Can you take Mirabegron with Sodium phenylbutyrate / taurursodiol?

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.

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.

Mirabegron has a moderate potential interaction with High Blood Pressure.

Mirabegron can increase blood pressure. In clinical studies, the use of mirabegron was associated with dose-related increases in supine blood pressure. At the maximum recommended dose of 50 mg, the mean maximum increase in systolic/diastolic blood pressure was approximately 3.5/1.5 mmHg greater than placebo in healthy volunteers and approximately 0.5 to 1 mmHg greater than placebo in patients with overactive bladder. Worsening of preexisting hypertension was reported infrequently in patients receiving mirabegron. Therapy with mirabegron should be administered cautiously in patients with hypertension. Periodic blood pressure determinations are recommended. Mirabegron is not recommended for use in patients with severe, uncontrolled hypertension, defined as systolic blood pressure >=180 mm Hg and/or diastolic blood pressure >=110 mm Hg.

Mirabegron has a moderate potential interaction with Liver Disease.

Mirebegron is partially metabolized by the liver through multiple pathways. Following administration of a single 100 mg dose, mean mirabegron peak plasma concentration (Cmax) and systemic exposure (AUC) increased by 9% and 19%, respectively, in volunteers with mild hepatic impairment (Child-Pugh Class A) and 175% and 65%, respectively, in volunteers with moderate hepatic impairment (Child-Pugh Class B) compared to volunteers with normal hepatic function. No dosage adjustment is necessary in patients with mild hepatic impairment. In patients with moderate hepatic impairment, the daily dosage of mirabegron should not exceed 25 mg. Mirabegron has not been studied in patients with severe hepatic impairment (Child-Pugh Class C). Mirabegron is not recommended for use in these patients.

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.

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.

Mirabegron has a moderate potential interaction with Renal Dysfunction.

Mirebegron is partially eliminated by the kidney through active tubular secretion and glomerular filtration, with renal clearance accounting for approximately 25% of the total clearance. Following administration of a single 100 mg dose, mean mirabegron peak plasma concentration (Cmax) and systemic exposure (AUC) increased by 6% and 31%, respectively, in volunteers with mild renal impairment (estimated GFR 60 to 89 mL/min/1.73 m2), 23% and 66%, respectively, in volunteers with moderate renal impairment (estimated GFR 30 to 59 mL/min/1.73 m2), and 92% and 118%, respectively, in patients with severe renal impairment (estimated GFR 15 to 29 mL/min/1.73 m2) compared to volunteers with normal renal function. No dosage adjustment is necessary in patients with mild or moderate renal impairment. In patients with severe renal impairment, the daily dosage of mirabegron should not exceed 25 mg. Mirabegron has not been studied in patients with end stage renal disease (CrCl <15 mL/min or estimated GFR <15 mL/min/1.73 m2 or requirement for hemodialysis). Mirabegron is not recommended for use in these patients.

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.

Mirabegron has a moderate potential interaction with Urinary Retention.

Although an increased risk of urinary retention was not observed in a controlled clinical safety study in patients with bladder outlet obstruction, urinary retention has been reported in this population during postmarketing use. Therapy with mirabegron should be administered cautiously in patients with clinically significant bladder outlet obstruction and conditions predisposing to urinary retention.