BUPRENORPHINE Drug Interactions
Also known as: BUPRENORPHINE
BUPRENORPHINE (brand name: BUPRENORPHINE) is a Opioid Analgesics. 1 INDICATIONS AND USAGE Buprenorphine Sublingual Tablets are indicated for the treatment of opioid dependence and are preferred for induction. Buprenorphine sublingual tablets should be used as part of a complete treatment plan to include counseling and psychosocial support. Buprenorphine…BUPRENORPHINE has 17 documented drug interactions in our database, including 6 contraindicated, 11 major, 0 moderate, and 0 minor interactions.
6
Contraindicated
11
Major
0
Moderate
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Minor
Concomitant use significantly increases the risk of severe respiratory depression, profound sedation, coma, and death. Patients may experience decreased level of consciousness, bradycardia, hypotension, and hypoventilation.
Mechanism
Both buprenorphine (an opioid partial agonist) and clonazepam (a benzodiazepine) are central nervous system (CNS) depressants. Their co-administration leads to an additive depressant effect on the CNS, particularly on the brainstem respiratory centers, and can potentiate GABAergic neurotransmission, leading to profound sedation and respiratory depression.
Clinical Management
Concomitant use should generally be avoided due to the high risk of serious adverse outcomes, as highlighted by the FDA Black Box Warning. If co-prescription is absolutely necessary, the lowest effective doses should be used for the shortest possible duration, with close monitoring for respiratory depression and sedation. Consider alternative non-opioid or non-benzodiazepine treatments.
The 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.
Mechanism
Buprenorphine, a partial opioid agonist, and oxazepam, a benzodiazepine, both exert central nervous system (CNS) depressant effects. Their co-administration leads to an additive pharmacodynamic interaction, significantly enhancing GABAergic inhibition and opioid receptor activation, thereby profoundly depressing CNS and respiratory function.
Clinical Management
Concomitant use of buprenorphine and oxazepam is generally contraindicated due to the high risk of severe adverse outcomes, including death. If co-administration is absolutely necessary and no alternatives exist, it should be done with extreme caution, initiating with the lowest possible doses of both drugs, for the shortest duration, and with close monitoring for respiratory depression and sedation. Consider naloxone availability and educate patients on signs of overdose.
This combination significantly increases the risk of severe respiratory depression, profound sedation, hypotension, psychomotor impairment, coma, and death. Patients may experience decreased level of consciousness, bradycardia, and hypoxemia.
Mechanism
Buprenorphine, a partial opioid agonist, and temazepam, a benzodiazepine, both exert central nervous system (CNS) depressant effects. The co-administration leads to synergistic depression of the CNS, primarily by enhancing GABAergic neurotransmission (benzodiazepines) and inhibiting neuronal activity via opioid receptors (buprenorphine), particularly affecting brainstem respiratory centers.
Clinical Management
Concomitant use of buprenorphine and temazepam is generally contraindicated due to the high risk of severe adverse outcomes, as highlighted by an FDA Black Box Warning. If co-administration is unavoidable, such as in patients already on stable buprenorphine therapy who require a benzodiazepine for a severe, acute indication, extreme caution is warranted. Initiate the benzodiazepine at the lowest effective dose and for the shortest possible duration, with close monitoring for signs of respiratory depression and sedation. Consider non-benzodiazepine alternatives for anxiety or insomnia.
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 combination significantly increases the risk of severe respiratory depression, profound sedation, coma, and death. Patients may experience decreased respiratory rate, hypoventilation, hypoxia, hypotension, and impaired mental status. The onset of these effects can be rapid and life-threatening.
Mechanism
Both buprenorphine, an opioid partial agonist, and midazolam, 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 via opioid receptors (buprenorphine). This synergistic depression significantly impairs respiratory drive and consciousness.
Clinical Management
Concomitant use of buprenorphine and midazolam is generally contraindicated due to the high risk of severe adverse events, as highlighted by an FDA Black Box Warning. If co-administration is absolutely unavoidable, it should be reserved for patients for whom alternative treatment options are inadequate, and only under close medical supervision with immediate availability of resuscitative equipment and naloxone. Doses of both drugs should be reduced, and patients must be continuously monitored for respiratory depression and sedation.
The combination significantly increases the risk of severe respiratory depression, profound sedation, coma, and death. Patients may exhibit somnolence, decreased respiratory rate, hypoxemia, and unresponsiveness. This can rapidly progress to life-threatening respiratory arrest.
Mechanism
Both buprenorphine (an opioid partial agonist) and chlordiazepoxide (a benzodiazepine) are central nervous system (CNS) depressants. Their co-administration leads to an additive depressant effect on the CNS, particularly affecting the respiratory drive and level of consciousness. This synergistic depression is primarily mediated through their respective actions on opioid receptors and GABA-A receptors.
Clinical Management
Concurrent use of buprenorphine and chlordiazepoxide is generally contraindicated due to the high risk. If co-administration is unavoidable and strictly medically necessary, use the lowest effective doses for the shortest duration possible, and monitor patients closely for signs of respiratory depression and sedation. Consider alternative treatments that do not involve concurrent opioid and benzodiazepine use.
Patients may experience profound sedation, respiratory depression, hypotension, and psychomotor impairment. This can lead to increased risk of falls, accidental injury, coma, and potentially fatal respiratory arrest. The impairment of motor function and cognitive abilities can significantly impact daily activities and safety.
Mechanism
Buprenorphine, an opioid partial agonist, exerts its primary effects through mu-opioid receptor agonism, leading to central nervous system (CNS) depression. Cyclobenzaprine, a skeletal muscle relaxant, also causes significant CNS depression primarily through its action on the brainstem and its anticholinergic properties. The concomitant use of these agents results in an additive depressant effect on the CNS.
Clinical Management
Concomitant use should generally be avoided due to the high risk of severe CNS and respiratory depression. If co-administration is unavoidable, reduce the starting dose of one or both drugs, monitor patients closely for signs of sedation and respiratory depression, and educate them on the risks. Consider alternative non-pharmacological treatments or muscle relaxants with less sedating profiles if possible.
Patients may experience profound sedation, respiratory depression, hypotension, and psychomotor impairment, including dizziness and ataxia. In severe cases, this interaction can lead to coma, respiratory arrest, and death. Impaired motor function can also increase the risk of falls and accidents.
Mechanism
Both buprenorphine, an opioid partial agonist, and methocarbamol, a centrally acting muscle relaxant, exert depressant effects on the central nervous system (CNS). The coadministration of these agents leads to an additive pharmacological effect, significantly enhancing CNS depression. This synergistic action can compromise vital functions regulated by the CNS.
Clinical Management
Concomitant use should generally be avoided. If coadministration is deemed necessary, initiate buprenorphine at the lowest effective dose and titrate slowly, and consider reducing the methocarbamol dose. Closely monitor patients for signs of respiratory depression, sedation, and altered mental status, especially during initiation or dose escalation of either drug. Educate patients on the risks and advise against operating heavy machinery or driving.
Patients may experience profound sedation, respiratory depression, hypotension, and psychomotor impairment. This can lead to increased risk of falls, accidental injury, and potentially life-threatening respiratory arrest. The combination significantly impairs the ability to operate machinery or drive safely.
Mechanism
Buprenorphine, an opioid partial agonist, and carisoprodol, a centrally acting muscle relaxant, both exert central nervous system (CNS) depressant effects. This combination leads to an additive pharmacological effect on GABAergic and opioid receptors, enhancing CNS depression. Carisoprodol's active metabolite, meprobamate, also contributes significantly to this depressant effect.
Clinical Management
Avoid concomitant use of buprenorphine and carisoprodol due to the high risk of severe CNS and respiratory depression. If co-administration is unavoidable, initiate at the lowest effective doses, monitor patients closely for signs of sedation and respiratory depression, and consider alternative non-opioid pain management or non-benzodiazepine muscle relaxants. Educate patients on the risks and advise against driving or operating heavy machinery.
Patients may experience profound sedation, respiratory depression, hypotension, and psychomotor impairment. In severe cases, this can progress to coma and death due to respiratory arrest. The risk is heightened in patients with pre-existing respiratory compromise or those receiving higher doses of either medication.
Mechanism
Both buprenorphine, an opioid partial agonist, and baclofen, a GABA-B receptor agonist, exert depressant effects on the central nervous system (CNS). When co-administered, their individual CNS depressant effects are additive, leading to an enhanced overall CNS depression. This synergistic action can compromise vital functions regulated by the brainstem, such as respiration.
Clinical Management
Avoid concomitant use of buprenorphine and baclofen if possible. If co-administration is unavoidable, initiate treatment with the lowest effective doses and titrate slowly, monitoring closely for signs of CNS and respiratory depression. Educate patients and caregivers about the risks and symptoms of CNS depression, and consider prescribing naloxone for at-risk patients.
Patients may experience increased sedation, somnolence, dizziness, and psychomotor impairment. The most serious clinical effect is an enhanced risk of respiratory depression, which can be life-threatening. Other effects include hypotension and profound bradycardia.
Mechanism
Buprenorphine, a partial opioid agonist, exerts its analgesic and CNS depressant effects primarily through mu-opioid receptor agonism. Tizanidine, an alpha-2 adrenergic agonist, reduces spasticity by increasing presynaptic inhibition of motor neurons in the spinal cord, which also leads to CNS depression. The co-administration of these two agents results in additive CNS depression.
Clinical Management
Concomitant use should generally be avoided due to the high risk of additive CNS and respiratory depression. If co-administration is unavoidable, initiate both medications at lower doses and titrate cautiously, monitoring closely for signs of sedation and respiratory compromise. Educate patients about the risks and advise against operating heavy machinery or driving.
Patients may experience increased sedation, dizziness, confusion, and psychomotor impairment. The most serious clinical effect is an increased risk of respiratory depression, which can be life-threatening, especially in opioid-naive patients or those with underlying respiratory compromise.
Mechanism
Buprenorphine, an opioid partial agonist, and metaxalone, a central nervous system (CNS) depressant muscle relaxant, both exert their primary effects by depressing CNS activity. The co-administration of these agents leads to an additive pharmacodynamic effect, increasing the overall CNS depression.
Clinical Management
Avoid concomitant use if possible. If co-administration is necessary, initiate buprenorphine at a lower dose and titrate slowly while closely monitoring for signs of respiratory depression and excessive sedation. Educate patients about the risks and advise against driving or operating heavy machinery.
Patients may experience increased sedation, dizziness, and psychomotor impairment. The most serious clinical effect is an enhanced risk of respiratory depression, which can be life-threatening. Other effects include profound somnolence, confusion, and difficulty concentrating.
Mechanism
Buprenorphine, an opioid partial agonist, exerts its primary effects through mu-opioid receptor agonism, leading to central nervous system (CNS) depression. Chlorzoxazone, a centrally acting muscle relaxant, also causes CNS depression by acting on subcortical and spinal cord levels. The co-administration of these agents results in an additive depressant effect on the CNS.
Clinical Management
Avoid concomitant use of buprenorphine and chlorzoxazone if possible. If co-administration is unavoidable, initiate both medications at the lowest effective doses and titrate carefully, monitoring closely for signs of CNS and respiratory depression. Educate patients about the risks and advise them to avoid driving or operating heavy machinery.
Patients may experience profound sedation, respiratory depression, coma, and even death. Other symptoms include dizziness, confusion, impaired psychomotor function, and hypotension. The risk of falls and accidental injury is significantly increased.
Mechanism
Buprenorphine, an opioid partial agonist, causes central nervous system (CNS) depression through its activity at mu-opioid receptors. Orphenadrine citrate, a skeletal muscle relaxant with anticholinergic properties, also exerts CNS depressant effects. The co-administration of these agents results in an additive depressant effect on the CNS.
Clinical Management
Avoid concomitant use of buprenorphine and orphenadrine citrate if possible. If co-administration is necessary, use the lowest effective doses and monitor patients closely for signs of CNS depression, particularly respiratory depression and sedation. Advise patients against operating heavy machinery or driving and educate them on the risks.
The primary clinical effects include profound sedation, respiratory depression, coma, and potentially death. Patients may exhibit reduced respiratory rate, shallow breathing, hypoxemia, and decreased level of consciousness. Other effects can include hypotension, bradycardia, and psychomotor impairment.
Mechanism
Buprenorphine, a partial opioid agonist, and lorazepam, a benzodiazepine, both exert central nervous system (CNS) depressant effects. Their co-administration leads to an additive and synergistic depression of the CNS, primarily by enhancing gamma-aminobutyric acid (GABA) activity (benzodiazepines) and opioid receptor agonism (buprenorphine). This combined effect significantly impairs respiratory drive and consciousness.
Clinical Management
Co-prescription of buprenorphine and lorazepam should generally be avoided due to the high risk of severe adverse outcomes, as highlighted by the FDA Black Box Warning. If co-administration is deemed absolutely necessary and no alternatives exist, it must be done with extreme caution, initiating with the lowest effective doses of both medications and titrating slowly while closely monitoring for signs of respiratory depression and sedation. Patients and caregivers must be educated about the risks and symptoms of overdose.
The concurrent use of buprenorphine and diazepam significantly increases the risk of severe adverse events including profound sedation, respiratory depression, coma, and death. Patients may exhibit somnolence, decreased level of consciousness, bradycardia, hypotension, and hypoventilation. The risk is heightened in opioid-naive individuals or those with underlying respiratory compromise.
Mechanism
Buprenorphine, a partial opioid agonist, and diazepam, a benzodiazepine, both cause central nervous system (CNS) depression. This interaction is primarily pharmacodynamic, as both drugs potentiate the inhibitory effects of gamma-aminobutyric acid (GABA) at different receptor sites, leading to additive CNS and respiratory depressant effects. Buprenorphine's respiratory depressant effects are mediated via mu-opioid receptors, while diazepam enhances GABAergic transmission.
Clinical Management
Concomitant use should generally be avoided due to the significant risks. If co-prescription is absolutely necessary, the lowest effective doses of both medications should be used for the shortest possible duration, with careful monitoring for signs of respiratory depression and sedation. Patients and caregivers must be educated on the risks and symptoms, and naloxone should be considered for at-home use. Gradual dose reduction of one or both agents may be necessary if adverse effects occur.
The combination significantly increases the risk of severe respiratory depression, profound sedation, coma, and death. Patients may experience decreased respiratory rate, shallow breathing, hypoxemia, altered mental status, somnolence, and psychomotor impairment. These effects can be life-threatening and require immediate medical intervention.
Mechanism
Buprenorphine, an opioid partial agonist, and alprazolam, a benzodiazepine, both exert central nervous system (CNS) depressant effects. Buprenorphine acts primarily on mu-opioid receptors, while alprazolam enhances the inhibitory effects of gamma-aminobutyric acid (GABA) at GABA-A receptors. The concomitant use leads to synergistic CNS depression, exacerbating effects on respiratory drive and consciousness.
Clinical Management
Avoid concomitant prescribing of buprenorphine and alprazolam whenever possible. If co-prescribing is unavoidable and alternative treatments are inadequate, use the lowest effective doses and shortest possible duration. Closely monitor patients for signs of respiratory depression and sedation, and educate them and their caregivers on these risks, including the availability of naloxone.
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