Drug Interaction Report

GENERALLY AVOID: Theoretically, proton pump inhibitors may decrease the gastrointestinal absorption of enteric-coated naproxen, which requires an acidic environment for dissolution. The proposed mechanism is an increase in gastric pH (i.e. decreased gastric acidity) induced by proton pump inhibitors. In patients treated with proton pump inhibitors, the possibility of a reduced or subtherapeutic response to enteric-coated naproxen should be considered.

MANAGEMENT: Concomitant use of these drugs is generally not recommended.

ADJUST DOSING INTERVAL: Administration of enteric-coated, gastro-resistant formulations of peppermint oil (e.g., delayed or sustained release capsules) concurrently with antacids may cause premature dissolution of the enteric coating and early release of the peppermint oil, which could lead to gastrointestinal irritation and reduced therapeutic effects. The use of other medications that can reduce gastric acid, such as H2-receptor antagonists and proton pump inhibitors, may also cause similar issues.

MANAGEMENT: Acid-lowering medications should not be administered at the same time as enteric-coated, gastro-resistant formulations of peppermint oil. In general, H2-receptor antagonists and proton pump inhibitors should preferably be avoided, while antacids should be administered at least 2 hours before or 2 hours after the peppermint oil preparation. The labeling for the specific product should be consulted for administration recommendations and other guidance.

ADJUST DOSING INTERVAL: Administration of enteric-coated, gastro-resistant formulations of peppermint oil (e.g., delayed or sustained release capsules) with food may cause premature dissolution of the enteric coating and early release of the peppermint oil, which could lead to gastrointestinal irritation and reduced therapeutic effects.

MANAGEMENT: Enteric-coated, gastro-resistant formulations of peppermint oil should not be taken immediately after eating. These products should preferably be taken 30 to 90 minutes before a meal with water. The labeling for the specific product should be consulted for administration recommendations and other guidance.

GENERALLY AVOID: The concurrent use of aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) and ethanol may lead to gastrointestinal (GI) blood loss. The mechanism may be due to a combined local effect as well as inhibition of prostaglandins leading to decreased integrity of the GI lining.

MANAGEMENT: Patients should be counseled on this potential interaction and advised to refrain from alcohol consumption while taking aspirin or NSAIDs.

MONITOR: Smoking cessation may lead to elevated plasma concentrations and enhanced pharmacologic effects of drugs that are substrates of CYP450 1A2 (and possibly CYP450 1A1) and/or certain drugs with a narrow therapeutic index (e.g., flecainide, pentazocine). One proposed mechanism is related to the loss of CYP450 1A2 and 1A1 induction by polycyclic aromatic hydrocarbons in tobacco smoke; when smoking cessation agents are initiated and smoking stops, the metabolism of certain drugs may decrease leading to increased plasma concentrations. The mechanism by which smoking cessation affects narrow therapeutic index drugs that are not known substrates of CYP450 1A2 or 1A1 is unknown. The clinical significance of this interaction is unknown as clinical data are lacking.

MANAGEMENT: Until more information is available, caution is advisable if smoking cessation agents are used concomitantly with drugs that are substrates of CYP450 1A2 or 1A1 and/or those with a narrow therapeutic range. Patients receiving smoking cessation agents may require periodic dose adjustments and closer clinical and laboratory monitoring of medications that are substrates of CYP450 1A2 or 1A1.