowitz NL. Drug interactions with tobacco smoking. Clin Pharmacokinet 1999;36:425–438.
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