Zodorm Drug Interactions

Not recommended: Concomitant intake with alcohol: The sedative effect may be enhanced when the product is used in combination with alcohol. This affects the ability to drive or use machines.
Take into account: Combination with CNS depressants: Enhancement of the central depressive effect may occur in cases of concomitant use with antipsychotics (neuroleptics), hypnotics, anxiolytics/sedatives, antidepressant agents, narcotic analgesics, antiepileptic drugs, anaesthetics and sedative antihistamines. Therefore, concomitant use of zolpidem with these drugs may increase drowsiness and next-day psychomotor impairment, including impaired driving ability (see Precautions). Also, isolated cases of visual hallucinations were reported in patients taking zolpidem with antidepressants including bupropion, desipramine, fluoxetine, sertraline and venlafaxine.
Co-administration of fluvoxamine may increase blood levels of zolpidem; concurrent use is not recommended.
In the case of narcotic analgesics, enhancement of euphoria may also occur leading to an increase in psychological dependence.
Opioids: The concomitant use of sedative medicines such as benzodiazepines or related drugs such as zolpidem with opioids increases the risk of sedation, respiratory depression, coma and death because of additive CNS depressant effect. The dosage and duration of concomitant use should be limited (see Precautions).
CYP450 inhibitors and inducers: Co-administration of ciprofloxacin may increase blood levels of zolpidem; concurrent use is not recommended.
Compounds which inhibit certain hepatic enzymes (particularly cytochrome P450) may enhance the activity of benzodiazepines and benzodiazepine-like agents.
Zolpidem is metabolised via several hepatic cytochrome P450 enzymes, the main enzyme being CYP3A4 with the contribution of CYP1A2. The pharmacodynamic effect of zolpidem is decreased when it is administered with a CYP3A4 inducer such as rifampicin and St. John's Wort. St. John's Wort has been shown to have a pharmacokinetic interaction with zolpidem. Mean Cmax and AUC were decreased (33.7 and 30.0% lower, respectively) for zolpidem administered with St. John's Wort compared to zolpidem administered alone. Co-administration of St. John's Wort may decrease blood levels of zolpidem; concurrent use is not recommended.
However, when zolpidem was administered with itraconazole (a CYP3A4 inhibitor), its pharmacokinetics and pharmacodynamics were not significantly modified. The clinical relevance of these results is unknown. Co-administration of zolpidem with ketoconazole (200 mg twice daily), a potent CYP3A4 inhibitor, prolonged zolpidem elimination half-life, increased total AUC, and decreased apparent oral clearance when compared to zolpidem plus placebo. The total AUC for zolpidem, when co-administered with ketoconazole, increased by a factor of 1.83 when compared to zolpidem alone. A routine dosage adjustment of zolpidem is not considered necessary, but patients should be advised that use of zolpidem with ketoconazole may enhance the sedative effects.
Since CYP3A4 plays an important role in zolpidem metabolism, possible interactions with drugs that are substrates or inducers of CYP3A4 should be considered.
Other drugs: When zolpidem was administered with ranitidine, no significant pharmacokinetic interactions were observed.