Can you take Sodium phenylbutyrate / taurursodiol with Thioridazine?

Thioridazine has a major potential interaction with Abnormal Electrocardiogram.

The use of thioridazine is contraindicated in patients with congenital or acquired QT interval prolongation syndromes or a history of cardiac arrhythmias. Thioridazine can prolong the QT interval of the electrocardiogram in a dose-related manner. The risk of torsade de pointes is progressively increased as the degree of prolongation becomes greater. In a crossover study of nine patients, a single 50 mg dose of thioridazine increased the QTc interval by a mean maximum of 23 msec compared to placebo. During postmarketing experience, torsade de pointes and sudden death have been reported, although a causal relationship has not been determined. The manufacturer states that thioridazine should not be administered in patients with a baseline QTc interval greater than 450 msec, and that it should be discontinued in patients with QTc measurements exceeding 500 msec during therapy. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of thioridazine on the QT interval and should be corrected prior to institution of therapy. Patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with thioridazine.

Thioridazine has a major potential interaction with Acute Alcohol Intoxication.

Phenothiazines are contraindicated in the presence of large amounts of central nervous system depressants such as alcohol. The risk of suicide and the danger of overdose may be increased in patients who use alcohol excessively. Phenothiazines should be used with caution in patients experiencing alcohol withdrawal.

Thioridazine has a major potential interaction with Alcoholism.

Phenothiazines are contraindicated in the presence of large amounts of central nervous system depressants such as alcohol. The risk of suicide and the danger of overdose may be increased in patients who use alcohol excessively. Phenothiazines should be used with caution in patients experiencing alcohol withdrawal.

Thioridazine has a major potential interaction with Altered Consciousness.

The use of phenothiazines is contraindicated in comatose patients and patients with severe central nervous system depression. Phenothiazines may potentiate the CNS and respiratory depression in these patients.

Thioridazine has a major potential interaction with Arrhythmia.

The use of thioridazine is contraindicated in patients with congenital or acquired QT interval prolongation syndromes or a history of cardiac arrhythmias. Thioridazine can prolong the QT interval of the electrocardiogram in a dose-related manner. The risk of torsade de pointes is progressively increased as the degree of prolongation becomes greater. In a crossover study of nine patients, a single 50 mg dose of thioridazine increased the QTc interval by a mean maximum of 23 msec compared to placebo. During postmarketing experience, torsade de pointes and sudden death have been reported, although a causal relationship has not been determined. The manufacturer states that thioridazine should not be administered in patients with a baseline QTc interval greater than 450 msec, and that it should be discontinued in patients with QTc measurements exceeding 500 msec during therapy. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of thioridazine on the QT interval and should be corrected prior to institution of therapy. Patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with thioridazine.

Thioridazine has a major potential interaction with Arrhythmia.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

The taurursodiol in sodium phenylbutyrate / taurursodiol has a moderate potential interaction with Biliary Obstruction.

Sodium phenylbutyrate-taurursodiol contains taurursodiol, a bile acid. In patients with disorders that interfere with bile acid circulation, there may be an increased risk for diarrhea and patients should be monitored appropriately. Other conditions such as pancreatic insufficiency, intestinal malabsorption, or intestinal diseases that may alter the concentration of bile acids, may also lead to decreased absorption of this drug and its components. Consider consulting with a GI specialists with experience managing these GI disorders. Patients with disorders of enterohepatic circulation (e.g., biliary infection, active cholecystitis, etc.), severe pancreatic disorders (e.g., pancreatitis), and intestinal disorders that may alter concentrations of bile acids (e.g., ileal resection, regional ileitis, etc.) were excluded from clinical studies and there is no experience in patients with these conditions. Caution is advised.

Thioridazine has a major potential interaction with Bone Marrow Depression/Low Blood Counts.

Phenothiazines may cause hematologic toxicity. In patients with preexisting blood dyscrasias, bone marrow suppression, or a history of drug-induced leukopenia or neutropenia, phenothiazines should not be used or are contraindicated. Complete blood counts should be regularly monitored in patients with risk factors for blood dyscrasias. If white blood cell counts indicate cellular depression, discontinue treatment and institute appropriate therapy.

Thioridazine has a moderate potential interaction with Breast Cancer.

The chronic use of phenothiazines is associated with persistent elevations in prolactin levels. The clinical significance in patients with a history of breast cancer is unknown and should be considered prior to therapy; approximately one-third of human breast cancers are thought to be prolactin-dependent. Chronic administration of neuroleptic drugs has been associated with mammary tumorigenesis in animal studies; however, evidence is inconclusive in humans.

Thioridazine has a major potential interaction with Cardiovascular Conditions and Disorders.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

The sodium phenylbutyrate in sodium phenylbutyrate / taurursodiol has a moderate potential interaction with Central Nervous System Disorders.

Sodium phenylbutyrate is a pro-drug and is rapidly metabolized to the active, phenylacetate. Neurotoxicity, including exacerbation of a preexisting neuropathy, has been reported with the use of intravenous phenylacetate. The acute onset and reversibility when the phenylacetate infusion was discontinued suggested a drug effect. Care should be exercised when prescribing sodium phenylbutyrate to patients at risk for neurotoxicity.

Thioridazine has a moderate potential interaction with Central Nervous System Disorders.

Phenothiazines can lower the seizure threshold. Caution is recommended during administration in patients with a history of convulsive disorders or EEG abnormalities. Anticonvulsant therapy should be maintained or adequately adjusted during phenothiazine treatment.

Thioridazine has a major potential interaction with Cerebrovascular Insufficiency.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

Thioridazine has a major potential interaction with Dementia.

Antipsychotic drugs are not approved for the treatment of patients with dementia-related psychosis. Older patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death; although the causes were varied, most of the deaths appeared to be either cardiovascular (e.g., heart failure, sudden death) or infectious (e.g., pneumonia) in nature. A causal relationship with antipsychotic use has not been established. In controlled trials in older patients with dementia-related psychosis, patients randomized to risperidone, aripiprazole, and olanzapine had higher incidence of cerebrovascular adverse events (e.g., stroke, transient ischemic attack), including fatalities, compared to patients treated with placebo.

Thioridazine has a major potential interaction with Diarrhea.

The use of thioridazine is contraindicated in patients with congenital or acquired QT interval prolongation syndromes or a history of cardiac arrhythmias. Thioridazine can prolong the QT interval of the electrocardiogram in a dose-related manner. The risk of torsade de pointes is progressively increased as the degree of prolongation becomes greater. In a crossover study of nine patients, a single 50 mg dose of thioridazine increased the QTc interval by a mean maximum of 23 msec compared to placebo. During postmarketing experience, torsade de pointes and sudden death have been reported, although a causal relationship has not been determined. The manufacturer states that thioridazine should not be administered in patients with a baseline QTc interval greater than 450 msec, and that it should be discontinued in patients with QTc measurements exceeding 500 msec during therapy. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of thioridazine on the QT interval and should be corrected prior to institution of therapy. Patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with thioridazine.

Thioridazine has a major potential interaction with Electrolyte Abnormalities.

The use of thioridazine is contraindicated in patients with congenital or acquired QT interval prolongation syndromes or a history of cardiac arrhythmias. Thioridazine can prolong the QT interval of the electrocardiogram in a dose-related manner. The risk of torsade de pointes is progressively increased as the degree of prolongation becomes greater. In a crossover study of nine patients, a single 50 mg dose of thioridazine increased the QTc interval by a mean maximum of 23 msec compared to placebo. During postmarketing experience, torsade de pointes and sudden death have been reported, although a causal relationship has not been determined. The manufacturer states that thioridazine should not be administered in patients with a baseline QTc interval greater than 450 msec, and that it should be discontinued in patients with QTc measurements exceeding 500 msec during therapy. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of thioridazine on the QT interval and should be corrected prior to institution of therapy. Patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with thioridazine.

The sodium phenylbutyrate in sodium phenylbutyrate / taurursodiol has a major potential interaction with Fluid Retention.

The use of sodium phenylbutyrate may cause fluid retention in patients with congestive heart failure, renal dysfunction, or sodium retention with edema. Sodium phenylbutyrate is primarily excreted by the kidney and these patients may exhibit reduced excretion. Therapy with sodium phenylbutyrate should be administered cautiously in these patients. Monitoring plasma levels of ammonia, arginine, branched-chain amino acids and serum proteins to maintain within normal limits and glutamine to less than 1000 mcmol/L is recommended.

The taurursodiol in sodium phenylbutyrate / taurursodiol has a moderate potential interaction with Gallbladder Disease.

Sodium phenylbutyrate-taurursodiol contains taurursodiol, a bile acid. In patients with disorders that interfere with bile acid circulation, there may be an increased risk for diarrhea and patients should be monitored appropriately. Other conditions such as pancreatic insufficiency, intestinal malabsorption, or intestinal diseases that may alter the concentration of bile acids, may also lead to decreased absorption of this drug and its components. Consider consulting with a GI specialists with experience managing these GI disorders. Patients with disorders of enterohepatic circulation (e.g., biliary infection, active cholecystitis, etc.), severe pancreatic disorders (e.g., pancreatitis), and intestinal disorders that may alter concentrations of bile acids (e.g., ileal resection, regional ileitis, etc.) were excluded from clinical studies and there is no experience in patients with these conditions. Caution is advised.

The sodium phenylbutyrate in sodium phenylbutyrate / taurursodiol has a major potential interaction with Heart Failure.

The use of sodium phenylbutyrate may cause fluid retention in patients with congestive heart failure, renal dysfunction, or sodium retention with edema. Sodium phenylbutyrate is primarily excreted by the kidney and these patients may exhibit reduced excretion. Therapy with sodium phenylbutyrate should be administered cautiously in these patients. Monitoring plasma levels of ammonia, arginine, branched-chain amino acids and serum proteins to maintain within normal limits and glutamine to less than 1000 mcmol/L is recommended.

Thioridazine has a major potential interaction with High Blood Pressure.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

Thioridazine has a major potential interaction with History - Cerebrovascular Disease.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

Thioridazine has a major potential interaction with History - Myocardial Infarction.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

Thioridazine has a major potential interaction with Hypokalemia.

The use of thioridazine is contraindicated in patients with congenital or acquired QT interval prolongation syndromes or a history of cardiac arrhythmias. Thioridazine can prolong the QT interval of the electrocardiogram in a dose-related manner. The risk of torsade de pointes is progressively increased as the degree of prolongation becomes greater. In a crossover study of nine patients, a single 50 mg dose of thioridazine increased the QTc interval by a mean maximum of 23 msec compared to placebo. During postmarketing experience, torsade de pointes and sudden death have been reported, although a causal relationship has not been determined. The manufacturer states that thioridazine should not be administered in patients with a baseline QTc interval greater than 450 msec, and that it should be discontinued in patients with QTc measurements exceeding 500 msec during therapy. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of thioridazine on the QT interval and should be corrected prior to institution of therapy. Patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with thioridazine.

Thioridazine has a major potential interaction with Hypotension.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

Thioridazine has a major potential interaction with Liver Disease.

Therapy with phenothiazines should be administered cautiously or are contraindicated in patients with preexisting liver disease or with a history of jaundice due to phenothiazine hypersensitivity. Patients with a history of hepatic encephalopathy due to cirrhosis may have increased sensitivity to the central nervous system effects of some phenothiazines (e.g., chlorpromazine). Treatment should be discontinued if jaundice occurs.

The sodium phenylbutyrate in sodium phenylbutyrate / taurursodiol has a moderate potential interaction with Liver Disease.

Sodium phenylbutyrate is primarily metabolized in the liver and kidney. Therapy with sodium phenylbutyrate should be administered cautiously in patients with liver disease. Monitoring plasma levels of ammonia, arginine, branched-chain amino acids and serum proteins to maintain within normal limits and glutamine to less than 1000 mcmol/L is recommended.

Thioridazine has a major potential interaction with Magnesium Imbalance.

The use of thioridazine is contraindicated in patients with congenital or acquired QT interval prolongation syndromes or a history of cardiac arrhythmias. Thioridazine can prolong the QT interval of the electrocardiogram in a dose-related manner. The risk of torsade de pointes is progressively increased as the degree of prolongation becomes greater. In a crossover study of nine patients, a single 50 mg dose of thioridazine increased the QTc interval by a mean maximum of 23 msec compared to placebo. During postmarketing experience, torsade de pointes and sudden death have been reported, although a causal relationship has not been determined. The manufacturer states that thioridazine should not be administered in patients with a baseline QTc interval greater than 450 msec, and that it should be discontinued in patients with QTc measurements exceeding 500 msec during therapy. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of thioridazine on the QT interval and should be corrected prior to institution of therapy. Patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with thioridazine.

The taurursodiol in sodium phenylbutyrate / taurursodiol has a moderate potential interaction with Malabsorption Syndrome.

Sodium phenylbutyrate-taurursodiol contains taurursodiol, a bile acid. In patients with disorders that interfere with bile acid circulation, there may be an increased risk for diarrhea and patients should be monitored appropriately. Other conditions such as pancreatic insufficiency, intestinal malabsorption, or intestinal diseases that may alter the concentration of bile acids, may also lead to decreased absorption of this drug and its components. Consider consulting with a GI specialists with experience managing these GI disorders. Patients with disorders of enterohepatic circulation (e.g., biliary infection, active cholecystitis, etc.), severe pancreatic disorders (e.g., pancreatitis), and intestinal disorders that may alter concentrations of bile acids (e.g., ileal resection, regional ileitis, etc.) were excluded from clinical studies and there is no experience in patients with these conditions. Caution is advised.

The sodium phenylbutyrate in sodium phenylbutyrate / taurursodiol has a moderate potential interaction with Myoneural Disorder.

Sodium phenylbutyrate is a pro-drug and is rapidly metabolized to the active, phenylacetate. Neurotoxicity, including exacerbation of a preexisting neuropathy, has been reported with the use of intravenous phenylacetate. The acute onset and reversibility when the phenylacetate infusion was discontinued suggested a drug effect. Care should be exercised when prescribing sodium phenylbutyrate to patients at risk for neurotoxicity.

Thioridazine has a moderate potential interaction with Neuroleptic Malignant Syndrome.

Therapy with phenothiazines may precipitate or aggravate a potentially fatal symptom complex known as neuroleptic malignant syndrome (NMS). Treatment should not be initiated in patients with active NMS, and should be immediately discontinued if currently administered in such patients. In patients with a history of NMS, introduction or reintroduction of phenothiazines should be carefully considered, since NMS may recur.

The sodium phenylbutyrate in sodium phenylbutyrate / taurursodiol has a moderate potential interaction with Peripheral Neuropathy.

Sodium phenylbutyrate is a pro-drug and is rapidly metabolized to the active, phenylacetate. Neurotoxicity, including exacerbation of a preexisting neuropathy, has been reported with the use of intravenous phenylacetate. The acute onset and reversibility when the phenylacetate infusion was discontinued suggested a drug effect. Care should be exercised when prescribing sodium phenylbutyrate to patients at risk for neurotoxicity.

Thioridazine has a major potential interaction with Pheochromocytoma.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

The sodium phenylbutyrate in sodium phenylbutyrate / taurursodiol has a major potential interaction with Renal Dysfunction.

The use of sodium phenylbutyrate may cause fluid retention in patients with congestive heart failure, renal dysfunction, or sodium retention with edema. Sodium phenylbutyrate is primarily excreted by the kidney and these patients may exhibit reduced excretion. Therapy with sodium phenylbutyrate should be administered cautiously in these patients. Monitoring plasma levels of ammonia, arginine, branched-chain amino acids and serum proteins to maintain within normal limits and glutamine to less than 1000 mcmol/L is recommended.

The sodium phenylbutyrate in sodium phenylbutyrate / taurursodiol has a moderate potential interaction with Renal Dysfunction.

Sodium phenylbutyrate is primarily metabolized in the liver and kidney. Therapy with sodium phenylbutyrate should be administered cautiously in patients with liver disease. Monitoring plasma levels of ammonia, arginine, branched-chain amino acids and serum proteins to maintain within normal limits and glutamine to less than 1000 mcmol/L is recommended.

Thioridazine has a major potential interaction with Respiratory Arrest.

The use of phenothiazines is contraindicated in comatose patients and patients with severe central nervous system depression. Phenothiazines may potentiate the CNS and respiratory depression in these patients.

Thioridazine has a moderate potential interaction with Seizures.

Phenothiazines can lower the seizure threshold. Caution is recommended during administration in patients with a history of convulsive disorders or EEG abnormalities. Anticonvulsant therapy should be maintained or adequately adjusted during phenothiazine treatment.

Thioridazine has a major potential interaction with Valvular Heart Disease.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.