I came across an article about drug interactions with smoking, by Dr. Geraldine Moses, a consultant drug information pharmacist from Brisbane, Australia). Here are some of the highlights: tobacco smoke interacts with medications through pharmacokinetic and pharmacodynamic mechanisms PK interactions affect the absorption, distribution, metabolism and elimination of other drugs, and with smoking, occur mainly because [...]
I came across an article about drug interactions with smoking, by Dr. Geraldine Moses, a consultant drug information pharmacist from Brisbane, Australia). Here are some of the highlights:
- tobacco smoke interacts with medications through pharmacokinetic and pharmacodynamic mechanisms
- PK interactions affect the absorption, distribution, metabolism and elimination of other drugs, and with smoking, occur mainly because of the induction of CYP1A2 enzymes
- PD interactions occur when the effects of interacting drugs overlap (can be additive, synergystic, or antagonistic)
- the polycyclic aromatic hydrocarbons (PAHs) in tobacco smoke are the culprits for inducing liver metabolism in smokers
- when a smoker quits, CYP1A2 substrate doses should be decreased so that drug toxicity can be avoided–>of utmost importance when a patient must stop smoking immediately, i.e. when they are admitted to the hospital
- Remember, nicotine doesn’t cause the CYP1A2 interactions–the PAHs do, so there’s no PK effect with nicotine replacement therapy
- plasma concentrations of clozapine (a CYP1A2 substrate) are 35% lower than in non smokers
- benzodiazepine levels are also affected by smoking–alprazolam serum concentrations can be reduced up to half in smokers compared to non-smokers, and half life is also reduced
- the interaction between oral contraceptives and smoking is pharmacodynamic in nature–the risk for thromboembolism is synergistic when the drugs are used together
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