Interactions between AK-Beta and Levamlodipine

The levobunolol ophthalmic in AK-Beta has a major potential interaction with Allergies.

Topically applied beta-adrenergic receptor blocking agents (aka beta-blockers) are systemically absorbed, with the potential for producing clinically significant systemic effects even at low or undetectable plasma levels. The use of beta-blockers in patients with a history of allergic reactions or anaphylaxis may be associated with heightened reactivity to culprit allergens. The frequency and/or severity of attacks may be increased during beta-blocker therapy. In addition, these patients may be refractory to the usual doses of epinephrine used to treat acute hypersensitivity reactions and may require a beta-agonist such as isoproterenol.

Levamlodipine has a major potential interaction with Aortic Stenosis.

In general, calcium channel blockers (CCBs) should not be used in patients with hypotension (systolic pressure < 90 mm Hg) or cardiogenic shock. Due to potential negative inotropic and peripheral vasodilating effects, the use of CCBs may further depress cardiac output and blood pressure, which can be detrimental in these patients. The use of verapamil and diltiazem is specifically contraindicated under these circumstances.

The levobunolol ophthalmic in AK-Beta has a major potential interaction with Asthma.

Ophthalmic beta-adrenergic receptor blocking agents (aka beta-blockers) in general should not be used in patients with a current or past history of bronchial asthma or chronic obstructive pulmonary disease. Topically applied beta-blockers are systemically absorbed, with the potential for producing clinically significant systemic effects even at low or undetectable plasma levels. In the respiratory tract, beta blockade may adversely affect pulmonary function by counteracting the bronchodilation produced by catecholamine stimulation of beta-2 receptors. Although agents with beta-1 selectivity (e.g., betaxolol) are considered safer in patients with bronchospastic diseases, cardioselectivity is not absolute and may be lost with larger doses or higher plasma levels.

The levobunolol ophthalmic in AK-Beta has a major potential interaction with Cardiogenic Shock.

The use of ophthalmic beta-adrenergic receptor blocking agents (aka beta-blockers) is considered by manufacturers to be contraindicated in patients with cardiogenic shock. Topically applied beta-blockers are systemically absorbed, with the potential for producing clinically significant systemic effects even at low or undetectable plasma levels. In cardiac tissues, beta blockade causes a reduction in inotropic as well as chronotropic activity, which may further depress cardiac output and blood pressure in such patients.

Levamlodipine has a major potential interaction with Cardiogenic Shock.

In general, calcium channel blockers (CCBs) should not be used in patients with hypotension (systolic pressure < 90 mm Hg) or cardiogenic shock. Due to potential negative inotropic and peripheral vasodilating effects, the use of CCBs may further depress cardiac output and blood pressure, which can be detrimental in these patients. The use of verapamil and diltiazem is specifically contraindicated under these circumstances.

The levobunolol ophthalmic in AK-Beta has a major potential interaction with Cerebrovascular Insufficiency.

Due to their negative inotropic and chronotropic effects on the heart, beta-adrenergic receptor blocking agents (aka beta-blockers) reduce cardiac output and may precipitate or aggravate symptoms of arterial insufficiency in patients with peripheral vascular disease. In addition, the nonselective beta-blockers (e.g., timolol, carteolol) may attenuate catecholamine-mediated vasodilation during exercise by blocking beta-2 receptors in peripheral vessels. Since topically applied beta-blockers are systemically absorbed and may produce clinically significant systemic effects even at low or undetectable plasma levels, therapy with ophthalmic beta-blockers should be administered cautiously in patients with peripheral vascular disease. Close monitoring for progression of arterial obstruction is advised.

The levobunolol ophthalmic in AK-Beta has a major potential interaction with COPD.

Ophthalmic beta-adrenergic receptor blocking agents (aka beta-blockers) in general should not be used in patients with a current or past history of bronchial asthma or chronic obstructive pulmonary disease. Topically applied beta-blockers are systemically absorbed, with the potential for producing clinically significant systemic effects even at low or undetectable plasma levels. In the respiratory tract, beta blockade may adversely affect pulmonary function by counteracting the bronchodilation produced by catecholamine stimulation of beta-2 receptors. Although agents with beta-1 selectivity (e.g., betaxolol) are considered safer in patients with bronchospastic diseases, cardioselectivity is not absolute and may be lost with larger doses or higher plasma levels.

The levobunolol ophthalmic in AK-Beta has a major potential interaction with Diabetes Mellitus.

Beta-adrenergic receptor blocking agents (aka beta-blockers) may mask symptoms of hypoglycemia such as tremors, tachycardia and blood pressure changes. In addition, the nonselective beta-blockers (e.g., timolol, carteolol) may inhibit catecholamine-mediated glycogenolysis, thereby potentiating insulin-induced hypoglycemia and delaying the recovery of normal blood glucose levels. Since topically applied beta-blockers are systemically absorbed and may produce clinically significant systemic effects even at low or undetectable plasma levels, therapy with ophthalmic beta-blockers should be administered cautiously in patients with diabetes or predisposed to spontaneous hypoglycemia.

The levobunolol ophthalmic in AK-Beta has a major potential interaction with Heart Block.

The use of ophthalmic beta-adrenergic receptor blocking agents (aka beta-blockers) is considered by manufacturers to be contraindicated in patients with sinus bradyarrhythmia or heart block greater than the first degree (unless a functioning pacemaker is present). Topically applied beta-blockers are systemically absorbed, with the potential for producing clinically significant systemic effects even at low or undetectable plasma levels. In cardiac tissues, beta blockade causes a reduction in inotropic as well as chronotropic activity, which may further depress cardiac function in such patients.

The levobunolol ophthalmic in AK-Beta has a major potential interaction with Heart Failure.

The use of ophthalmic beta-adrenergic receptor blocking agents (aka beta-blockers) is considered by manufacturers to be contraindicated in patients with overt congestive heart failure (CHF). Topically applied beta-blockers are systemically absorbed, with the potential for producing clinically significant systemic effects even at low or undetectable plasma levels. Since sympathetic stimulation may be important in maintaining the hemodynamic function in patients with CHF, beta blockade can worsen the heart failure. However, therapy with ophthalmic beta-blockers can be administered cautiously in some CHF patients provided they are well compensated and receiving digitalis, diuretics, an ACE inhibitor, and/or nitrates. Beta-blockers should be discontinued if cardiac failure develops or worsens during therapy.

The levobunolol ophthalmic in AK-Beta has a major potential interaction with Hyperthyroidism.

Beta-adrenergic receptor blocking agents (aka beta-blockers) may mask some symptoms of hyperthyroidism such as tachycardia, anxiety, tremor, and heat intolerance. Abrupt withdrawal of beta-blocker therapy in thyrotoxic patients may exacerbate symptoms of hyperthyroidism or precipitate a thyroid storm. Since topically applied beta-blockers are systemically absorbed and may produce clinically significant systemic effects even at low or undetectable plasma levels, therapy with ophthalmic beta-blockers should be administered cautiously in patients with or suspected of having hyperthyroidism. Cessation of beta-blocker therapy, when necessary, should occur gradually over a period of 1 to 2 weeks. Patients should be advised not to discontinue treatment without first consulting with the physician. Close monitoring is recommended during and after therapy withdrawal.

Levamlodipine has a major potential interaction with Hypotension.

In general, calcium channel blockers (CCBs) should not be used in patients with hypotension (systolic pressure < 90 mm Hg) or cardiogenic shock. Due to potential negative inotropic and peripheral vasodilating effects, the use of CCBs may further depress cardiac output and blood pressure, which can be detrimental in these patients. The use of verapamil and diltiazem is specifically contraindicated under these circumstances.

Levamlodipine has a major potential interaction with Ischemic Heart Disease.

Increased frequency, duration, and/or severity of angina, as well as acute myocardial infarction, have rarely developed during initiation or dosage increase of calcium channel blockers (CCBs), particularly in patients with severe obstructive coronary artery disease and those treated with immediate-release formulations. The mechanism of this effect is not established. Therapy with CCBs should be administered cautiously in patients with significant coronary artery disease.

Levamlodipine has a major potential interaction with Liver Disease.

Calcium channel blockers (CCBs) are extensively metabolized by the liver. The half-lives of CCBs may be prolonged substantially in patients with severe hepatic impairment, with the potential for significant drug accumulation. In addition, the use of some CCBs has been associated with elevations in serum transaminases, both with and without concomitant elevations in alkaline phosphatase and bilirubin. While these effects may be transient and reversible, some patients have developed cholestasis or hepatocellular injury. Therapy with CCBs should be administered cautiously and often at reduced dosages in patients with significantly impaired hepatic function. Periodic monitoring of liver function is advised.

The levobunolol ophthalmic in AK-Beta has a moderate potential interaction with Myoneural Disorder.

Topically applied beta-adrenergic receptor blocking agents (aka beta-blockers) are systemically absorbed, with the potential for producing clinically significant systemic effects even at low or undetectable plasma levels. In the nervous and musculoskeletal systems, beta blockade may potentiate muscle weakness consistent with certain myasthenic symptoms such as diplopia, ptosis, and generalized weakness. Several beta-blockers have been associated rarely with aggravation of muscle weakness in patients with preexisting myasthenia gravis or myasthenic symptoms.

The levobunolol ophthalmic in AK-Beta has a major potential interaction with Peripheral Arterial Disease.

Due to their negative inotropic and chronotropic effects on the heart, beta-adrenergic receptor blocking agents (aka beta-blockers) reduce cardiac output and may precipitate or aggravate symptoms of arterial insufficiency in patients with peripheral vascular disease. In addition, the nonselective beta-blockers (e.g., timolol, carteolol) may attenuate catecholamine-mediated vasodilation during exercise by blocking beta-2 receptors in peripheral vessels. Since topically applied beta-blockers are systemically absorbed and may produce clinically significant systemic effects even at low or undetectable plasma levels, therapy with ophthalmic beta-blockers should be administered cautiously in patients with peripheral vascular disease. Close monitoring for progression of arterial obstruction is advised.

The levobunolol ophthalmic in AK-Beta has a major potential interaction with Sinus Node Dysfunction.

The use of ophthalmic beta-adrenergic receptor blocking agents (aka beta-blockers) is considered by manufacturers to be contraindicated in patients with sinus bradyarrhythmia or heart block greater than the first degree (unless a functioning pacemaker is present). Topically applied beta-blockers are systemically absorbed, with the potential for producing clinically significant systemic effects even at low or undetectable plasma levels. In cardiac tissues, beta blockade causes a reduction in inotropic as well as chronotropic activity, which may further depress cardiac function in such patients.