Can you take Eplerenone 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.

Eplerenone has a major potential interaction with Hyperkalemia.

The use of eplerenone is contraindicated in the presence of elevated serum potassium concentrations (> 5.5 mEq/L). Eplerenone is a blocker of aldosterone binding at the mineralocorticoid receptor and can cause hyperkalemia, which may result in life-threatening cardiac arrhythmias. Careful monitoring of serum potassium levels is necessary in patients who are at risk for the development of hyperkalemia (including those receiving concomitant ACE inhibitors or angiotensin II receptor antagonists), especially during initiation of therapy, after dosage adjustment, and during illness that could alter renal function. In clinical trials, monitoring occurred every 2 weeks for the first 1 to 2 months, then monthly thereafter. Eplerenone should be withdrawn immediately if hyperkalemia develops, and measures should be initiated to lower serum potassium if it exceeds 6.5 mEq/L.

Eplerenone has a moderate potential interaction with Liver Disease.

Eplerenone is primarily metabolized by the liver. In patients with moderate (Child-Pugh Class B) hepatic impairment given eplerenone 400 mg, the steady-state peak plasma concentration (Cmax) and systemic exposure (AUC) of eplerenone were increased by 3.6% and 42%, respectively, compared to those in normal subjects. In 16 patients with mild to moderate hepatic impairment who received 400 mg of eplerenone, no elevations in serum potassium above 5.5 mmol/L were observed. Their mean increase in serum potassium was 0.12 mEq/L compared to 0.13 mEq/L in normal controls. No adjustment of the starting dosage is recommended for patients with mild to moderate hepatic impairment. The use of eplerenone in patients with severe hepatic impairment has not been evaluated, thus caution is advised.

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.

Eplerenone has a major potential interaction with Renal Dysfunction.

The use of eplerenone is contraindicated in patients with renal impairment as defined by serum creatinine above 2.0 mg/dL for males or 1.8 mg/dL for females, or a creatinine clearance (CrCl) below 50 mL/min. These patients are at increased risk of developing persistent hyperkalemia, which is the principal adverse effect of eplerenone and can lead to potentially life-threatening cardiac arrhythmias. The incidence of hyperkalemia increases with decreasing renal function. In clinical studies of eplerenone, serum potassium levels exceeding 5.5 mEq/L were observed in 10.4% of treated patients with baseline calculated CrCl less than 70 mL/min, 5.6% of patients with baseline CrCl 70 to 100 mL/min, and 2.6% of patients with baseline CrCl greater than 100 mL/min. Careful monitoring of serum potassium levels is necessary in patients treated with eplerenone who are at risk for the development of hyperkalemia, especially during initiation of therapy, after dosage adjustment, and during illness that could alter renal function. In clinical trials, monitoring occurred every 2 weeks for the first 1 to 2 months, then monthly thereafter. Eplerenone should be withdrawn immediately if hyperkalemia develops, and measures should be initiated to lower serum potassium if it exceeds 6.5 mEq/L.

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.

Eplerenone has a major potential interaction with Type 2 Diabetes.

The use of eplerenone is contraindicated in patients with type II diabetes mellitus and microalbuminuria. These patients are at increased risk of developing persistent hyperkalemia, which is the principal adverse effect of eplerenone and can lead to potentially life-threatening cardiac arrhythmias. In a study of such patients treated with a 200 mg/day dose, the frequency of maximum serum potassium levels exceeding 5.5 mEq/L was 33% with eplerenone alone and 38% in combination with enalapril. In other patient populations, the frequency has been reported at 1% for the 200 mg/day dose and 8.7% for the 400 mg/day dose. Careful monitoring of serum potassium levels is necessary in patients treated with eplerenone who are at risk for the development of hyperkalemia, especially during initiation of therapy, after dosage adjustment, and during illness that could alter renal function. In clinical trials, monitoring occurred every 2 weeks for the first 1 to 2 months, then monthly thereafter. Eplerenone should be withdrawn immediately if hyperkalemia develops, and measures should be initiated to lower serum potassium if it exceeds 6.5 mEq/L.