Can you take Buprenorphine with Clobazam?

cloBAZam has a major potential interaction with Acute Alcohol Intoxication.

The use of benzodiazepines with alcohol is not recommended. Patients with acute alcohol intoxication exhibit depressed vital signs. The central nervous system depressant effects of benzodiazepines may be additive with those of alcohol, and severe respiratory depression and death may occur. Therapy with benzodiazepines should be administered cautiously in patients who might be prone to acute alcohol intake.

Buprenorphine has a moderate potential interaction with Adrenal Insufficiency.

Buprenorphine should be used with caution in patients with adrenal insufficiency (e.g., Addison's disease). Cases of adrenal insufficiency have been reported with opioid use, more often with use beyond 1 month. If adrenal insufficiency has occurred with a particular opioid, other opioids may be tried as some cases reported use of a different opioid without recurrence of adrenal insufficiency. Available information does not identify which opioids are more likely to be associated with adrenal insufficiency.

Buprenorphine has a major potential interaction with Alcoholism.

Buprenorphine exposes users to the risks of addiction, abuse, and misuse. Each patient's risk should be assessed before prescribing buprenorphine analgesics, and all patients should be monitored regularly for development of such behaviors and conditions. Risks are increased in patients with personal or family history of substance abuse (including drug or alcohol abuse or addiction) or mental illness (e.g., major depression); the potential for such risks should not prevent proper pain management in any given patient. Patients at increased risk may be prescribed buprenorphine analgesics but use in such patients requires intensive counseling about the risks and proper use of buprenorphine, as well as intensive monitoring for signs of addiction, abuse, and misuse; prescribing naloxone for the emergency treatment of opioid overdose should be considered. All patients using buprenorphine for opioid dependence should be monitored for progression of opioid use disorder and addictive behaviors.

Buprenorphine is sought for nonmedical use (including by individuals with opioid use disorder) and is subject to criminal diversion. These risks should be considered when prescribing or dispensing buprenorphine. Strategies to reduce such risks should be used (e.g., prescribe smallest appropriate quantity, careful storage during use, proper disposal of unused drug).

Buprenorphine has a major potential interaction with Altered Consciousness.

Buprenorphine analgesics are contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with buprenorphine. Patients should be monitored closely for respiratory depression, especially during initiation of therapy or after a dosage increase. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; however, naloxone may not be effective in reversing respiratory depression produced by buprenorphine due to its slow rate of dissociation from mu receptors.

The use of buprenorphine analgesics in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Buprenorphine-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of buprenorphine analgesics; buprenorphine for opioid dependence should be used with caution in such patients with compromised respiratory function. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), buprenorphine analgesics may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting therapy. Buprenorphine for opioid dependence should be used with caution in patients with head injury, intracranial lesions, and other circumstances where cerebrospinal pressure may be increased. Opioids may obscure the clinical course in a patient with a head injury; use of buprenorphine analgesics should be avoided in patients with impaired consciousness or coma.

Life-threatening respiratory depression is more likely to occur in older adult, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating buprenorphine analgesics and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered. Buprenorphine should be used with caution in patients with kyphoscoliosis.

Buprenorphine has a moderate potential interaction with Arrhythmia.

Thorough QT studies with buprenorphine have shown QT prolongation 15 msec or less; this QTc prolongation effect does not appear to be mediated by hERG channels. Based on these 2 findings, buprenorphine is unlikely to be proarrhythmic when used alone in patients without risk factors. However, these observations should be considered in clinical decisions when prescribing buprenorphine to patients with risk factors (e.g., hypokalemia, bradycardia, recent conversion from atrial fibrillation, congestive heart failure, baseline QT prolongation, subclinical long-QT syndrome, severe hypomagnesemia).

Buprenorphine has a major potential interaction with Asphyxia.

Buprenorphine analgesics are contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with buprenorphine. Patients should be monitored closely for respiratory depression, especially during initiation of therapy or after a dosage increase. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; however, naloxone may not be effective in reversing respiratory depression produced by buprenorphine due to its slow rate of dissociation from mu receptors.

The use of buprenorphine analgesics in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Buprenorphine-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of buprenorphine analgesics; buprenorphine for opioid dependence should be used with caution in such patients with compromised respiratory function. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), buprenorphine analgesics may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting therapy. Buprenorphine for opioid dependence should be used with caution in patients with head injury, intracranial lesions, and other circumstances where cerebrospinal pressure may be increased. Opioids may obscure the clinical course in a patient with a head injury; use of buprenorphine analgesics should be avoided in patients with impaired consciousness or coma.

Life-threatening respiratory depression is more likely to occur in older adult, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating buprenorphine analgesics and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered. Buprenorphine should be used with caution in patients with kyphoscoliosis.

Buprenorphine has a moderate potential interaction with Benign Prostatic Hyperplasia.

Buprenorphine should be used with caution in patients with prostatic hypertrophy or urethral stricture. Urinary retention has been reported with buprenorphine.

Buprenorphine has a moderate potential interaction with Biliary Obstruction.

Opioid agonists may cause spasm of the sphincter of Oddi, which may increase biliary tract pressure. Other opioid-induced effects may include a reduction in biliary and pancreatic secretions and transient elevations in serum amylase. Patients with biliary tract disease (including acute pancreatitis) should be regularly evaluated for worsening symptoms. Therapy with opioids should be administered cautiously in patients with biliary tract disease, gallbladder disease, or acute pancreatitis.

Buprenorphine has a major potential interaction with Brain Tumor.

The hypoventilation associated with administration of opioid partial agonists can induce cerebral hypoxia and vasodilatation with resultant increase in intracranial pressure. Unless mechanical ventilation is provided, extreme caution is advised when opioid partial agonists are given to patients with head injury, intracranial lesions, or a preexisting elevated CSF pressure. Also, clinicians treating such patients should be aware that opioid partial agonists may interfere with the evaluation of CNS function, especially with respect to consciousness levels, respiratory status, and pupillary changes.

Buprenorphine has a major potential interaction with Brain Tumor.

Buprenorphine analgesics are contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with buprenorphine. Patients should be monitored closely for respiratory depression, especially during initiation of therapy or after a dosage increase. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; however, naloxone may not be effective in reversing respiratory depression produced by buprenorphine due to its slow rate of dissociation from mu receptors.

The use of buprenorphine analgesics in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Buprenorphine-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of buprenorphine analgesics; buprenorphine for opioid dependence should be used with caution in such patients with compromised respiratory function. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), buprenorphine analgesics may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting therapy. Buprenorphine for opioid dependence should be used with caution in patients with head injury, intracranial lesions, and other circumstances where cerebrospinal pressure may be increased. Opioids may obscure the clinical course in a patient with a head injury; use of buprenorphine analgesics should be avoided in patients with impaired consciousness or coma.

Life-threatening respiratory depression is more likely to occur in older adult, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating buprenorphine analgesics and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered. Buprenorphine should be used with caution in patients with kyphoscoliosis.

Buprenorphine has a major potential interaction with Cachexia.

Buprenorphine analgesics are contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with buprenorphine. Patients should be monitored closely for respiratory depression, especially during initiation of therapy or after a dosage increase. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; however, naloxone may not be effective in reversing respiratory depression produced by buprenorphine due to its slow rate of dissociation from mu receptors.

The use of buprenorphine analgesics in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Buprenorphine-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of buprenorphine analgesics; buprenorphine for opioid dependence should be used with caution in such patients with compromised respiratory function. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), buprenorphine analgesics may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting therapy. Buprenorphine for opioid dependence should be used with caution in patients with head injury, intracranial lesions, and other circumstances where cerebrospinal pressure may be increased. Opioids may obscure the clinical course in a patient with a head injury; use of buprenorphine analgesics should be avoided in patients with impaired consciousness or coma.

Life-threatening respiratory depression is more likely to occur in older adult, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating buprenorphine analgesics and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered. Buprenorphine should be used with caution in patients with kyphoscoliosis.

Buprenorphine has a major potential interaction with Cerebral Vascular Disorder.

Buprenorphine analgesics are contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with buprenorphine. Patients should be monitored closely for respiratory depression, especially during initiation of therapy or after a dosage increase. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; however, naloxone may not be effective in reversing respiratory depression produced by buprenorphine due to its slow rate of dissociation from mu receptors.

The use of buprenorphine analgesics in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Buprenorphine-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of buprenorphine analgesics; buprenorphine for opioid dependence should be used with caution in such patients with compromised respiratory function. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), buprenorphine analgesics may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting therapy. Buprenorphine for opioid dependence should be used with caution in patients with head injury, intracranial lesions, and other circumstances where cerebrospinal pressure may be increased. Opioids may obscure the clinical course in a patient with a head injury; use of buprenorphine analgesics should be avoided in patients with impaired consciousness or coma.

Life-threatening respiratory depression is more likely to occur in older adult, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating buprenorphine analgesics and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered. Buprenorphine should be used with caution in patients with kyphoscoliosis.

Buprenorphine has a major potential interaction with Cerebral Vascular Disorder.

The hypoventilation associated with administration of opioid partial agonists can induce cerebral hypoxia and vasodilatation with resultant increase in intracranial pressure. Unless mechanical ventilation is provided, extreme caution is advised when opioid partial agonists are given to patients with head injury, intracranial lesions, or a preexisting elevated CSF pressure. Also, clinicians treating such patients should be aware that opioid partial agonists may interfere with the evaluation of CNS function, especially with respect to consciousness levels, respiratory status, and pupillary changes.

Buprenorphine has a major potential interaction with Cor Pulmonale.

Buprenorphine analgesics are contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with buprenorphine. Patients should be monitored closely for respiratory depression, especially during initiation of therapy or after a dosage increase. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; however, naloxone may not be effective in reversing respiratory depression produced by buprenorphine due to its slow rate of dissociation from mu receptors.

The use of buprenorphine analgesics in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Buprenorphine-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of buprenorphine analgesics; buprenorphine for opioid dependence should be used with caution in such patients with compromised respiratory function. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), buprenorphine analgesics may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting therapy. Buprenorphine for opioid dependence should be used with caution in patients with head injury, intracranial lesions, and other circumstances where cerebrospinal pressure may be increased. Opioids may obscure the clinical course in a patient with a head injury; use of buprenorphine analgesics should be avoided in patients with impaired consciousness or coma.

Life-threatening respiratory depression is more likely to occur in older adult, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating buprenorphine analgesics and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered. Buprenorphine should be used with caution in patients with kyphoscoliosis.

Buprenorphine has a moderate potential interaction with Dehydration.

Buprenorphine may cause severe hypotension (including orthostatic hypotension, syncope) in ambulatory patients. Risk is increased in patients whose ability to maintain blood pressure has already been compromised by reduced blood volume or coadministration of certain CNS depressant drugs; these patients should be monitored for signs of hypotension after starting or titrating buprenorphine. In patients with circulatory shock, buprenorphine may cause vasodilation that can further reduce cardiac output and blood pressure; buprenorphine analgesics should be avoided in patients with circulatory shock.

Buprenorphine has a major potential interaction with Depression.

Buprenorphine exposes users to the risks of addiction, abuse, and misuse. Each patient's risk should be assessed before prescribing buprenorphine analgesics, and all patients should be monitored regularly for development of such behaviors and conditions. Risks are increased in patients with personal or family history of substance abuse (including drug or alcohol abuse or addiction) or mental illness (e.g., major depression); the potential for such risks should not prevent proper pain management in any given patient. Patients at increased risk may be prescribed buprenorphine analgesics but use in such patients requires intensive counseling about the risks and proper use of buprenorphine, as well as intensive monitoring for signs of addiction, abuse, and misuse; prescribing naloxone for the emergency treatment of opioid overdose should be considered. All patients using buprenorphine for opioid dependence should be monitored for progression of opioid use disorder and addictive behaviors.

Buprenorphine is sought for nonmedical use (including by individuals with opioid use disorder) and is subject to criminal diversion. These risks should be considered when prescribing or dispensing buprenorphine. Strategies to reduce such risks should be used (e.g., prescribe smallest appropriate quantity, careful storage during use, proper disposal of unused drug).

cloBAZam has a moderate potential interaction with Depression.

Benzodiazepines depress the central nervous system and may cause or exacerbate mental depression and cause suicidal behavior and ideation. Episodes of mania and hypomania have also been reported in depressed patients treated with some of these agents. Therapy with benzodiazepines should be administered cautiously in patients with a history of depression or other psychiatric disorders. Patients should be monitored for any changes in mood or behavior. It may be prudent to refrain from dispensing large quantities of medication to these patients.

Buprenorphine has a major potential interaction with Drug Dependence.

Buprenorphine exposes users to the risks of addiction, abuse, and misuse. Each patient's risk should be assessed before prescribing buprenorphine analgesics, and all patients should be monitored regularly for development of such behaviors and conditions. Risks are increased in patients with personal or family history of substance abuse (including drug or alcohol abuse or addiction) or mental illness (e.g., major depression); the potential for such risks should not prevent proper pain management in any given patient. Patients at increased risk may be prescribed buprenorphine analgesics but use in such patients requires intensive counseling about the risks and proper use of buprenorphine, as well as intensive monitoring for signs of addiction, abuse, and misuse; prescribing naloxone for the emergency treatment of opioid overdose should be considered. All patients using buprenorphine for opioid dependence should be monitored for progression of opioid use disorder and addictive behaviors.

Buprenorphine is sought for nonmedical use (including by individuals with opioid use disorder) and is subject to criminal diversion. These risks should be considered when prescribing or dispensing buprenorphine. Strategies to reduce such risks should be used (e.g., prescribe smallest appropriate quantity, careful storage during use, proper disposal of unused drug).

cloBAZam has a major potential interaction with Drug Dependence.

Benzodiazepines have the potential to cause dependence and abuse. Tolerance as well as physical and psychological dependence can develop, particularly after prolonged use and/or excessive dosages. However, abrupt cessation following continual use of as few as 6 weeks at therapeutic levels has occasionally precipitated withdrawal symptoms. Addiction- prone individuals, such as those with a history of alcohol or substance abuse, should be under careful surveillance when treated with benzodiazepines. It may be prudent to refrain from dispensing large quantities of medication to these patients. After prolonged use or if dependency is suspected, withdrawal of benzodiazepine therapy should be undertaken gradually using a dosage- tapering schedule. If withdrawal symptoms occur, temporary reinstitution of benzodiazepines may be necessary.

Buprenorphine has a moderate potential interaction with Gallbladder Disease.

Opioid agonists may cause spasm of the sphincter of Oddi, which may increase biliary tract pressure. Other opioid-induced effects may include a reduction in biliary and pancreatic secretions and transient elevations in serum amylase. Patients with biliary tract disease (including acute pancreatitis) should be regularly evaluated for worsening symptoms. Therapy with opioids should be administered cautiously in patients with biliary tract disease, gallbladder disease, or acute pancreatitis.

Buprenorphine has a major potential interaction with Gastrointestinal Obstruction.

Opioid analgesics are contraindicated in patients with known or suspected gastrointestinal obstruction, including paralytic ileus.

Buprenorphine has a major potential interaction with Head Injury.

The hypoventilation associated with administration of opioid partial agonists can induce cerebral hypoxia and vasodilatation with resultant increase in intracranial pressure. Unless mechanical ventilation is provided, extreme caution is advised when opioid partial agonists are given to patients with head injury, intracranial lesions, or a preexisting elevated CSF pressure. Also, clinicians treating such patients should be aware that opioid partial agonists may interfere with the evaluation of CNS function, especially with respect to consciousness levels, respiratory status, and pupillary changes.

Buprenorphine has a major potential interaction with Head Injury.

Buprenorphine analgesics are contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with buprenorphine. Patients should be monitored closely for respiratory depression, especially during initiation of therapy or after a dosage increase. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; however, naloxone may not be effective in reversing respiratory depression produced by buprenorphine due to its slow rate of dissociation from mu receptors.

The use of buprenorphine analgesics in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Buprenorphine-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of buprenorphine analgesics; buprenorphine for opioid dependence should be used with caution in such patients with compromised respiratory function. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), buprenorphine analgesics may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting therapy. Buprenorphine for opioid dependence should be used with caution in patients with head injury, intracranial lesions, and other circumstances where cerebrospinal pressure may be increased. Opioids may obscure the clinical course in a patient with a head injury; use of buprenorphine analgesics should be avoided in patients with impaired consciousness or coma.

Life-threatening respiratory depression is more likely to occur in older adult, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating buprenorphine analgesics and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered. Buprenorphine should be used with caution in patients with kyphoscoliosis.

Buprenorphine has a moderate potential interaction with Heart Failure.

Thorough QT studies with buprenorphine have shown QT prolongation 15 msec or less; this QTc prolongation effect does not appear to be mediated by hERG channels. Based on these 2 findings, buprenorphine is unlikely to be proarrhythmic when used alone in patients without risk factors. However, these observations should be considered in clinical decisions when prescribing buprenorphine to patients with risk factors (e.g., hypokalemia, bradycardia, recent conversion from atrial fibrillation, congestive heart failure, baseline QT prolongation, subclinical long-QT syndrome, severe hypomagnesemia).

Buprenorphine has a moderate potential interaction with Hypokalemia.

Thorough QT studies with buprenorphine have shown QT prolongation 15 msec or less; this QTc prolongation effect does not appear to be mediated by hERG channels. Based on these 2 findings, buprenorphine is unlikely to be proarrhythmic when used alone in patients without risk factors. However, these observations should be considered in clinical decisions when prescribing buprenorphine to patients with risk factors (e.g., hypokalemia, bradycardia, recent conversion from atrial fibrillation, congestive heart failure, baseline QT prolongation, subclinical long-QT syndrome, severe hypomagnesemia).

Buprenorphine has a moderate potential interaction with Hypotension.

Buprenorphine may cause severe hypotension (including orthostatic hypotension, syncope) in ambulatory patients. Risk is increased in patients whose ability to maintain blood pressure has already been compromised by reduced blood volume or coadministration of certain CNS depressant drugs; these patients should be monitored for signs of hypotension after starting or titrating buprenorphine. In patients with circulatory shock, buprenorphine may cause vasodilation that can further reduce cardiac output and blood pressure; buprenorphine analgesics should be avoided in patients with circulatory shock.

Buprenorphine has a moderate potential interaction with Liver Disease.

Buprenorphine is metabolized in the liver, and its activity may be increased and/or extended in patients with impaired liver function.
-Buccal film or sublingual tablets: A dose adjustment is recommended for patients with severe liver dysfunction; patients with moderate or severe liver dysfunction should be periodically assessed for signs/symptoms of toxicity or overdose caused by increased buprenorphine levels.
-IM/IV injection: This product should be administered with caution in patients with severe liver dysfunction.
-Subcutaneous injection or subdermal implant: The effect of liver dysfunction on the pharmacokinetics of this product has not been studied. Due to the long-acting nature of the subcutaneous injection, dosage adjustments are not rapidly reflected in plasma buprenorphine levels. Because buprenorphine levels cannot be rapidly adjusted when using the subcutaneous injection, and because the subdermal implant cannot be titrated, patients with preexisting moderate to severe liver dysfunction are not candidates for treatment with these products.
-Transdermal system: This product has not been evaluated in patients with severe liver dysfunction; because this product is only intended for 7-day application, use of an alternate analgesic that may permit more flexibility with dosing in these patients should be considered.

Buprenorphine has a moderate potential interaction with Long QT Syndrome.

Thorough QT studies with buprenorphine have shown QT prolongation 15 msec or less; this QTc prolongation effect does not appear to be mediated by hERG channels. Based on these 2 findings, buprenorphine is unlikely to be proarrhythmic when used alone in patients without risk factors. However, these observations should be considered in clinical decisions when prescribing buprenorphine to patients with risk factors (e.g., hypokalemia, bradycardia, recent conversion from atrial fibrillation, congestive heart failure, baseline QT prolongation, subclinical long-QT syndrome, severe hypomagnesemia).

Buprenorphine has a moderate potential interaction with Magnesium Imbalance.

Thorough QT studies with buprenorphine have shown QT prolongation 15 msec or less; this QTc prolongation effect does not appear to be mediated by hERG channels. Based on these 2 findings, buprenorphine is unlikely to be proarrhythmic when used alone in patients without risk factors. However, these observations should be considered in clinical decisions when prescribing buprenorphine to patients with risk factors (e.g., hypokalemia, bradycardia, recent conversion from atrial fibrillation, congestive heart failure, baseline QT prolongation, subclinical long-QT syndrome, severe hypomagnesemia).

Buprenorphine has a moderate potential interaction with Pancreatitis.

Opioid agonists may cause spasm of the sphincter of Oddi, which may increase biliary tract pressure. Other opioid-induced effects may include a reduction in biliary and pancreatic secretions and transient elevations in serum amylase. Patients with biliary tract disease (including acute pancreatitis) should be regularly evaluated for worsening symptoms. Therapy with opioids should be administered cautiously in patients with biliary tract disease, gallbladder disease, or acute pancreatitis.

Buprenorphine has a major potential interaction with Psychiatric Disorders.

Buprenorphine exposes users to the risks of addiction, abuse, and misuse. Each patient's risk should be assessed before prescribing buprenorphine analgesics, and all patients should be monitored regularly for development of such behaviors and conditions. Risks are increased in patients with personal or family history of substance abuse (including drug or alcohol abuse or addiction) or mental illness (e.g., major depression); the potential for such risks should not prevent proper pain management in any given patient. Patients at increased risk may be prescribed buprenorphine analgesics but use in such patients requires intensive counseling about the risks and proper use of buprenorphine, as well as intensive monitoring for signs of addiction, abuse, and misuse; prescribing naloxone for the emergency treatment of opioid overdose should be considered. All patients using buprenorphine for opioid dependence should be monitored for progression of opioid use disorder and addictive behaviors.

Buprenorphine is sought for nonmedical use (including by individuals with opioid use disorder) and is subject to criminal diversion. These risks should be considered when prescribing or dispensing buprenorphine. Strategies to reduce such risks should be used (e.g., prescribe smallest appropriate quantity, careful storage during use, proper disposal of unused drug).

cloBAZam has a moderate potential interaction with Psychosis.

Benzodiazepines depress the central nervous system and may cause or exacerbate mental depression and cause suicidal behavior and ideation. Episodes of mania and hypomania have also been reported in depressed patients treated with some of these agents. Therapy with benzodiazepines should be administered cautiously in patients with a history of depression or other psychiatric disorders. Patients should be monitored for any changes in mood or behavior. It may be prudent to refrain from dispensing large quantities of medication to these patients.

Buprenorphine has a major potential interaction with Pulmonary Impairment.

Buprenorphine analgesics are contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with buprenorphine. Patients should be monitored closely for respiratory depression, especially during initiation of therapy or after a dosage increase. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; however, naloxone may not be effective in reversing respiratory depression produced by buprenorphine due to its slow rate of dissociation from mu receptors.

The use of buprenorphine analgesics in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Buprenorphine-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of buprenorphine analgesics; buprenorphine for opioid dependence should be used with caution in such patients with compromised respiratory function. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), buprenorphine analgesics may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting therapy. Buprenorphine for opioid dependence should be used with caution in patients with head injury, intracranial lesions, and other circumstances where cerebrospinal pressure may be increased. Opioids may obscure the clinical course in a patient with a head injury; use of buprenorphine analgesics should be avoided in patients with impaired consciousness or coma.

Life-threatening respiratory depression is more likely to occur in older adult, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating buprenorphine analgesics and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered. Buprenorphine should be used with caution in patients with kyphoscoliosis.

Buprenorphine has a moderate potential interaction with Renal Dysfunction.

Buprenorphine is substantially excreted by the kidney; the risk of adverse reactions to this drug may be greater in patients with impaired renal function. Buprenorphine has not been studied in patients with renal dysfunction; caution is recommended when used in patients with severe renal dysfunction.

cloBAZam has a moderate potential interaction with Renal Dysfunction.

Benzodiazepines are excreted by the kidneys and should be used with caution in patients with impaired renal function and end-stage kidney disease.

Buprenorphine has a major potential interaction with Respiratory Arrest.

Buprenorphine analgesics are contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with buprenorphine. Patients should be monitored closely for respiratory depression, especially during initiation of therapy or after a dosage increase. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; however, naloxone may not be effective in reversing respiratory depression produced by buprenorphine due to its slow rate of dissociation from mu receptors.

The use of buprenorphine analgesics in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Buprenorphine-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of buprenorphine analgesics; buprenorphine for opioid dependence should be used with caution in such patients with compromised respiratory function. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), buprenorphine analgesics may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting therapy. Buprenorphine for opioid dependence should be used with caution in patients with head injury, intracranial lesions, and other circumstances where cerebrospinal pressure may be increased. Opioids may obscure the clinical course in a patient with a head injury; use of buprenorphine analgesics should be avoided in patients with impaired consciousness or coma.

Life-threatening respiratory depression is more likely to occur in older adult, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating buprenorphine analgesics and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered. Buprenorphine should be used with caution in patients with kyphoscoliosis.

Buprenorphine has a major potential interaction with Scoliosis.

Buprenorphine analgesics are contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with buprenorphine. Patients should be monitored closely for respiratory depression, especially during initiation of therapy or after a dosage increase. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; however, naloxone may not be effective in reversing respiratory depression produced by buprenorphine due to its slow rate of dissociation from mu receptors.

The use of buprenorphine analgesics in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Buprenorphine-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of buprenorphine analgesics; buprenorphine for opioid dependence should be used with caution in such patients with compromised respiratory function. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), buprenorphine analgesics may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting therapy. Buprenorphine for opioid dependence should be used with caution in patients with head injury, intracranial lesions, and other circumstances where cerebrospinal pressure may be increased. Opioids may obscure the clinical course in a patient with a head injury; use of buprenorphine analgesics should be avoided in patients with impaired consciousness or coma.

Life-threatening respiratory depression is more likely to occur in older adult, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating buprenorphine analgesics and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered. Buprenorphine should be used with caution in patients with kyphoscoliosis.

Buprenorphine has a moderate potential interaction with Seizures.

Narcotic (opioid) analgesic agents may increase the frequency of seizures in patients with seizure disorders, may increase the risk of seizures occurring in other clinical settings associated with seizures, and, at higher dosages, have been reported to induce seizures in patients without history of seizures. Patients with history of seizure disorders should be regularly evaluated for worsened seizure control during therapy. Prolonged meperidine use may increase the risk of toxicity (e.g., seizures) from the accumulation of the active metabolite (normeperidine).

Buprenorphine has a moderate potential interaction with Shock.

Buprenorphine may cause severe hypotension (including orthostatic hypotension, syncope) in ambulatory patients. Risk is increased in patients whose ability to maintain blood pressure has already been compromised by reduced blood volume or coadministration of certain CNS depressant drugs; these patients should be monitored for signs of hypotension after starting or titrating buprenorphine. In patients with circulatory shock, buprenorphine may cause vasodilation that can further reduce cardiac output and blood pressure; buprenorphine analgesics should be avoided in patients with circulatory shock.

Buprenorphine has a moderate potential interaction with Urinary Retention.

Buprenorphine should be used with caution in patients with prostatic hypertrophy or urethral stricture. Urinary retention has been reported with buprenorphine.