Can you take Combigan with Rasagiline?

The timolol ophthalmic in Combigan 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.

The timolol ophthalmic in Combigan 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 timolol ophthalmic in Combigan 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.

The brimonidine ophthalmic in Combigan has a moderate potential interaction with Cardiovascular Conditions and Disorders.

Topically applied alpha-2 adrenergic receptor agonists are systemically absorbed, with the potential for producing rare but clinically significant systemic effects. In the central nervous system, alpha adrenergic stimulation causes an inhibition of sympathetic vasomotor centers, resulting in decreased peripheral resistance and bradycardia. While the commercially available agents in the U.S. (apraclonidine and brimonidine) are hydrophilic and do not readily distribute across the ocular-blood barrier into the CNS, prolonged use may increase the risk of systemic effects. There have been occasional reports of bradycardia, chest heaviness or burning, palpitation, reduced blood pressure, and orthostatic hypotension when apraclonidine 1% was administered once or twice a day for 4 weeks to individuals not undergoing laser surgery. Therapy with ophthalmic alpha-2 adrenergic agents should be administered cautiously in patients with severe, uncontrolled cardiovascular disease, including hypertension, coronary or cerebrovascular insufficiency, recent myocardial infarction, chronic renal failure, Raynaud's disease, thromboangiitis obliterans, and a predisposition for orthostatic hypotension.

The timolol ophthalmic in Combigan 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 brimonidine ophthalmic in Combigan has a moderate potential interaction with Cerebrovascular Insufficiency.

Topically applied alpha-2 adrenergic receptor agonists are systemically absorbed, with the potential for producing rare but clinically significant systemic effects. In the central nervous system, alpha adrenergic stimulation causes an inhibition of sympathetic vasomotor centers, resulting in decreased peripheral resistance and bradycardia. While the commercially available agents in the U.S. (apraclonidine and brimonidine) are hydrophilic and do not readily distribute across the ocular-blood barrier into the CNS, prolonged use may increase the risk of systemic effects. There have been occasional reports of bradycardia, chest heaviness or burning, palpitation, reduced blood pressure, and orthostatic hypotension when apraclonidine 1% was administered once or twice a day for 4 weeks to individuals not undergoing laser surgery. Therapy with ophthalmic alpha-2 adrenergic agents should be administered cautiously in patients with severe, uncontrolled cardiovascular disease, including hypertension, coronary or cerebrovascular insufficiency, recent myocardial infarction, chronic renal failure, Raynaud's disease, thromboangiitis obliterans, and a predisposition for orthostatic hypotension.

The timolol ophthalmic in Combigan 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 brimonidine ophthalmic in Combigan has a moderate potential interaction with Depression.

Topically applied alpha-2 adrenergic receptor agonists are systemically absorbed, with the potential for producing rare but clinically significant systemic effects. Depression has infrequently been associated with the ocular use of these drugs due to their inhibiting effect on the sympathetic nervous system. Depressed patients should be monitored for exacerbation of their condition during therapy with ophthalmic alpha-2 adrenergic agents.

The timolol ophthalmic in Combigan 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 timolol ophthalmic in Combigan 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 timolol ophthalmic in Combigan 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.

Rasagiline has a moderate potential interaction with High Blood Pressure.

Exacerbation of hypertension may occur during treatment with rasagiline. Dosage adjustment may be necessary if the elevation is sustained. Patients should be monitored for new onset hypertension or hypertension that is not well controlled after starting treatment.

The timolol ophthalmic in Combigan 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.

The brimonidine ophthalmic in Combigan has a moderate potential interaction with Hypotension.

Topically applied alpha-2 adrenergic receptor agonists are systemically absorbed, with the potential for producing rare but clinically significant systemic effects. In the central nervous system, alpha adrenergic stimulation causes an inhibition of sympathetic vasomotor centers, resulting in decreased peripheral resistance and bradycardia. While the commercially available agents in the U.S. (apraclonidine and brimonidine) are hydrophilic and do not readily distribute across the ocular-blood barrier into the CNS, prolonged use may increase the risk of systemic effects. There have been occasional reports of bradycardia, chest heaviness or burning, palpitation, reduced blood pressure, and orthostatic hypotension when apraclonidine 1% was administered once or twice a day for 4 weeks to individuals not undergoing laser surgery. Therapy with ophthalmic alpha-2 adrenergic agents should be administered cautiously in patients with severe, uncontrolled cardiovascular disease, including hypertension, coronary or cerebrovascular insufficiency, recent myocardial infarction, chronic renal failure, Raynaud's disease, thromboangiitis obliterans, and a predisposition for orthostatic hypotension.

Rasagiline has a moderate potential interaction with Hypotension.

Dopamine agonists may impair the systemic regulation of blood pressure, with resultant orthostatic hypotension at any time, but especially during dose escalation. Additionally, patients with Parkinson's disease may have an impaired capacity to respond to an orthostatic challenge. For these reasons, patients with Parkinson's disease (or restless legs syndrome) who are being treated with dopaminergic agonists typically require careful monitoring for signs/symptoms of orthostatic hypotension, especially during dose escalation, and should be advised of this risk.

Rasagiline has a major potential interaction with Liver Disease.

Rasagiline should not be used in patients with moderate to severe hepatic impairment. Patients with mild hepatic impairment should not exceed a dose of 0.5 mg daily.

The brimonidine ophthalmic in Combigan has a moderate potential interaction with Liver Disease.

Topically applied alpha-2 adrenergic receptor agonists are systemically absorbed, with the potential for producing rare but clinically significant systemic effects. There are limited data concerning the pharmacokinetic disposition or the clinical use of these drugs in patients with renal and/or liver disease. Therapy with ophthalmic alpha-2 adrenergic agents should be administered cautiously in patients with significantly impaired renal or hepatic function.

The timolol ophthalmic in Combigan 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 timolol ophthalmic in Combigan 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.

Rasagiline has a moderate potential interaction with Psychosis.

Ordinarily, patients with major psychotic disorder should not be treated with dopaminergic antiparkinsonian agents, because of the risk of exacerbating psychosis. Hallucinations and psychotic-like behavior have been reported with dopaminergic medications. In addition, certain medications used to treat psychosis may exacerbate the symptoms of Parkinson's disease and may decrease the effectiveness of these drugs. The use of bromocriptine in patients with severe psychotic disorders is not recommended.

The brimonidine ophthalmic in Combigan has a moderate potential interaction with Renal Dysfunction.

Topically applied alpha-2 adrenergic receptor agonists are systemically absorbed, with the potential for producing rare but clinically significant systemic effects. There are limited data concerning the pharmacokinetic disposition or the clinical use of these drugs in patients with renal and/or liver disease. Therapy with ophthalmic alpha-2 adrenergic agents should be administered cautiously in patients with significantly impaired renal or hepatic function.

Rasagiline has a moderate potential interaction with Renal Dysfunction.

Dose adjustment of rasagiline is not required for patients with mild or moderate renal impairment. However, rasagiline has not been studied in patients with severe renal impairment. Caution is advised if used.

The timolol ophthalmic in Combigan 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.