Can you take Dezocine with Duloxetine?

Dezocine has a major potential interaction with Acute Alcohol Intoxication.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; 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 opioid partial 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 routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

Dezocine 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.

Dezocine has a major potential interaction with Alcoholism.

Opioid partial agonists have the potential to cause dependence and abuse, particularly in patients with a history of drug abuse. Tolerance as well as physical and psychological dependence can develop after prolonged use, and abrupt cessation or a significant reduction in dosage may precipitate withdrawal symptoms. Because of their opioid antagonistic effect, withdrawal symptoms may also occur if opioid partial agonists are administered to patients with an opioid dependence or in whom substantial amounts of narcotics have recently been administered. Therapy with opioid partial agonists is not recommended in patients who are physically dependent on narcotics. Addiction-prone individuals, such as those with a history of alcohol or substance abuse, should be under careful surveillance or medical supervision when treated with opioid partial agonists. It may be prudent to refrain from dispensing large quantities of medication to these patients. After prolonged use or if dependency is suspected, withdrawal of opioid therapy should be undertaken gradually using a dosage-tapering schedule.

Dezocine has a major potential interaction with Altered Consciousness.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; 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 opioid partial 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 routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

Dezocine has a major potential interaction with Asphyxia.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; 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 opioid partial 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 routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

Dezocine 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.

DULoxetine has a major potential interaction with Bipolar Disorder.

Adult and pediatric patients with depression and other psychiatric disorders may experience worsening of their symptoms and may have the emergence of suicidal thoughts and behavior. Patients should be monitored appropriately and observed closely for worsening of their symptoms, suicidality or changes in their behavior, especially during the first few months of treatment, and at times of dose changes. Discontinuing the medication should be considered if symptoms are persistently worse, or abrupt in onset. It may be prudent to refrain from dispensing large quantities of medication to these patients.

DULoxetine has a moderate potential interaction with Bipolar Disorder.

Therapy with SNRI antidepressants can cause activation of mania and hypomania and should be used with caution in patients with personal or family history of mania, hypomania, bipolar disorder, and other mood disorders.

Dezocine 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.

Dezocine has a major potential interaction with Brain Tumor.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; 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 opioid partial 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 routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

Dezocine 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.

Dezocine has a major potential interaction with Cerebral Vascular Disorder.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; 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 opioid partial 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 routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

Dezocine has a major potential interaction with Constipation.

Narcotic (opioid) analgesic agents increase smooth muscle tone in the gastrointestinal tract and decrease peristalsis, which can lead to elevated intraluminal pressure, spasm, and constipation following prolonged use. In patients with severe or acute inflammatory bowel disease, the decrease in colonic motility may induce toxic megacolon. Therapy with opioids should be administered cautiously in patients with gastrointestinal obstruction, constipation, inflammatory bowel disease, or recent gastrointestinal tract surgery. Gastrointestinal effects appear to be the most pronounced with morphine.

DULoxetine has a moderate potential interaction with Dehydration.

Treatment with SNRI antidepressants can cause hyponatremia. Caution should be used when treating patients with hyponatremia or at greater risk of hyponatremia such as the elderly, patients taking diuretics or who are volume depleted.

DULoxetine has a major potential interaction with Depression.

Adult and pediatric patients with depression and other psychiatric disorders may experience worsening of their symptoms and may have the emergence of suicidal thoughts and behavior. Patients should be monitored appropriately and observed closely for worsening of their symptoms, suicidality or changes in their behavior, especially during the first few months of treatment, and at times of dose changes. Discontinuing the medication should be considered if symptoms are persistently worse, or abrupt in onset. It may be prudent to refrain from dispensing large quantities of medication to these patients.

DULoxetine has a moderate potential interaction with Diabetes Mellitus.

In clinical trials, treatment with duloxetine delayed-release worsened the glycemic control in some patients with diabetes. Caution should be used when using duloxetine in diabetic patients and their glycemic levels should be checked regularly.

Dezocine has a major potential interaction with Drug Dependence.

Opioid partial agonists have the potential to cause dependence and abuse, particularly in patients with a history of drug abuse. Tolerance as well as physical and psychological dependence can develop after prolonged use, and abrupt cessation or a significant reduction in dosage may precipitate withdrawal symptoms. Because of their opioid antagonistic effect, withdrawal symptoms may also occur if opioid partial agonists are administered to patients with an opioid dependence or in whom substantial amounts of narcotics have recently been administered. Therapy with opioid partial agonists is not recommended in patients who are physically dependent on narcotics. Addiction-prone individuals, such as those with a history of alcohol or substance abuse, should be under careful surveillance or medical supervision when treated with opioid partial agonists. It may be prudent to refrain from dispensing large quantities of medication to these patients. After prolonged use or if dependency is suspected, withdrawal of opioid therapy should be undertaken gradually using a dosage-tapering schedule.

Dezocine 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.

Dezocine has a major potential interaction with Gastrointestinal Obstruction.

Narcotic (opioid) analgesic agents increase smooth muscle tone in the gastrointestinal tract and decrease peristalsis, which can lead to elevated intraluminal pressure, spasm, and constipation following prolonged use. In patients with severe or acute inflammatory bowel disease, the decrease in colonic motility may induce toxic megacolon. Therapy with opioids should be administered cautiously in patients with gastrointestinal obstruction, constipation, inflammatory bowel disease, or recent gastrointestinal tract surgery. Gastrointestinal effects appear to be the most pronounced with morphine.

Dezocine has a major potential interaction with Gastrointestinal Obstruction.

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

DULoxetine has a moderate potential interaction with Glaucoma, Narrow Angle.

SNRI antidepressants cause pupillary dilation that may trigger an angle closure attack in patients with anatomically narrow angle without iridectomy.

Dezocine has a major potential interaction with Head Injury.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; 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 opioid partial 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 routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

Dezocine 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.

DULoxetine has a moderate potential interaction with High Blood Pressure.

Selective serotonin and norepinephrine reuptake inhibitor antidepressants (SNRIs) have been associated with sustained increases in blood pressure. Therapy with SNRI antidepressants should be administered cautiously in patients with preexisting hypertension. Blood pressure should be assessed prior to initiating treatment and monitored regularly. The dose should be reduced or discontinued if necessary.

DULoxetine has a moderate potential interaction with Hyponatremia.

Treatment with SNRI antidepressants can cause hyponatremia. Caution should be used when treating patients with hyponatremia or at greater risk of hyponatremia such as the elderly, patients taking diuretics or who are volume depleted.

Dezocine has a major potential interaction with Infectious Gastroenteritis.

Narcotic (opioid) analgesic agents may prolong and/or worsen diarrhea associated with organisms that invade the intestinal mucosa, such as toxigenic Escherichia coli, Salmonella, Shigella, and pseudomembranous colitis due to broad-spectrum antibiotics. These agents decrease gastrointestinal motility, which may delay the excretion of infective gastroenteric organisms and/or their toxins. Other symptoms and complications such as fever, shedding of organisms, and extraintestinal illness may also be increased or prolonged. Therapy with opioids should be avoided or administered cautiously in patients with infectious diarrhea, particularly that due to pseudomembranous enterocolitis or enterotoxin-producing bacteria or if accompanied by high fever, pus, or blood in the stool.

Dezocine has a major potential interaction with Inflammatory Bowel Disease.

Narcotic (opioid) analgesic agents increase smooth muscle tone in the gastrointestinal tract and decrease peristalsis, which can lead to elevated intraluminal pressure, spasm, and constipation following prolonged use. In patients with severe or acute inflammatory bowel disease, the decrease in colonic motility may induce toxic megacolon. Therapy with opioids should be administered cautiously in patients with gastrointestinal obstruction, constipation, inflammatory bowel disease, or recent gastrointestinal tract surgery. Gastrointestinal effects appear to be the most pronounced with morphine.

Dezocine has a major potential interaction with Intestinal Anastomoses.

Narcotic (opioid) analgesic agents increase smooth muscle tone in the gastrointestinal tract and decrease peristalsis, which can lead to elevated intraluminal pressure, spasm, and constipation following prolonged use. In patients with severe or acute inflammatory bowel disease, the decrease in colonic motility may induce toxic megacolon. Therapy with opioids should be administered cautiously in patients with gastrointestinal obstruction, constipation, inflammatory bowel disease, or recent gastrointestinal tract surgery. Gastrointestinal effects appear to be the most pronounced with morphine.

Dezocine has a major potential interaction with Ischemic Heart Disease.

Opioid partial agonists may increase systemic and pulmonary arterial pressure and systemic vascular resistance, particularly when given by IV administration. Data are available for pentazocine and butorphanol. Therapy with opioid partial agonists should be administered cautiously and only if the benefit justifies the risk in patients with acute myocardial infarction (especially if accompanied by hypertension or left ventricular failure) or coronary insufficiency.

DULoxetine has a major potential interaction with Liver Disease.

Postmarketing studies have reported that duloxetine and some other SNRIs like milnacipran may aggravate preexisting liver disease. The use of duloxetine delayed-release and milnacipran should be avoided in patients with chronic liver disease or cirrhosis.

Dezocine 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.

DULoxetine has a moderate potential interaction with Mania.

Therapy with SNRI antidepressants can cause activation of mania and hypomania and should be used with caution in patients with personal or family history of mania, hypomania, bipolar disorder, and other mood disorders.

Dezocine 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.

Dezocine 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.

Dezocine has a major potential interaction with Pulmonary Impairment.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; 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 opioid partial 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 routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

DULoxetine has a major potential interaction with Renal Dysfunction.

The use of duloxetine should be avoided in patients with severe renal impairment (GFR <30 mL/min).

Dezocine 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.

Dezocine has a major potential interaction with Respiratory Arrest.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; 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 opioid partial 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 routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

Dezocine 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).

DULoxetine has a moderate potential interaction with Seizures.

SNRI antidepressants may trigger seizures and should be administered with caution in patients with a seizure disorder.

Dezocine 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.

DULoxetine has a moderate potential interaction with Urinary Tract Infection.

SNRI antidepressants have a noradrenergic effect and can affect urethral resistance. Caution should be used in patients with a history of dysuria, prostatic hypertrophy, prostatitis, and other lower urinary tract obstructive disorders.

DULoxetine has a moderate potential interaction with Urinary Tract Obstruction.

SNRI antidepressants have a noradrenergic effect and can affect urethral resistance. Caution should be used in patients with a history of dysuria, prostatic hypertrophy, prostatitis, and other lower urinary tract obstructive disorders.