Drug Interactions between buprenorphine and chlorpheniramine / guaifenesin / phenylephrine

Do not use alcohol or medications that contain alcohol while you are receiving treatment with buprenorphine. This may increase nervous system side effects such as drowsiness, dizziness, lightheadedness, difficulty concentrating, and impairment in thinking and judgment. In severe cases, low blood pressure, respiratory distress, fainting, coma, or even death may occur. You should also avoid consuming grapefruit and grapefruit juice, as this may increase the blood levels and effects of buprenorphine. Talk to your doctor or pharmacist if you have questions on how to take this or other medications you are prescribed. Do not exceed the dose of buprenorphine prescribed for you or use the medication more frequently or for a longer duration than prescribed by your doctor. Also avoid activities requiring mental alertness such as driving or operating hazardous machinery until you know how the medication affects you. It is important to tell your doctor about all other medications you use, including vitamins and herbs. Do not stop using any medication without first talking to your doctor.

Alcohol can increase the nervous system side effects of chlorpheniramine such as dizziness, drowsiness, and difficulty concentrating. Some people may also experience impairment in thinking and judgment. You should avoid or limit the use of alcohol while being treated with chlorpheniramine. Do not use more than the recommended dose of chlorpheniramine, and avoid activities requiring mental alertness such as driving or operating hazardous machinery until you know how the medication affects you. Talk to your doctor or pharmacist if you have any questions or concerns.

Both phenylephrine and caffeine can increase blood pressure and heart rate, and combining them may enhance these effects. Talk to your doctor before using these medications, especially if you have a history of high blood pressure or heart disease. You may need a dose adjustment or more frequent monitoring by your doctor to safely use both medications. Contact your doctor if your condition changes or you experience increased side effects. It is important to tell your doctor about all other medications you use, including vitamins and herbs. Do not stop using any medications without first talking to your doctor.

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 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 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 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.

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 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.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

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.

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.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

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 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 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).

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

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.

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 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).

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

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 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 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 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.

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).

It has been suggested that the anticholinergic effect of antihistamines may reduce the volume and cause thickening of bronchial secretions, resulting in obstruction of respiratory tract. Some manufacturers and clinicians recommend that therapy with antihistamines be administered cautiously in patients with asthma or chronic obstructive pulmonary disease.

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

Sympathomimetic agents may cause or worsen urinary difficulty in patients with prostate enlargement due to smooth muscle contraction in the bladder neck via stimulation of alpha-1 adrenergic receptors. Therapy with sympathomimetic agents should be administered cautiously in patients with hypertrophy or neoplasm of the prostate.

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.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

It has been suggested that the anticholinergic effect of antihistamines may reduce the volume and cause thickening of bronchial secretions, resulting in obstruction of respiratory tract. Some manufacturers and clinicians recommend that therapy with antihistamines be administered cautiously in patients with asthma or chronic obstructive pulmonary disease.

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 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.

Sympathomimetic agents may cause increases in blood glucose concentrations. These effects are usually transient and slight but may be significant with dosages higher than those normally recommended. Therapy with sympathomimetic agents should be administered cautiously in patients with diabetes mellitus. Closer monitoring of blood glucose concentrations may be appropriate.

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.

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.

Sympathomimetic agents can induce transient mydriasis via stimulation of alpha-1 adrenergic receptors. In patients with anatomically narrow angles or narrow-angle glaucoma, pupillary dilation can provoke an acute attack. In patients with other forms of glaucoma, mydriasis may occasionally increase intraocular pressure. Therapy with sympathomimetic agents should be administered cautiously in patients with or predisposed to glaucoma, particularly narrow-angle glaucoma.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

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 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.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

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.

Limited pharmacokinetic data are available for the older, first-generation antihistamines. Many appear to be primarily metabolized by the liver, and both parent drugs and metabolites are excreted in the urine. Patients with renal and/or liver disease may be at greater risk for adverse effects from antihistamines due to drug and metabolite accumulation. Therapy with antihistamines should be administered cautiously in such patients. Lower initial dosages may be appropriate.

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).

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).

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.

Sympathomimetic agents may cause or worsen urinary difficulty in patients with prostate enlargement due to smooth muscle contraction in the bladder neck via stimulation of alpha-1 adrenergic receptors. Therapy with sympathomimetic agents should be administered cautiously in patients with hypertrophy or neoplasm of the prostate.

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.

Limited pharmacokinetic data are available for the older, first-generation antihistamines. Many appear to be primarily metabolized by the liver, and both parent drugs and metabolites are excreted in the urine. Patients with renal and/or liver disease may be at greater risk for adverse effects from antihistamines due to drug and metabolite accumulation. Therapy with antihistamines should be administered cautiously in such patients. Lower initial dosages may be appropriate.

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

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.