Can you take Midodrine 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.

Midodrine has a major potential interaction with Diabetes Mellitus.

Midodrine can cause marked elevation of supine blood pressure (BP>200 mmHg systolic) and should not be used in patients with persistent and excessive supine hypertension. Systolic elevations of this degree are most likely to be observed in patients with relatively elevated pre-treatment systolic blood pressures (mean 170 mmHg). There is no experience in patients with initial supine systolic pressure above 180 mmHg, as those patients were excluded from the clinical trials. Use of midodrine in such patients is not recommended. Additionally, care should be taken when using this agent in orthostatic hypotensive patients who are also diabetic. Supine and sitting hypertension should be evaluated at the beginning of therapy, and blood pressure (supine, sitting, and orthostatic) should be monitored regularly.

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.

Midodrine has a major potential interaction with Heart Disease.

The use of midodrine is contraindicated in patients with severe organic heart disease, pheochromocytoma, or thyrotoxicosis.

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.

Midodrine has a major potential interaction with High Blood Pressure.

Midodrine can cause marked elevation of supine blood pressure (BP>200 mmHg systolic) and should not be used in patients with persistent and excessive supine hypertension. Systolic elevations of this degree are most likely to be observed in patients with relatively elevated pre-treatment systolic blood pressures (mean 170 mmHg). There is no experience in patients with initial supine systolic pressure above 180 mmHg, as those patients were excluded from the clinical trials. Use of midodrine in such patients is not recommended. Additionally, care should be taken when using this agent in orthostatic hypotensive patients who are also diabetic. Supine and sitting hypertension should be evaluated at the beginning of therapy, and blood pressure (supine, sitting, and orthostatic) should be monitored regularly.

Midodrine has a moderate potential interaction with Liver Disease.

Midodrine, a prodrug, undergoes bioactivation in a variety of tissues to desglymidodrine, an alpha-1 agonist. The liver functions in the metabolism of midodrine and desglymidodrine. The pharmacokinetic disposition of midodrine has not been studied in patients with hepatic impairment. Therapy with midodrine should be administered cautiously in patients with compromised hepatic function. Clinical monitoring of hepatic function prior to initiation of therapy.

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.

Midodrine has a major potential interaction with Pheochromocytoma.

The use of midodrine is contraindicated in patients with severe organic heart disease, pheochromocytoma, or thyrotoxicosis.

Midodrine has a major potential interaction with Renal Dysfunction.

The use of midodrine is contraindicated in patients with acute renal disease or urinary retention/obstruction disorder. Midodrine is primarily eliminated by the kidney as desglymidodrine (active metabolite). The serum concentration of midodrine is expected to be increased in patients with renal impairment. Desglymidodrine induces urinary retention by increasing bladder neck tone. Therapy with midodrine should be administered cautiously and initiated at 2.5 mg doses in patients with compromised renal function. Clinical monitoring of renal function prior to initiation of therapy and subsequently as appropriate and blood pressure (supine, sitting, and orthostatic) is recommended. Midodrine is removed by dialysis.

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.

Midodrine has a major potential interaction with Thyrotoxicosis.

The use of midodrine is contraindicated in patients with severe organic heart disease, pheochromocytoma, or thyrotoxicosis.

Midodrine has a major potential interaction with Urinary Retention.

The use of midodrine is contraindicated in patients with acute renal disease or urinary retention/obstruction disorder. Midodrine is primarily eliminated by the kidney as desglymidodrine (active metabolite). The serum concentration of midodrine is expected to be increased in patients with renal impairment. Desglymidodrine induces urinary retention by increasing bladder neck tone. Therapy with midodrine should be administered cautiously and initiated at 2.5 mg doses in patients with compromised renal function. Clinical monitoring of renal function prior to initiation of therapy and subsequently as appropriate and blood pressure (supine, sitting, and orthostatic) is recommended. Midodrine is removed by dialysis.