Naloxone/pentazocine and Alcohol/Food Interactions

MONITOR: This warning does not apply to the naloxone component in non-injectable formulations of naloxone-containing combination medicines. Naloxone injection is an antagonist that will reverse the actions of opiates. This reversal can occur when the opiate drug is being used clinically and when it is being abused. Physically dependent patients may experience withdrawal symptoms. Abrupt postoperative opioid reversal has resulted in hypotension, ventricular tachycardia and fibrillation, pulmonary edema, cardiac arrest, encephalopathy, and death.

MANAGEMENT: Patients receiving naloxone injection should be monitored for changes in vital signs, nausea, vomiting, diarrhea, aches, fever, runny nose, sneezing, nervousness, irritability, shivering, abdominal cramps.

GENERALLY AVOID: Ethanol may potentiate the central nervous system (CNS) depressant effects of opioid analgesics. Concomitant use may result in additive CNS depression and impairment of judgment, thinking, and psychomotor skills. In more severe cases, hypotension, respiratory depression, profound sedation, coma, or even death may occur.

MANAGEMENT: Concomitant use of opioid analgesics with ethanol should be avoided.

MONITOR: This warning does not apply to the naloxone component in non-injectable formulations of naloxone-containing combination medicines. Naloxone injection is an antagonist that will reverse the actions of opiates. This reversal can occur when the opiate drug is being used clinically and when it is being abused. Physically dependent patients may experience withdrawal symptoms. Abrupt postoperative opioid reversal has resulted in hypotension, ventricular tachycardia and fibrillation, pulmonary edema, cardiac arrest, encephalopathy, and death.

MANAGEMENT: Patients receiving naloxone injection should be monitored for changes in vital signs, nausea, vomiting, diarrhea, aches, fever, runny nose, sneezing, nervousness, irritability, shivering, abdominal cramps.

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.

MONITOR: Smoking tobacco may decrease the plasma concentrations and effects of pentazocine by enhancing its metabolic clearance.

MANAGEMENT: The possibility of reduced therapeutic effects of pentazocine should be considered in smokers.