Can you take Bitolterol with Nilotinib?

Nilotinib has a moderate potential interaction with Cardiovascular Conditions and Disorders.

Cardiovascular events (including arterial vascular occlusive events, peripheral arterial occlusive disease, and ischemic cerebrovascular events) have been reported in patients receiving BCR-ABL tyrosine kinase inhibitors. Patients should seek immediate medical attention if acute signs or symptoms of cardiovascular events occur. Cardiovascular status should be evaluated, and cardiovascular risk factors should be monitored and actively managed during treatment.

Bitolterol has a moderate potential interaction with Diabetes Mellitus.

Adrenergic bronchodilators may cause increases in blood glucose concentrations. These effects are usually transient and slight, but may be significant with dosages higher than those normally recommended. Large doses of IV albuterol (not commercially available in the U.S.) and terbutaline sulfate have been reported to cause exacerbation of preexisting diabetes mellitus and ketoacidosis. Therapy with adrenergic bronchodilators should be administered cautiously in patients with diabetes mellitus. Closer monitoring of blood glucose concentrations may be appropriate. Systemic adverse effects are minimized, but not abolished, by administration of these agents via oral inhalation.

Nilotinib has a moderate potential interaction with Electrolyte Abnormalities.

Nilotinib can cause hypophosphatemia, hypokalemia, hyperkalemia, hypocalcemia, and hyponatremia. Electrolyte abnormalities should be corrected prior to initiating nilotinib and during therapy; these electrolytes should be monitored periodically during therapy.

Bitolterol has a moderate potential interaction with Heart Disease.

Adrenergic bronchodilators can stimulate cardiovascular beta- 1 and beta- 2 receptors, resulting in adverse effects such as tachycardia, palpitation, peripheral vasodilation, blood pressure changes, and ECG changes (e.g., flattening of the T wave; prolongation of the QT interval; ST segment depression). Direct stimulation of cardiac tissues is mediated by beta- 1 receptors and thus less likely to occur with beta-2-selective agents such as albuterol. However, beta-2-selectivity is not absolute and can be lost with larger doses. High dosages of these agents have been associated with precipitation or aggravation of angina, myocardial ischemia, and cardiac arrhythmias. Therapy with adrenergic bronchodilators should be administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, and/or underlying cardiovascular disorders such as coronary insufficiency, cardiac arrhythmias, or hypertension. The recommended dosages should not be exceeded.

Bitolterol has a moderate potential interaction with High Blood Pressure.

Adrenergic bronchodilators can stimulate cardiovascular beta- 1 and beta- 2 receptors, resulting in adverse effects such as tachycardia, palpitation, peripheral vasodilation, blood pressure changes, and ECG changes (e.g., flattening of the T wave; prolongation of the QT interval; ST segment depression). Direct stimulation of cardiac tissues is mediated by beta- 1 receptors and thus less likely to occur with beta-2-selective agents such as albuterol. However, beta-2-selectivity is not absolute and can be lost with larger doses. High dosages of these agents have been associated with precipitation or aggravation of angina, myocardial ischemia, and cardiac arrhythmias. Therapy with adrenergic bronchodilators should be administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, and/or underlying cardiovascular disorders such as coronary insufficiency, cardiac arrhythmias, or hypertension. The recommended dosages should not be exceeded.

Bitolterol has a moderate potential interaction with Hyperthyroidism.

Adrenergic bronchodilators can stimulate cardiovascular beta- 1 and beta- 2 receptors, resulting in adverse effects such as tachycardia, palpitation, peripheral vasodilation, blood pressure changes, and ECG changes (e.g., flattening of the T wave; prolongation of the QT interval; ST segment depression). Direct stimulation of cardiac tissues is mediated by beta- 1 receptors and thus less likely to occur with beta-2-selective agents such as albuterol. However, beta-2-selectivity is not absolute and can be lost with larger doses. High dosages of these agents have been associated with precipitation or aggravation of angina, myocardial ischemia, and cardiac arrhythmias. Therapy with adrenergic bronchodilators should be administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, and/or underlying cardiovascular disorders such as coronary insufficiency, cardiac arrhythmias, or hypertension. The recommended dosages should not be exceeded.

Nilotinib has a major potential interaction with Hypokalemia.

The use of nilotinib is contraindicated in patients with hypokalemia, hypomagnesemia, or long QT syndrome. Nilotinib prolongs the QT interval in a concentration-dependent manner; QT prolongation may lead to torsade de pointes, which can result in syncope, seizures, and/or death. Before initiating nilotinib and periodically, electrolyte, calcium, and magnesium blood levels should be tested. Hypokalemia or hypomagnesemia must be corrected before starting treatment and these electrolytes should be monitored periodically. ECGs should be obtained at baseline, 7 days after starting nilotinib, following dose adjustments, and periodically as clinically indicated.

Bitolterol has a moderate potential interaction with Hypokalemia.

Adrenergic bronchodilators may cause decreases in serum potassium concentrations, primarily when given by nebulization or intravenous administration. Although this effect is usually transient and does not require supplementation, clinically significant hypokalemia may occur in some patients, with the potential to induce cardiovascular adverse effects. The relevance of these observations to oral or oral aerosol/powder for inhalation therapy is unknown. Therapy with adrenergic bronchodilators should be administered cautiously in patients with or predisposed to hypokalemia.

Nilotinib has a moderate potential interaction with Intestinal Anastomoses.

Nilotinib exposure is reduced in patients with total gastrectomy. More frequent monitoring of these patients is recommended; a dose increase or alternative therapy should be considered.

Nilotinib has a moderate potential interaction with Lactose Intolerance.

Nilotinib capsule formulations contain lactose and are not recommended for patients with rare hereditary problems of galactose intolerance, severe lactase deficiency with a severe degree of intolerance to lactose-containing products, or glucose-galactose malabsorption.

Nilotinib has a moderate potential interaction with Liver Disease.

Nilotinib exposure is increased in patients with hepatic impairment. If possible, alternative therapies should be considered; if nilotinib use is necessary, the dosage should be reduced and the QT interval should be monitored closely. Nilotinib may cause hepatotoxicity as measured by elevations in bilirubin, AST, ALT, and alkaline phosphatase; liver function tests should be monitored monthly or as clinically indicated and after dosage adjustments.

Nilotinib has a major potential interaction with Long QT Syndrome.

The use of nilotinib is contraindicated in patients with hypokalemia, hypomagnesemia, or long QT syndrome. Nilotinib prolongs the QT interval in a concentration-dependent manner; QT prolongation may lead to torsade de pointes, which can result in syncope, seizures, and/or death. Before initiating nilotinib and periodically, electrolyte, calcium, and magnesium blood levels should be tested. Hypokalemia or hypomagnesemia must be corrected before starting treatment and these electrolytes should be monitored periodically. ECGs should be obtained at baseline, 7 days after starting nilotinib, following dose adjustments, and periodically as clinically indicated.

Nilotinib has a major potential interaction with Magnesium Imbalance.

The use of nilotinib is contraindicated in patients with hypokalemia, hypomagnesemia, or long QT syndrome. Nilotinib prolongs the QT interval in a concentration-dependent manner; QT prolongation may lead to torsade de pointes, which can result in syncope, seizures, and/or death. Before initiating nilotinib and periodically, electrolyte, calcium, and magnesium blood levels should be tested. Hypokalemia or hypomagnesemia must be corrected before starting treatment and these electrolytes should be monitored periodically. ECGs should be obtained at baseline, 7 days after starting nilotinib, following dose adjustments, and periodically as clinically indicated.

Nilotinib has a moderate potential interaction with Pancreatitis.

Nilotinib can increase serum lipase. Patients with a history of pancreatitis may be at greater risk of elevated serum lipase. Serum lipase should be monitored monthly or as clinically indicated. If lipase elevations occur with abdominal symptoms, treatment should be interrupted and appropriate diagnostic evaluation should be considered to exclude pancreatitis.

Bitolterol has a moderate potential interaction with Seizures.

Adrenergic bronchodilators may cause CNS stimulation. Therapy with adrenergic bronchodilators should be administered cautiously in patients with seizure disorders. Systemic adverse effects are minimized, but not abolished, by administration of these agents via oral inhalation.