Can you take Apresazide with Buprenorphine?

The hydroCHLOROthiazide in Apresazide has a moderate potential interaction with Abnormal Glucose Tolerance.

Thiazide diuretics may cause hyperglycemia and glycosuria in patients with diabetes. They may also precipitate diabetes in prediabetic patients. These effects are usually reversible following discontinuation of the drugs. Therapy with thiazide diuretics should be administered cautiously in patients with diabetes mellitus, glucose intolerance, or a predisposition to hyperglycemia. Patients with diabetes mellitus should be monitored more closely during thiazide therapy, and their antidiabetic regimen adjusted accordingly.

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.

The hydroCHLOROthiazide in Apresazide has a major potential interaction with Anuria.

The use of thiazide diuretics is contraindicated in patients with anuria.

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.

The hydroCHLOROthiazide in Apresazide has a moderate potential interaction with Asthma.

Thiazide diuretics should be used with caution in patients with history of bronchial asthma as sensitivity reactions may occur.

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.

The hydrALAZINE in Apresazide has a major potential interaction with Bone Marrow Depression/Low Blood Counts.

Hydralazine may rarely cause blood dyscrasias at recommended dosages. Reduction in hemoglobin, red cell count, agranulocytosis, leukopenia, and purpura have been reported. Therapy with hydralazine should be administered cautiously in patients with these preexisting conditions and if such abnormalities develop during the course of therapy, treatment should be discontinued. Monitoring blood counts should be considered for those patients at higher risk.

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.

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 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.

The hydrALAZINE in Apresazide has a moderate potential interaction with Cerebral Vascular Disorder.

The vasodilatory effects of hydralazine may aggravate cerebral vasculopathy. Therapy with hydralazine should be administered cautiously in patients with cerebral vasculopathy.

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.

The hydroCHLOROthiazide in Apresazide has a major potential interaction with Dehydration.

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.

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).

The hydroCHLOROthiazide in Apresazide has a moderate potential interaction with Diabetes Mellitus.

Thiazide diuretics may cause hyperglycemia and glycosuria in patients with diabetes. They may also precipitate diabetes in prediabetic patients. These effects are usually reversible following discontinuation of the drugs. Therapy with thiazide diuretics should be administered cautiously in patients with diabetes mellitus, glucose intolerance, or a predisposition to hyperglycemia. Patients with diabetes mellitus should be monitored more closely during thiazide therapy, and their antidiabetic regimen adjusted accordingly.

The hydroCHLOROthiazide in Apresazide has a major potential interaction with Diarrhea.

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.

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).

The hydroCHLOROthiazide in Apresazide has a major potential interaction with Electrolyte Abnormalities.

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.

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.

The hydrALAZINE in Apresazide has a moderate potential interaction with Glomerulonephritis.

The use of hydralazine has been associated with the development of glomerulonephritis. Hydralazine should be used with caution in patients with advanced renal damage and these patients may require a lower dose. Renal function should be monitored and supported as required.

The hydroCHLOROthiazide in Apresazide has a moderate potential interaction with Gout.

Thiazide diuretics decrease the rate of uric acid excretion. Hyperuricemia occurs frequently but is usually asymptomatic and rarely leads to clinical gout except in patients with a history of gout or chronic renal failure. Therapy with thiazide diuretics should be administered cautiously in such patients.

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).

The hydroCHLOROthiazide in Apresazide has a moderate potential interaction with High Cholesterol.

Thiazide diuretics may increase serum triglyceride and cholesterol levels, primarily LDL and VLDL. Whether these effects are dose-related and sustained during chronic therapy are unknown. Patients with preexisting hyperlipidemia may require closer monitoring during thiazide therapy, and adjustments made accordingly in their lipid-lowering regimen

The hydroCHLOROthiazide in Apresazide has a major potential interaction with Hyperaldosteronism.

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.

The hydroCHLOROthiazide in Apresazide has a moderate potential interaction with Hyperparathyroidism.

Urinary calcium excretion is decreased by thiazide diuretics during chronic administration. Pathologic changes in the parathyroid gland with hypercalcemia and hypophosphatemia have been reported during prolonged therapy. However, the common complications of hyperparathyroidism such as renal lithiasis, bone resorption, and peptic ulceration have not been seen. Clinicians should be cognizant of these effects when prescribing or administering thiazide therapy to patients with hyperparathyroidism. These drugs should be discontinued before carrying out tests for parathyroid function.

The hydroCHLOROthiazide in Apresazide has a major potential interaction with Hypokalemia.

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.

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).

The hydroCHLOROthiazide in Apresazide has a major potential interaction with Hyponatremia.

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.

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.

The hydrALAZINE in Apresazide has a major potential interaction with Ischemic Heart Disease.

The use of hydralazine is contraindicated in patients with coronary artery disease. Reflex tachycardia may commonly occur. Palpitations and chest pain have also been reported. Myocardial infarction has been associated with the use of hydralazine.

The hydroCHLOROthiazide in Apresazide has a major potential interaction with Liver Disease.

Patients with severe liver disease or cirrhosis are very susceptible to thiazide-induced hypokalemic hypochloremic alkalosis. Blood ammonia concentrations may be further increased in patients with previously elevated concentrations. Hepatic encephalopathy and death have occurred secondary to the electrolyte alterations accompanying diuretic use. Therapy with thiazide diuretics should be administered cautiously in patients with impaired hepatic function or progressive liver disease, and discontinued promptly if signs of impending hepatic coma appear (e.g., tremors, confusion, and increased jaundice).

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).

The hydrALAZINE in Apresazide has a major potential interaction with Lupus Erythematosus.

The use of hydralazine has been associated with the development of lupus erythematosus and lupus-like syndromes, as well as exacerbation of the disease. Hydralazine therapy should be withdrawn in patients experiencing worsening of preexisting lupus. Monitoring complete blood counts, and antinuclear antibody titers before and during prolonged therapy is recommended.

The hydroCHLOROthiazide in Apresazide has a major potential interaction with Lupus Erythematosus.

The use of thiazide diuretics has been reported to possibly exacerbate or activate systemic lupus erythematosus. Reported cases have generally been associated with chlorothiazide and hydrochlorothiazide. Therapy with thiazide diuretics should be administered cautiously in patients with a history or risk of SLE.

The hydroCHLOROthiazide in Apresazide has a major potential interaction with Magnesium Imbalance.

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.

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).

The hydroCHLOROthiazide in Apresazide has a major potential interaction with Malnourishment.

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.

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).

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.

The hydroCHLOROthiazide in Apresazide has a major potential interaction with Renal Dysfunction.

Thiazide diuretics may be ineffective when the glomerular filtration rate is low (GFR < 25 mL/min) because they are not expected to be filtered into the renal tubule, their site of action. In addition, thiazide diuretics decrease the GFR and may precipitate azotemia in renal disease. Cumulative effects may also develop because most of these drugs are excreted unchanged in the urine by glomerular filtration and active tubular secretion. Therapy with thiazide diuretics should be administered cautiously at reduced dosages in patients with renal impairment. If renal function becomes progressively worse, as indicated by rising BUN or serum creatinine levels, an interruption or discontinuation of thiazide therapy should be considered.

The hydrALAZINE in Apresazide has a moderate potential interaction with Renal Dysfunction.

The use of hydralazine has been associated with the development of glomerulonephritis. Hydralazine should be used with caution in patients with advanced renal damage and these patients may require a lower dose. Renal function should be monitored and supported as required.

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.

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.

The hydroCHLOROthiazide in Apresazide has a moderate potential interaction with Thyroid Disease.

Thiazide diuretics may decrease serum PBI (protein-bound iodine) levels without associated thyroid disturbance. Clinicians should be cognizant of this effect when prescribing or administering thiazide therapy to patients with thyroid disorders.

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.

The hydrALAZINE in Apresazide has a major potential interaction with Valvular Heart Disease.

The use of hydralazine is contraindicated in patients with mitral valvular rheumatic heart disease.

The hydroCHLOROthiazide in Apresazide has a major potential interaction with Ventricular Arrhythmia.

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.

The hydroCHLOROthiazide in Apresazide has a major potential interaction with Vomiting.

The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.