Interactions between Sanorex and Sufentanil

SUFentanil has a major potential interaction with Acute Alcohol Intoxication.

The use of opiate agonists is contraindicated in patients with acute alcohol intoxication exhibiting depressed vital signs. The central nervous system depressant effects of opiate agonists may be additive with those of alcohol. Severe respiratory depression and death may occur. Therapy with opiate agonists should be administered cautiously in patients who might be prone to acute alcohol intake.

SUFentanil has a moderate potential interaction with Adrenal Insufficiency.

Patients with Addison's disease may have increased risk of respiratory depression and prolonged CNS depression associated with the use of narcotic (opioid) analgesic agents. Conversely, these agents may cause or potentiate adrenal insufficiency. Therapy with opioids should be administered cautiously and initiated at reduced dosages in patients with adrenocortical insufficiency. Subsequent doses should be titrated based on individual response rather than a fixed dosing schedule.

The mazindol in Sanorex has a major potential interaction with Alcoholism.

CNS stimulants (especially amphetamines) have a high potential for abuse and misuse, which can lead to development of a substance use disorder, including addiction. Misuse and abuse of CNS stimulants can result in overdose and death; this risk is increased with higher doses or unapproved methods of administration (e.g., snorting, injection). Before prescribing a CNS stimulant, each patient's risk for abuse, misuse, and addiction should be assessed. Throughout therapy, it is recommended to reassess each patient's risk and frequently monitor for signs/symptoms of abuse, misuse, and addiction. Therapy with CNS stimulants should be administered cautiously, if at all, in patients with a history of alcohol or substance abuse. The use of some agents is contraindicated in patients with a history of drug abuse.

SUFentanil has a major potential interaction with Altered Consciousness.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

The mazindol in Sanorex has a major potential interaction with Anxiety and Stress.

Some CNS stimulants are contraindicated in patients with marked agitation and/or anxiety since these symptoms may be aggravated. CNS stimulants may also exacerbate symptoms of behavior disturbance and thought disorder in psychotic patients, particularly children. Therapy with CNS stimulants should be administered cautiously in patients with a history of psychosis or a predisposition to agitated states.

SUFentanil has a moderate potential interaction with Arrhythmia.

Opiate agonists have cholinergic activity. Large doses and/or rapid intravenous administration may produce bradycardia and arrhythmias via stimulation of medullary vagal nuclei. Therapy with opiate agonists should be administered cautiously in patients with a history of arrhythmias. Clinical monitoring of cardiovascular status is recommended during therapy.

SUFentanil has a major potential interaction with Asphyxia.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

SUFentanil has a major potential interaction with Brain Tumor.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

SUFentanil has a major potential interaction with Brain Tumor.

The hypoventilation associated with administration of opiate agonists, particularly by the intravenous route, can induce cerebral hypoxia and vasodilatation with resultant increase in intracranial pressure. Opiate agonists should not be used in patients with suspected or known head injury or increased intracranial pressure. Also, clinicians treating such patients should be aware that opiate agonists may interfere with the evaluation of CNS function, especially with respect to consciousness levels, respiratory status, and pupillary changes.

The mazindol in Sanorex has a major potential interaction with Cardiovascular Conditions and Disorders.

Many amphetamines and amphetamine-like drugs are contraindicated in patients with advanced arteriosclerosis, symptomatic or unstable cardiac or cerebrovascular disease, moderate to severe hypertension, or hyperthyroidism. Like other sympathomimetic amines, amphetamines may cause cardiovascular adverse effects such as palpitation, tachycardia, cardiac arrhythmias, and elevation of blood pressure. Rarely, cardiomyopathy manifested as ventricular hypertrophy and/or congestive heart failure has been reported during chronic amphetamine use. In addition, sudden death has been reported in association with amphetamine therapy at usual dosages in children with structural cardiac abnormalities. In general, amphetamines should not be used in patients with structural cardiac abnormalities. If not otherwise contraindicated, therapy with amphetamines should be administered cautiously in patients with a current or past history of cardiovascular or cerebrovascular disease.

The mazindol in Sanorex has a major potential interaction with Cerebral Vascular Disorder.

Many amphetamines and amphetamine-like drugs are contraindicated in patients with advanced arteriosclerosis, symptomatic or unstable cardiac or cerebrovascular disease, moderate to severe hypertension, or hyperthyroidism. Like other sympathomimetic amines, amphetamines may cause cardiovascular adverse effects such as palpitation, tachycardia, cardiac arrhythmias, and elevation of blood pressure. Rarely, cardiomyopathy manifested as ventricular hypertrophy and/or congestive heart failure has been reported during chronic amphetamine use. In addition, sudden death has been reported in association with amphetamine therapy at usual dosages in children with structural cardiac abnormalities. In general, amphetamines should not be used in patients with structural cardiac abnormalities. If not otherwise contraindicated, therapy with amphetamines should be administered cautiously in patients with a current or past history of cardiovascular or cerebrovascular disease.

SUFentanil has a major potential interaction with Cerebral Vascular Disorder.

The hypoventilation associated with administration of opiate agonists, particularly by the intravenous route, can induce cerebral hypoxia and vasodilatation with resultant increase in intracranial pressure. Opiate agonists should not be used in patients with suspected or known head injury or increased intracranial pressure. Also, clinicians treating such patients should be aware that opiate agonists may interfere with the evaluation of CNS function, especially with respect to consciousness levels, respiratory status, and pupillary changes.

SUFentanil has a major potential interaction with Cerebral Vascular Disorder.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

SUFentanil has a major potential interaction with Dehydration.

Opiate agonists can induce vasodilation and significant hypotension, particularly when given in high dosages and/or by rapid intravenous administration. Opiate analgesics cause vasodilatation that may exacerbate hypotension and hypoperfusion and, therefore, are contraindicated in circulatory shock. At therapeutic analgesic dosages, ambulatory patients are more likely to experience dizziness and hypotension than patients who are confined to bed. However, orthostatic hypotension may occur in supine patients upon rising. Therapy with opiate agonists should be administered cautiously and initiated at reduced dosages in patients with hypovolemia, or a predisposition to hypotension. When given by intramuscular or subcutaneous administration, clinicians should also be aware that impaired perfusion in these patients may prevent complete absorption of the drug. With repeated injections, an excessive amount may be absorbed suddenly if normal circulation is reestablished.

The mazindol in Sanorex has a major potential interaction with Depression.

The use of CNS stimulants can cause psychotic symptoms, suicidal ideation, and aggression, and can exacerbate symptoms of behavior disturbance and thought disorder; CNS stimulants may induce a manic or mixed episode in patients with bipolar disorder. Psychiatric symptoms have been reported in patients with and without history of psychiatric disorders. All patients (particularly those with psychotic or bipolar disorders) should be monitored closely, especially during treatment initiation and at times of dose changes. Extreme caution should be exercised when CNS stimulants are given to patients with a history of psychosis, depression, mania, or bipolar disorder. Prior to initiating therapy, all patients should be screened for risk factors for developing a manic episode (e.g., comorbid or history of depressive symptoms or family history of suicide, bipolar disease, or depression). If any psychiatric symptoms emerge or are exacerbated, treatment suspension should be considered. Some CNS stimulants are contraindicated in patients with marked agitation or anxiety.

The mazindol in Sanorex has a major potential interaction with Drug Dependence.

CNS stimulants (especially amphetamines) have a high potential for abuse and misuse, which can lead to development of a substance use disorder, including addiction. Misuse and abuse of CNS stimulants can result in overdose and death; this risk is increased with higher doses or unapproved methods of administration (e.g., snorting, injection). Before prescribing a CNS stimulant, each patient's risk for abuse, misuse, and addiction should be assessed. Throughout therapy, it is recommended to reassess each patient's risk and frequently monitor for signs/symptoms of abuse, misuse, and addiction. Therapy with CNS stimulants should be administered cautiously, if at all, in patients with a history of alcohol or substance abuse. The use of some agents is contraindicated in patients with a history of drug abuse.

SUFentanil has a major potential interaction with Gastrointestinal Obstruction.

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

The mazindol in Sanorex has a major potential interaction with Glaucoma/Intraocular Hypertension.

Some amphetamines and amphetamine-like drugs are contraindicated in patients with narrow-angle glaucoma or anatomically narrow angles. Like other sympathomimetic amines, amphetamines can induce transient mydriasis. In patients with narrow angles, pupillary dilation can provoke an acute attack of angle-closure glaucoma. If possible, these agents should also be avoided in patients with other forms of glaucoma since mydriasis may occasionally increase intraocular pressure.

SUFentanil has a major potential interaction with Head Injury.

The hypoventilation associated with administration of opiate agonists, particularly by the intravenous route, can induce cerebral hypoxia and vasodilatation with resultant increase in intracranial pressure. Opiate agonists should not be used in patients with suspected or known head injury or increased intracranial pressure. Also, clinicians treating such patients should be aware that opiate agonists may interfere with the evaluation of CNS function, especially with respect to consciousness levels, respiratory status, and pupillary changes.

SUFentanil has a major potential interaction with Head Injury.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

The mazindol in Sanorex has a major potential interaction with Heart Disease.

Many amphetamines and amphetamine-like drugs are contraindicated in patients with advanced arteriosclerosis, symptomatic or unstable cardiac or cerebrovascular disease, moderate to severe hypertension, or hyperthyroidism. Like other sympathomimetic amines, amphetamines may cause cardiovascular adverse effects such as palpitation, tachycardia, cardiac arrhythmias, and elevation of blood pressure. Rarely, cardiomyopathy manifested as ventricular hypertrophy and/or congestive heart failure has been reported during chronic amphetamine use. In addition, sudden death has been reported in association with amphetamine therapy at usual dosages in children with structural cardiac abnormalities. In general, amphetamines should not be used in patients with structural cardiac abnormalities. If not otherwise contraindicated, therapy with amphetamines should be administered cautiously in patients with a current or past history of cardiovascular or cerebrovascular disease.

The mazindol in Sanorex has a major potential interaction with Heart Disease.

Many CNS stimulants are contraindicated in patients with significant cardiovascular impairment such as uncompensated heart failure, severe coronary disease, severe hypertension (including that associated with hyperthyroidism or pheochromocytoma), cardiac structural abnormalities, serious arrhythmias, etc. Sudden death has been reported in patients with structural cardiac abnormalities or other serious cardiac disease who are treated with CNS stimulants at the recommended dosages for attention deficit hyperactivity disorder; use of these agents should be avoided in patients with known structural cardiac abnormalities, cardiomyopathy, serious cardiac arrhythmia, coronary artery disease, or other serious cardiac disease. Additionally, stroke, myocardial infarction, chest pain, syncope, arrhythmias, and other symptoms have been reported in adults under treatment. A careful assessment of the cardiovascular status should be done in patients being considered for treatment. This includes family history, physical exam, and further cardiac evaluation (EKG and echocardiogram). Patients who develop symptoms should have a detailed cardiac evaluation and if needed, treatment should be suspended.

The mazindol in Sanorex has a major potential interaction with High Blood Pressure.

Many CNS stimulants are contraindicated in patients with significant cardiovascular impairment such as uncompensated heart failure, severe coronary disease, severe hypertension (including that associated with hyperthyroidism or pheochromocytoma), cardiac structural abnormalities, serious arrhythmias, etc. Sudden death has been reported in patients with structural cardiac abnormalities or other serious cardiac disease who are treated with CNS stimulants at the recommended dosages for attention deficit hyperactivity disorder; use of these agents should be avoided in patients with known structural cardiac abnormalities, cardiomyopathy, serious cardiac arrhythmia, coronary artery disease, or other serious cardiac disease. Additionally, stroke, myocardial infarction, chest pain, syncope, arrhythmias, and other symptoms have been reported in adults under treatment. A careful assessment of the cardiovascular status should be done in patients being considered for treatment. This includes family history, physical exam, and further cardiac evaluation (EKG and echocardiogram). Patients who develop symptoms should have a detailed cardiac evaluation and if needed, treatment should be suspended.

The mazindol in Sanorex has a major potential interaction with High Blood Pressure.

CNS stimulants increase blood pressure and heart rate; the use of some agents may be contraindicated in patients with severe/uncontrolled hypertension. Caution should be used when administering to patients with preexisting high blood pressure (even mild hypertension) and other cardiovascular conditions. All patients under treatment should be regularly monitored for potential tachycardia and hypertension.

The mazindol in Sanorex has a major potential interaction with History - Cerebrovascular Disease.

Many amphetamines and amphetamine-like drugs are contraindicated in patients with advanced arteriosclerosis, symptomatic or unstable cardiac or cerebrovascular disease, moderate to severe hypertension, or hyperthyroidism. Like other sympathomimetic amines, amphetamines may cause cardiovascular adverse effects such as palpitation, tachycardia, cardiac arrhythmias, and elevation of blood pressure. Rarely, cardiomyopathy manifested as ventricular hypertrophy and/or congestive heart failure has been reported during chronic amphetamine use. In addition, sudden death has been reported in association with amphetamine therapy at usual dosages in children with structural cardiac abnormalities. In general, amphetamines should not be used in patients with structural cardiac abnormalities. If not otherwise contraindicated, therapy with amphetamines should be administered cautiously in patients with a current or past history of cardiovascular or cerebrovascular disease.

The mazindol in Sanorex has a major potential interaction with History - Myocardial Infarction.

Many amphetamines and amphetamine-like drugs are contraindicated in patients with advanced arteriosclerosis, symptomatic or unstable cardiac or cerebrovascular disease, moderate to severe hypertension, or hyperthyroidism. Like other sympathomimetic amines, amphetamines may cause cardiovascular adverse effects such as palpitation, tachycardia, cardiac arrhythmias, and elevation of blood pressure. Rarely, cardiomyopathy manifested as ventricular hypertrophy and/or congestive heart failure has been reported during chronic amphetamine use. In addition, sudden death has been reported in association with amphetamine therapy at usual dosages in children with structural cardiac abnormalities. In general, amphetamines should not be used in patients with structural cardiac abnormalities. If not otherwise contraindicated, therapy with amphetamines should be administered cautiously in patients with a current or past history of cardiovascular or cerebrovascular disease.

The mazindol in Sanorex has a major potential interaction with Hyperthyroidism.

Many amphetamines and amphetamine-like drugs are contraindicated in patients with advanced arteriosclerosis, symptomatic or unstable cardiac or cerebrovascular disease, moderate to severe hypertension, or hyperthyroidism. Like other sympathomimetic amines, amphetamines may cause cardiovascular adverse effects such as palpitation, tachycardia, cardiac arrhythmias, and elevation of blood pressure. Rarely, cardiomyopathy manifested as ventricular hypertrophy and/or congestive heart failure has been reported during chronic amphetamine use. In addition, sudden death has been reported in association with amphetamine therapy at usual dosages in children with structural cardiac abnormalities. In general, amphetamines should not be used in patients with structural cardiac abnormalities. If not otherwise contraindicated, therapy with amphetamines should be administered cautiously in patients with a current or past history of cardiovascular or cerebrovascular disease.

The mazindol in Sanorex has a major potential interaction with Hyperthyroidism.

Many CNS stimulants are contraindicated in patients with significant cardiovascular impairment such as uncompensated heart failure, severe coronary disease, severe hypertension (including that associated with hyperthyroidism or pheochromocytoma), cardiac structural abnormalities, serious arrhythmias, etc. Sudden death has been reported in patients with structural cardiac abnormalities or other serious cardiac disease who are treated with CNS stimulants at the recommended dosages for attention deficit hyperactivity disorder; use of these agents should be avoided in patients with known structural cardiac abnormalities, cardiomyopathy, serious cardiac arrhythmia, coronary artery disease, or other serious cardiac disease. Additionally, stroke, myocardial infarction, chest pain, syncope, arrhythmias, and other symptoms have been reported in adults under treatment. A careful assessment of the cardiovascular status should be done in patients being considered for treatment. This includes family history, physical exam, and further cardiac evaluation (EKG and echocardiogram). Patients who develop symptoms should have a detailed cardiac evaluation and if needed, treatment should be suspended.

SUFentanil has a major potential interaction with Hypotension.

Opiate agonists can induce vasodilation and significant hypotension, particularly when given in high dosages and/or by rapid intravenous administration. Opiate analgesics cause vasodilatation that may exacerbate hypotension and hypoperfusion and, therefore, are contraindicated in circulatory shock. At therapeutic analgesic dosages, ambulatory patients are more likely to experience dizziness and hypotension than patients who are confined to bed. However, orthostatic hypotension may occur in supine patients upon rising. Therapy with opiate agonists should be administered cautiously and initiated at reduced dosages in patients with hypovolemia, or a predisposition to hypotension. When given by intramuscular or subcutaneous administration, clinicians should also be aware that impaired perfusion in these patients may prevent complete absorption of the drug. With repeated injections, an excessive amount may be absorbed suddenly if normal circulation is reestablished.

The mazindol in Sanorex has a moderate potential interaction with Liver Disease.

In general, CNS stimulants are extensively metabolized by the liver. Their plasma clearance may be decreased and their half-life prolonged in patients with impaired hepatic function. Therapy with CNS stimulants should be administered cautiously in patients with moderate to severe liver disease, and the dosage should be adjusted accordingly in certain agents. Additionally, postmarketing reports have shown that atomoxetine can cause severe liver injury; laboratory testing should be done at the first sign/symptom of liver dysfunction (jaundice, dark urine, upper quadrant tenderness) and treatment should be discontinued in patients with evidence of liver injury.

SUFentanil has a moderate potential interaction with Liver Disease.

Narcotic (opioid) analgesic agents are extensively metabolized by the liver, and several of them (e.g., codeine, hydrocodone, meperidine, methadone, morphine, propoxyphene) have active metabolites that are further converted to inactive substances. The serum concentrations of these agents and their metabolites may be increased and the half-lives prolonged in patients with impaired hepatic function. Therapy with opioids should be administered cautiously and initiated at reduced dosages in patients with liver disease. Subsequent doses should be titrated based on individual response rather than a fixed dosing schedule.

The mazindol in Sanorex has a major potential interaction with Neurosis.

Some CNS stimulants are contraindicated in patients with marked agitation and/or anxiety since these symptoms may be aggravated. CNS stimulants may also exacerbate symptoms of behavior disturbance and thought disorder in psychotic patients, particularly children. Therapy with CNS stimulants should be administered cautiously in patients with a history of psychosis or a predisposition to agitated states.

The mazindol in Sanorex has a major potential interaction with Peripheral Arterial Disease.

Many CNS stimulants are contraindicated in patients with significant cardiovascular impairment such as uncompensated heart failure, severe coronary disease, severe hypertension (including that associated with hyperthyroidism or pheochromocytoma), cardiac structural abnormalities, serious arrhythmias, etc. Sudden death has been reported in patients with structural cardiac abnormalities or other serious cardiac disease who are treated with CNS stimulants at the recommended dosages for attention deficit hyperactivity disorder; use of these agents should be avoided in patients with known structural cardiac abnormalities, cardiomyopathy, serious cardiac arrhythmia, coronary artery disease, or other serious cardiac disease. Additionally, stroke, myocardial infarction, chest pain, syncope, arrhythmias, and other symptoms have been reported in adults under treatment. A careful assessment of the cardiovascular status should be done in patients being considered for treatment. This includes family history, physical exam, and further cardiac evaluation (EKG and echocardiogram). Patients who develop symptoms should have a detailed cardiac evaluation and if needed, treatment should be suspended.

The mazindol in Sanorex has a major potential interaction with Pheochromocytoma.

Many CNS stimulants are contraindicated in patients with significant cardiovascular impairment such as uncompensated heart failure, severe coronary disease, severe hypertension (including that associated with hyperthyroidism or pheochromocytoma), cardiac structural abnormalities, serious arrhythmias, etc. Sudden death has been reported in patients with structural cardiac abnormalities or other serious cardiac disease who are treated with CNS stimulants at the recommended dosages for attention deficit hyperactivity disorder; use of these agents should be avoided in patients with known structural cardiac abnormalities, cardiomyopathy, serious cardiac arrhythmia, coronary artery disease, or other serious cardiac disease. Additionally, stroke, myocardial infarction, chest pain, syncope, arrhythmias, and other symptoms have been reported in adults under treatment. A careful assessment of the cardiovascular status should be done in patients being considered for treatment. This includes family history, physical exam, and further cardiac evaluation (EKG and echocardiogram). Patients who develop symptoms should have a detailed cardiac evaluation and if needed, treatment should be suspended.

SUFentanil has a major potential interaction with Prematurity/Underweight in Infancy.

The use of narcotic (opioid) analgesic agents is contraindicated in premature infants. These agents may cross the immature blood-brain barrier to a greater extent than in adults, resulting in disproportionate respiratory depression.

The mazindol in Sanorex has a major potential interaction with Psychosis.

The use of CNS stimulants can cause psychotic symptoms, suicidal ideation, and aggression, and can exacerbate symptoms of behavior disturbance and thought disorder; CNS stimulants may induce a manic or mixed episode in patients with bipolar disorder. Psychiatric symptoms have been reported in patients with and without history of psychiatric disorders. All patients (particularly those with psychotic or bipolar disorders) should be monitored closely, especially during treatment initiation and at times of dose changes. Extreme caution should be exercised when CNS stimulants are given to patients with a history of psychosis, depression, mania, or bipolar disorder. Prior to initiating therapy, all patients should be screened for risk factors for developing a manic episode (e.g., comorbid or history of depressive symptoms or family history of suicide, bipolar disease, or depression). If any psychiatric symptoms emerge or are exacerbated, treatment suspension should be considered. Some CNS stimulants are contraindicated in patients with marked agitation or anxiety.

The mazindol in Sanorex has a major potential interaction with Psychosis.

Some CNS stimulants are contraindicated in patients with marked agitation and/or anxiety since these symptoms may be aggravated. CNS stimulants may also exacerbate symptoms of behavior disturbance and thought disorder in psychotic patients, particularly children. Therapy with CNS stimulants should be administered cautiously in patients with a history of psychosis or a predisposition to agitated states.

SUFentanil has a major potential interaction with Pulmonary Impairment.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

The mazindol in Sanorex has a moderate potential interaction with Renal Dysfunction.

Overall CNS stimulants should be administered with caution in patients with significantly impaired renal function as the reduction in the rate of elimination may alter the therapeutic response. The dosage should be adjusted accordingly in certain agents.

SUFentanil has a moderate potential interaction with Renal Dysfunction.

Although narcotic (opioid) analgesic agents are generally metabolized by the liver, renal impairment can alter the elimination of these agents and their metabolites (some of which are pharmacologically active), resulting in drug accumulation and increased risk of toxicity. Therapy with opioids should be administered cautiously and initiated at reduced dosages in patients with significantly impaired renal function. Subsequent doses should be titrated based on individual response rather than a fixed dosing schedule.

SUFentanil has a major potential interaction with Respiratory Arrest.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

The mazindol in Sanorex has a moderate potential interaction with Seizures.

Due to general central nervous system stimulation, therapy with CNS stimulant drugs may cause seizures. These drugs may lower the convulsive threshold in patients with history of seizures, with prior electroencephalogram (EEG) abnormalities without seizures, and very rarely, without history of seizures and no prior EEG evidence of seizures. Therapy with CNS stimulants should be used with caution in patients with or predisposed to seizures. If seizures occur, therapy should be discontinued.

SUFentanil 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).

SUFentanil has a major potential interaction with Shock.

Opiate agonists can induce vasodilation and significant hypotension, particularly when given in high dosages and/or by rapid intravenous administration. Opiate analgesics cause vasodilatation that may exacerbate hypotension and hypoperfusion and, therefore, are contraindicated in circulatory shock. At therapeutic analgesic dosages, ambulatory patients are more likely to experience dizziness and hypotension than patients who are confined to bed. However, orthostatic hypotension may occur in supine patients upon rising. Therapy with opiate agonists should be administered cautiously and initiated at reduced dosages in patients with hypovolemia, or a predisposition to hypotension. When given by intramuscular or subcutaneous administration, clinicians should also be aware that impaired perfusion in these patients may prevent complete absorption of the drug. With repeated injections, an excessive amount may be absorbed suddenly if normal circulation is reestablished.

The mazindol in Sanorex has a major potential interaction with Tic Disorder.

CNS stimulants have been reported to worsen Tourette's syndrome and exacerbate motor and verbal tics. Before initiating therapy, it is recommended to assess family history and clinically evaluate patients for tics or Tourette's syndrome. Therapy with CNS stimulants, if necessary, should be administered cautiously in patients with tic disorders or family history of Tourette's syndrome. The manufacturers of the CNS stimulants, methylphenidate (racemic) and dexmethylphenidate (the more pharmacologically active d-enantiomer), consider their use to be contraindicated in such patients.

The mazindol in Sanorex has a moderate potential interaction with Type 2 Diabetes.

Obese, type 2 diabetic patients who achieve weight loss may demonstrate improved metabolic control of their disease as a result of their reduced weight. Therefore, patients with type 2 diabetes mellitus should be monitored during weight-reduction therapy (or therapy that may be expected to induce significant weight loss as a secondary effect) for hypoglycemia and reduced need for oral hypoglycemic medication or insulin, and the dosages of these agents adjusted accordingly. Patients should be apprised of the risk of hypoglycemia and be alert to potential signs and symptoms such as headache, dizziness, drowsiness, nervousness, confusion, tremor, hunger, weakness, perspiration, and palpitation.

SUFentanil has a moderate potential interaction with Urinary Retention.

Narcotic (opioid) analgesic agents may inhibit the urinary voiding reflex and increase the tone of the vesical sphincter in the bladder. Acute urinary retention requiring catheterization may occur, particularly in patients with prostatic hypertrophy or urethral stricture and in older adult patients. These agents may also decrease urine production via direct effects on the kidney and central stimulation of the release of vasopressin. Therapy with opioids should be administered cautiously in patients with or predisposed to urinary retention and/or oliguria. The effects on smooth muscle tone appear to be the most pronounced with morphine.