TRIAZOLAM Drug Interactions
Also known as: Triazolam
Triazolam is a benzodiazepine medication prescribed for the short-term treatment of insomnia in adults. It works by enhancing the activity of a natural calming chemical in your brain, which helps you fall asleep. This medication is typically used for brief periods, usually 7 to 10 days.TRIAZOLAM has 10 documented drug interactions in our database, including 8 contraindicated, 2 major, 0 moderate, and 0 minor interactions.
8
Contraindicated
2
Major
0
Moderate
0
Minor
Patients may experience severe respiratory depression, profound sedation, hypotension, psychomotor impairment, coma, and death. Even at therapeutic doses, the combination can lead to life-threatening respiratory insufficiency and altered mental status. The risk is heightened in opioid-naive individuals or those with underlying respiratory conditions.
Mechanism
Both buprenorphine, an opioid partial agonist, and triazolam, a benzodiazepine, are central nervous system (CNS) depressants. Their co-administration leads to an additive depressant effect on the CNS, primarily by enhancing gamma-aminobutyric acid (GABA) activity and opioid receptor agonism, respectively. This synergistic depression significantly increases the risk of respiratory depression and profound sedation.
Clinical Management
Concomitant use of buprenorphine and triazolam is generally contraindicated due to the high risk of serious adverse outcomes, including death. If co-prescription is absolutely unavoidable, it should be done with extreme caution, initiating the lowest effective doses of both drugs and titrating slowly. Patients must be closely monitored for respiratory depression and sedation, and educated on the risks, with naloxone readily available.
The interaction can manifest as severe sedation, profound respiratory depression, coma, and death. Patients may experience decreased level of consciousness, bradycardia, hypotension, and hypoxia. These effects can be rapid in onset and life-threatening.
Mechanism
Oxycodone, an opioid agonist, and triazolam, a benzodiazepine, both exert central nervous system (CNS) depressant effects. Their co-administration leads to an additive or synergistic depression of the CNS, particularly affecting the medullary respiratory center, which can result in profound respiratory depression and hypoventilation.
Clinical Management
Concomitant use of opioids and benzodiazepines should be avoided due to the high risk of severe adverse outcomes, including respiratory depression and death. If no alternatives are available, prescribe the lowest effective doses and shortest possible duration, closely monitor patients for respiratory depression and sedation, and educate patients and caregivers on the risks. Consider naloxone availability.
Patients may experience severe respiratory depression, potentially leading to respiratory arrest, hypoxia, and death. Other clinical effects include profound sedation, somnolence, coma, hypotension, psychomotor impairment, and increased risk of accidental overdose or injury.
Mechanism
Tramadol, an opioid analgesic, and triazolam, a benzodiazepine, both depress the central nervous system (CNS). Opioids primarily act on mu-opioid receptors, while benzodiazepines enhance the effects of gamma-aminobutyric acid (GABA) at GABA-A receptors. The synergistic CNS depressant effects of these two drug classes lead to profound respiratory depression, sedation, and hypotension.
Clinical Management
Concomitant use of tramadol and triazolam is generally contraindicated due to the high risk of serious adverse outcomes, including respiratory depression and death. If no alternative treatments are available and co-prescription is absolutely necessary, use the lowest effective doses for the shortest possible duration, monitor patients closely for respiratory depression and sedation, and provide naloxone for opioid overdose reversal. Educate patients and caregivers on the risks and symptoms of respiratory depression.
The combination significantly increases the risk of profound sedation, respiratory depression, coma, and death. Patients may experience decreased level of consciousness, hypoventilation, bradycardia, and hypotension. This interaction can be life-threatening due to the synergistic depressant effects on the respiratory drive.
Mechanism
Codeine sulfate is an opioid analgesic that acts as an agonist at mu-opioid receptors in the central nervous system (CNS), leading to CNS depression, including respiratory depression and sedation. Triazolam is a benzodiazepine that enhances the effect of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) at GABA-A receptors, also resulting in CNS depression. The concomitant use of these two drug classes produces additive CNS depressant effects.
Clinical Management
Concomitant use of codeine sulfate and triazolam is contraindicated due to the severe risks. If no suitable alternatives exist, and the benefits outweigh the risks, the lowest effective doses should be used for the shortest duration possible, with close monitoring for respiratory depression and sedation. Patients and caregivers must be educated on the signs and symptoms of respiratory depression and sedation.
This interaction significantly increases the risk of severe respiratory depression, profound sedation, coma, and death. Patients may experience decreased level of consciousness, hypoventilation, and hypotension.
Mechanism
Methadone, an opioid agonist, and triazolam, a benzodiazepine, both cause central nervous system (CNS) depression. When co-administered, their individual depressant effects on the CNS are synergistic, leading to profound suppression of brain activity, particularly in respiratory centers.
Clinical Management
Co-administration of methadone and triazolam is contraindicated. If co-administration is unavoidable, extreme caution is warranted, with reduced dosages of both agents and close monitoring for respiratory depression and sedation. Naloxone should be readily available.
The combination significantly increases the risk of severe adverse events including profound sedation, respiratory depression, coma, and death. Patients may experience extreme drowsiness, confusion, dizziness, slowed or stopped breathing, and unresponsiveness.
Mechanism
Both hydromorphone (an opioid agonist) and triazolam (a benzodiazepine) are central nervous system (CNS) depressants. Their co-administration leads to additive pharmacodynamic effects, primarily by enhancing GABAergic neurotransmission (benzodiazepine) and agonizing mu-opioid receptors (opioid), resulting in profound CNS and respiratory depression.
Clinical Management
Concomitant use is contraindicated. If co-administration is unavoidable, the lowest effective doses should be used for the shortest possible duration, with close monitoring for respiratory depression and sedation. Naloxone should be readily available for opioid overdose reversal, and flumazenil for benzodiazepine reversal, though the latter is generally not recommended for benzodiazepine overdose due to seizure risk.
Patients may experience severe sedation, profound respiratory depression, coma, and death. Other effects can include hypotension, psychomotor impairment, and increased risk of accidental overdose.
Mechanism
Both oxymorphone, an opioid agonist, and triazolam, a benzodiazepine, are central nervous system (CNS) depressants. Their concomitant use leads to additive pharmacodynamic effects, primarily by enhancing GABAergic neurotransmission (benzodiazepine) and activating mu-opioid receptors (oxymorphone), resulting in profound CNS and respiratory depression.
Clinical Management
Concomitant use of oxymorphone and triazolam is generally contraindicated. If co-prescription is absolutely unavoidable, use the lowest effective doses and shortest possible duration, and closely monitor patients for signs of respiratory depression and sedation. Consider alternative non-opioid or non-benzodiazepine treatments when possible.
This combination significantly increases the risk of severe respiratory depression, profound sedation, coma, and death. Patients may experience decreased level of consciousness, hypoventilation, hypotension, and psychomotor impairment. Even with careful dose titration, the risk remains high.
Mechanism
Tapentadol, an opioid agonist, causes central nervous system (CNS) depression through mu-opioid receptor activation. Triazolam, a benzodiazepine, enhances the inhibitory effects of gamma-aminobutyric acid (GABA) at GABA-A receptors, also leading to CNS depression. The co-administration results in additive and synergistic CNS depressant effects.
Clinical Management
Concomitant use of opioids and benzodiazepines, including Tapentadol and Triazolam, is generally contraindicated due to the high risk of serious adverse outcomes. If no alternative treatment options are adequate, and the benefits outweigh the risks, prescribe the lowest effective doses for the shortest duration possible. Closely monitor patients for signs of respiratory depression and sedation, and educate them and their caregivers on these risks.
The concurrent use significantly increases the risk of severe respiratory depression, profound sedation, hypotension, psychomotor impairment, coma, and death. Patients may experience decreased respiratory rate and depth, somnolence, confusion, and unresponsiveness.
Mechanism
Both fentanyl, an opioid agonist, and triazolam, a benzodiazepine, are central nervous system (CNS) depressants. Their co-administration leads to an additive depressant effect on the CNS, primarily by enhancing GABAergic neurotransmission (benzodiazepines) and inhibiting neuronal activity (opioids), particularly in brainstem respiratory centers.
Clinical Management
Avoid concomitant use whenever possible. If co-prescription is unavoidable, use the lowest effective doses and shortest possible duration. Closely monitor patients for signs of respiratory depression and sedation, especially during initiation or dose escalation of either drug. Educate patients and caregivers on the risks and symptoms to watch for.
Concomitant use can lead to profound sedation, respiratory depression (decreased respiratory rate and depth), coma, and death. Patients may exhibit somnolence, dizziness, mental confusion, and psychomotor impairment. The combination significantly impairs cognitive and motor function.
Mechanism
Morphine, an opioid agonist, primarily acts on mu-opioid receptors to produce central nervous system (CNS) depression, including respiratory depression and sedation. Triazolam, a benzodiazepine, enhances the effect of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) at the GABA-A receptor, leading to further CNS depression. The synergistic CNS depressant effects of both drugs significantly increase the risk of severe adverse outcomes.
Clinical Management
Avoid concomitant use of morphine and triazolam whenever possible due to the high risk of severe adverse effects, including respiratory depression and death. If concurrent use is unavoidable, prescribe the lowest effective doses for the shortest possible duration, closely monitor patients for signs of respiratory depression and sedation, and educate patients and caregivers on the risks. Consider alternative therapies if clinically appropriate.
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