Can you take Amprenavir with Sodium phenylbutyrate / taurursodiol?

Amprenavir has a moderate potential interaction with Abnormal Glucose Tolerance.

New onset diabetes mellitus, exacerbation of preexisting diabetes mellitus, hyperglycemia, and some cases of diabetic ketoacidosis have been reported during postmarketing surveillance in HIV-infected patients treated with protease inhibitors. Some patients required either initiation or dosage adjustments of insulin or oral hypoglycemic agents for treatment of these events. In some cases, hyperglycemia persisted despite discontinuation of protease inhibitor therapy. A causal relationship has not been established between protease inhibitor therapy and these events. Monitoring patients for hyperglycemia, new onset diabetes mellitus, or exacerbation of diabetes mellitus should be considered during protease inhibitor therapy.

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.

Amprenavir has a moderate potential interaction with Dehydration.

Cases of nephrolithiasis have been reported during postmarketing surveillance in HIV-infected patients receiving amprenavir or fosamprenavir therapy. Because these events were reported voluntarily during clinical practice, estimates of frequency cannot be made. Therapy with amprenavir or fosamprenavir should be administered cautiously in patients with a current or past history of nephrolithiasis. Adequate hydration is recommended. Those who are dehydrated may be at increased risk and should be encouraged to consume additional amounts of liquid or given intravenous fluids if necessary. Patients should be instructed to seek medical attention if they experience potential signs and symptoms of urolithiasis such as flank pain, hematuria, dysuria, and urinary urgency. Temporary interruption or discontinuation of therapy may be required.

Amprenavir has a moderate potential interaction with Diabetes Mellitus.

New onset diabetes mellitus, exacerbation of preexisting diabetes mellitus, hyperglycemia, and some cases of diabetic ketoacidosis have been reported during postmarketing surveillance in HIV-infected patients treated with protease inhibitors. Some patients required either initiation or dosage adjustments of insulin or oral hypoglycemic agents for treatment of these events. In some cases, hyperglycemia persisted despite discontinuation of protease inhibitor therapy. A causal relationship has not been established between protease inhibitor therapy and these events. Monitoring patients for hyperglycemia, new onset diabetes mellitus, or exacerbation of diabetes mellitus should be considered during protease inhibitor therapy.

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.

Amprenavir has a moderate potential interaction with History, Nephrolithiasis.

Cases of nephrolithiasis have been reported during postmarketing surveillance in HIV-infected patients receiving amprenavir or fosamprenavir therapy. Because these events were reported voluntarily during clinical practice, estimates of frequency cannot be made. Therapy with amprenavir or fosamprenavir should be administered cautiously in patients with a current or past history of nephrolithiasis. Adequate hydration is recommended. Those who are dehydrated may be at increased risk and should be encouraged to consume additional amounts of liquid or given intravenous fluids if necessary. Patients should be instructed to seek medical attention if they experience potential signs and symptoms of urolithiasis such as flank pain, hematuria, dysuria, and urinary urgency. Temporary interruption or discontinuation of therapy may be required.

Amprenavir has a major potential interaction with Liver Disease.

The use of amprenavir oral solution is contraindicated in patients with renal and/or hepatic failure due to the large amount of excipient propylene glycol in the formulation. In general, use of the solution should be limited to patients in whom the capsule formulation or other protease inhibitors are not feasible options. Caution is advised in patients with renal or hepatic impairment due to increased risk of propylene glycol-associated adverse events. All patients receiving the oral solution should be monitored for signs of propylene glycol toxicity including seizures, stupor, tachycardia, hyperosmolality, lactic acidosis, renal toxicity, and hemolysis.

Amprenavir has a moderate potential interaction with Liver Disease.

Amprenavir is primarily metabolized by the liver. Patients with liver disease may be at greater risk for adverse effects from amprenavir due to decreased drug clearance. Therapy with amprenavir should be administered cautiously in patients with moderate or severe hepatic impairment, and the dosage should be reduced as follows: 450 mg (three 150 mg capsules) or 513 mg (34 mL oral solution) orally twice a day for Child-Pugh score 5 to 8; 300 mg (two 150 mg capsules) or 342 mg (23 mL oral solution) orally twice a day for Child-Pugh score 9 to 12.

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.

Amprenavir has a moderate potential interaction with Nephrolithiasis.

Cases of nephrolithiasis have been reported during postmarketing surveillance in HIV-infected patients receiving amprenavir or fosamprenavir therapy. Because these events were reported voluntarily during clinical practice, estimates of frequency cannot be made. Therapy with amprenavir or fosamprenavir should be administered cautiously in patients with a current or past history of nephrolithiasis. Adequate hydration is recommended. Those who are dehydrated may be at increased risk and should be encouraged to consume additional amounts of liquid or given intravenous fluids if necessary. Patients should be instructed to seek medical attention if they experience potential signs and symptoms of urolithiasis such as flank pain, hematuria, dysuria, and urinary urgency. Temporary interruption or discontinuation of therapy may be required.

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.

Amprenavir has a major potential interaction with Renal Dysfunction.

The use of amprenavir oral solution is contraindicated in patients with renal and/or hepatic failure due to the large amount of excipient propylene glycol in the formulation. In general, use of the solution should be limited to patients in whom the capsule formulation or other protease inhibitors are not feasible options. Caution is advised in patients with renal or hepatic impairment due to increased risk of propylene glycol-associated adverse events. All patients receiving the oral solution should be monitored for signs of propylene glycol toxicity including seizures, stupor, tachycardia, hyperosmolality, lactic acidosis, renal toxicity, and hemolysis.

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.

Amprenavir has a minor potential interaction with Vitamin K Deficiency.

Formulations of Agenerase (brand of amprenavir) provide high daily doses of vitamin E exceeding the Reference Daily Intake (adults 30 Intl units, pediatrics approximately 10 Intl units). The effects of long-term, high-dose vitamin E administration in humans are unclear. High levels of vitamin E may exacerbate the blood coagulation defect of vitamin K deficiency caused by anticoagulant therapy or malabsorption.