Cigarette smoking-induced alterations in
drug absorption, distribution, metabolism, excretion, and effectiveness are reviewed.
Drug therapy can be affected pharmacokinetically by polyaromatic
hydrocarbons and pharmacodynamically by
nicotine.
Pentazocine and
phenylbutazone show increased metabolism in smokers and may have to be given in higher dosages. Smokers experience less
pain relief with
propoxyphene than do nonsmokers.
Codeine,
meperidine, and
morphine are unaffected pharmacokinetically, and the effect on
acetaminophen is probably not clinically important.
Carbamazepine,
phenytoin, and
phenobarbital are not influenced.
Heparin metabolism is elevated in smokers; this effect may necessitate modest increases in dosage.
Warfarin clearance is increased, but this is not associated with a change in prothrombin time.
Pindolol and
propranolol are unaffected pharmacokinetically, but direct effects of
nicotine may interfere with blood pressure control. Smoking transiently diminishes the
diuretic effect of
furosemide, inconsistently affects protein binding of
lidocaine, and has no effect on
prednisone,
prednisolone, or
dexamethasone. The metabolism of
estrogens to less active metabolites is increased. Smoking is associated with decreased subcutaneous absorption of
insulin and increased dosage requirements. Healing of GI
ulcers with
histamine H2-receptor antagonists may be compromised in smokers;
sucralfate is probably more useful.
Imipramine,
benzodiazepines,
chlorpromazine, and
glutethimide may be influenced, and
theophylline metabolism is accelerated. Cigarette smoking can affect the pharmacokinetic and pharmacodynamic properties of many drugs.