Can you take Crizotinib with Sodium phenylbutyrate / taurursodiol?

Crizotinib has a moderate potential interaction with Arrhythmia.

The use of crizotinib can cause QTc prolongation. It is recommended to avoid the use of this agent in patients with congenital long QT syndrome. Care should be exercised when using this drug in patients with a history of or predisposition to QTc prolongation. ECGs and electrolytes should be monitored in patients with congestive heart failure, bradyarrhythmias, electrolyte abnormalities, or who are taking medications that prolong the QT interval. It is recommended to withhold, reduce dose, or permanently discontinue crizotinib for QT/QTc interval prolongation as recommended.

Crizotinib has a moderate potential interaction with Arrhythmia.

Crizotinib can cause symptomatic bradycardia. Heart rate and blood pressure should be monitored regularly. It is recommended to withhold, reduce dose, or permanently discontinue crizotinib for bradycardia as recommended.

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.

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.

Crizotinib has a moderate potential interaction with Diverticulitis.

The use of crizotinib can cause gastrointestinal (GI) perforations. This drug should be used with caution in patients at risk for GI perforation (e.g., history of diverticulitis, metastases to the gastrointestinal tract, concomitant use of medicinal products with a recognized risk of gastrointestinal perforation). It is recommended to discontinue treatment in patients who develop GI perforation.

Crizotinib has a moderate potential interaction with Electrolyte Abnormalities.

The use of crizotinib can cause QTc prolongation. It is recommended to avoid the use of this agent in patients with congenital long QT syndrome. Care should be exercised when using this drug in patients with a history of or predisposition to QTc prolongation. ECGs and electrolytes should be monitored in patients with congestive heart failure, bradyarrhythmias, electrolyte abnormalities, or who are taking medications that prolong the QT interval. It is recommended to withhold, reduce dose, or permanently discontinue crizotinib for QT/QTc interval prolongation as recommended.

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.

Crizotinib has a moderate potential interaction with Gastrointestinal Obstruction.

The use of crizotinib can cause gastrointestinal (GI) perforations. This drug should be used with caution in patients at risk for GI perforation (e.g., history of diverticulitis, metastases to the gastrointestinal tract, concomitant use of medicinal products with a recognized risk of gastrointestinal perforation). It is recommended to discontinue treatment in patients who develop GI perforation.

Crizotinib has a moderate potential interaction with Gastrointestinal Perforation.

The use of crizotinib can cause gastrointestinal (GI) perforations. This drug should be used with caution in patients at risk for GI perforation (e.g., history of diverticulitis, metastases to the gastrointestinal tract, concomitant use of medicinal products with a recognized risk of gastrointestinal perforation). It is recommended to discontinue treatment in patients who develop GI perforation.

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.

Crizotinib has a moderate potential interaction with Heart Failure.

The use of crizotinib can cause QTc prolongation. It is recommended to avoid the use of this agent in patients with congenital long QT syndrome. Care should be exercised when using this drug in patients with a history of or predisposition to QTc prolongation. ECGs and electrolytes should be monitored in patients with congestive heart failure, bradyarrhythmias, electrolyte abnormalities, or who are taking medications that prolong the QT interval. It is recommended to withhold, reduce dose, or permanently discontinue crizotinib for QT/QTc interval prolongation as recommended.

Crizotinib has a moderate potential interaction with Interstitial Lung Disease.

Severe, life-threatening, or fatal interstitial lung disease (ILD)/pneumonitis can occur with crizotinib. Care should be exercised when using this drug in patients with preexisting pulmonary impairment. Patients should be monitored for pulmonary symptoms indicative of ILD/pneumonitis. Crizotinib should be permanently discontinued in patients diagnosed with drug-related ILD/pneumonitis if no other potential causes of ILD/pneumonitis have been identified.

Crizotinib has a moderate potential interaction with Liver Disease.

Crizotinib concentrations increased in patients with preexisting moderate (any AST and total bilirubin greater than 1.5 to 3 times the upper limit of normal [1.5 to 3 x ULN]) or severe (any AST and total bilirubin greater than 3 x ULN) liver dysfunction; a reduced dosage of crizotinib is recommended in these patients. Caution is recommended in patients with moderate or severe liver dysfunction. No dose adjustment is recommended in patients with preexisting mild liver dysfunction (AST greater than ULN and total bilirubin up to 1 x ULN or any AST and total bilirubin greater than 1 to 1.5 x ULN).

Cases of drug-induced hepatotoxicity with fatal outcomes have been reported with the use of crizotinib. It is recommended to monitor liver function tests (including ALT, AST, total bilirubin) every 2 weeks during the first 2 months of therapy, then once a month, and as clinically indicated, with more frequent repeat testing for increased liver transaminases, alkaline phosphatase, or total bilirubin in patients who develop increased transaminases. It is recommended to withhold, reduce dose, or permanently discontinue crizotinib for hepatotoxicity as recommended.

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.

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.

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.

Crizotinib has a moderate potential interaction with Pulmonary Impairment.

Severe, life-threatening, or fatal interstitial lung disease (ILD)/pneumonitis can occur with crizotinib. Care should be exercised when using this drug in patients with preexisting pulmonary impairment. Patients should be monitored for pulmonary symptoms indicative of ILD/pneumonitis. Crizotinib should be permanently discontinued in patients diagnosed with drug-related ILD/pneumonitis if no other potential causes of ILD/pneumonitis have been identified.

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.

Crizotinib has a moderate potential interaction with Renal Dysfunction.

The exposure to crizotinib is increased in patients with preexisting severe renal dysfunction (CrCl less than 30 mL/min [calculated using the modified Cockcroft-Gault equation for adult patients and the Schwartz equation for pediatric patients]) not requiring dialysis; a reduced dosage of crizotinib is recommended in these patients. Care should be exercised when using this drug in patients with severe renal dysfunction not requiring dialysis. No dose adjustment is recommended in patients with mild to moderate renal dysfunction (CrCl 30 to 89 mL/min).

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.

Crizotinib has a moderate potential interaction with Visual Defect/Disturbance.

Cases of optic atrophy and optic nerve disorder leading to vision loss have been reported with the use of crizotinib. Assessment of visual symptoms for all patients is recommended monthly during therapy; new visual symptoms should be reported to an eye specialist. For pediatric and young adult patients with anaplastic large cell lymphoma or inflammatory myofibroblastic tumor, baseline and follow-up ophthalmologic examinations (including retinal examination) should be obtained within 1 month of starting crizotinib and every 3 months thereafter. The ophthalmological evaluation should consist of best corrected visual acuity, retinal photographs, visual fields, optical coherence tomography (OCT), and other evaluations as appropriate. Crizotinib should be permanently discontinued for grade 3 or 4 ocular disorders or severe visual loss (best corrected vision less than 20/200 in 1 or both eyes) unless another cause is identified. There is insufficient information to characterize the risks of resumption of crizotinib in patients who develop visual symptoms or visual loss; a decision to resume treatment with crizotinib should consider the potential benefits versus risks to the patient.