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Drug overview for TIMOLOL MALEATE (timolol maleate/pf):
Generic name: TIMOLOL MALEATE/PF (TIE-moh-lohl)
Drug class: Ophthalmic Beta-Blockers
Therapeutic class: Ophthalmic Agents
Timolol is a nonselective beta-adrenergic blocking agent.
No enhanced Uses information available for this drug.
Generic name: TIMOLOL MALEATE/PF (TIE-moh-lohl)
Drug class: Ophthalmic Beta-Blockers
Therapeutic class: Ophthalmic Agents
Timolol is a nonselective beta-adrenergic blocking agent.
No enhanced Uses information available for this drug.
DRUG IMAGES
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The following indications for TIMOLOL MALEATE (timolol maleate/pf) have been approved by the FDA:
Indications:
Ocular hypertension
Open angle glaucoma
Professional Synonyms:
Chronic glaucoma
Compensated glaucoma
Glaucoma simplex
Increased intraocular pressure
Increased IOP
Open-angle glaucoma
Raised intraocular pressure
Simple glaucoma
Indications:
Ocular hypertension
Open angle glaucoma
Professional Synonyms:
Chronic glaucoma
Compensated glaucoma
Glaucoma simplex
Increased intraocular pressure
Increased IOP
Open-angle glaucoma
Raised intraocular pressure
Simple glaucoma
The following dosing information is available for TIMOLOL MALEATE (timolol maleate/pf):
No enhanced Dosing information available for this drug.
Timolol or timolol maleate is applied topically to the eye as an ophthalmic solution. Timolol maleate also is applied topically to the eye as a gel-forming ophthalmic solution. Timolol maleate also is commercially available in fixed combination with dorzolamide hydrochloride or brimonidine tartrate (as ophthalmic solutions) for topical application to the eye.
Care should be taken to avoid contamination of the solution container. Some timolol ophthalmic solutions contain benzalkonium chloride, which may be absorbed by soft contact lenses. Contact lenses should be removed prior to administration of each dose of these solutions, but may be reinserted 15 minutes after the dose.
Preservative-free ophthalmic solutions containing timolol alone or in fixed combination with dorzolamide should be administered topically to one or both eyes immediately after the single-use container is opened; since sterility cannot be maintained after the individual unit is opened, any remaining contents should be discarded immediately after administration. If the patient is receiving more than one ophthalmic preparation, the preparations should be administered at least 5 minutes apart, although some manufacturers recommend an interval of at least 10 minutes. Containers of timolol maleate ophthalmic gel-forming solution should be inverted and shaken once just prior to administration of each dose. Patients receiving ophthalmic gel-forming solutions of the drug who also are receiving other ophthalmic preparations should be instructed that other topical preparations be administered at least 10 minutes before a dose of the gel-forming solution.
Care should be taken to avoid contamination of the solution container. Some timolol ophthalmic solutions contain benzalkonium chloride, which may be absorbed by soft contact lenses. Contact lenses should be removed prior to administration of each dose of these solutions, but may be reinserted 15 minutes after the dose.
Preservative-free ophthalmic solutions containing timolol alone or in fixed combination with dorzolamide should be administered topically to one or both eyes immediately after the single-use container is opened; since sterility cannot be maintained after the individual unit is opened, any remaining contents should be discarded immediately after administration. If the patient is receiving more than one ophthalmic preparation, the preparations should be administered at least 5 minutes apart, although some manufacturers recommend an interval of at least 10 minutes. Containers of timolol maleate ophthalmic gel-forming solution should be inverted and shaken once just prior to administration of each dose. Patients receiving ophthalmic gel-forming solutions of the drug who also are receiving other ophthalmic preparations should be instructed that other topical preparations be administered at least 10 minutes before a dose of the gel-forming solution.
| DRUG LABEL | DOSING TYPE | DOSING INSTRUCTIONS |
|---|---|---|
| TIMOLOL MALEATE 0.25% EYE DROP | Maintenance | Adults instill 1 drop into both eyes by ophthalmic route once daily |
| TIMOLOL MALEATE 0.5% EYE DROP | Maintenance | Adults instill 1 drop into both eyes by ophthalmic route once daily |
| DRUG LABEL | DOSING TYPE | DOSING INSTRUCTIONS |
|---|---|---|
| TIMOLOL MALEATE 0.5% EYE DROP | Maintenance | Adults instill 1 drop into both eyes by ophthalmic route once daily |
| TIMOLOL MALEATE 0.25% EYE DROP | Maintenance | Adults instill 1 drop into both eyes by ophthalmic route once daily |
The following drug interaction information is available for TIMOLOL MALEATE (timolol maleate/pf):
There are 0 contraindications.
There are 4 severe interactions.
These drug interactions can produce serious consequences in most patients. Actions required for severe interactions include, but are not limited to, discontinuing one or both agents, adjusting dosage, altering administration scheduling, and providing additional patient monitoring. Review the full interaction monograph for more information.
| Drug Interaction | Drug Names |
|---|---|
| Methyldopa/Beta-Blockers (Nonselective) SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Unopposed alpha-adrenergic vasoconstriction produced by alpha-methylnorepinephrine in the presence of beta-blockade. CLINICAL EFFECTS: Severe hypertension. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Monitor blood pressure during concomitant administration of methyldopa and a nonselective beta-blocker. If hypertension occurs, treatment with phentolamine should be considered. DISCUSSION: Although methyldopa and propranolol have been used together to treat hypertension, severe increases in blood pressure, including death in one patient, has been reported during administration of these drugs. In addition, methyldopa alone has been reported to cause paradoxical hypertension. Additional studies are needed to define the specific population at risk. |
METHYLDOPA, METHYLDOPA-HYDROCHLOROTHIAZIDE, METHYLDOPATE HCL |
| Beta-2 Agonists/Non-Cardioselective Beta-Blockers SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Non-cardioselective beta-blockers and beta-2 agonists may antagonize the effects of each other. CLINICAL EFFECTS: Diminished response to either the beta-agonist, beta-blocker, or both may occur. Beta-blockers may also induce bronchospasm. PREDISPOSING FACTORS: Patients receiving beta-2 agonists for the treatment of asthma may be more at risk for bronchospasm. PATIENT MANAGEMENT: If possible, avoid beta-blocker therapy in asthmatic patients requiring beta-2 agonist therapy. If beta-blocker therapy is required, use a cardio-selective beta-blocker. For timolol ophthalmic drops, counsel patients to apply pressure to the inner corner of the eye after administration to prevent systemic absorption. Monitor patients for decreased effects of either agent, such as increased need for/use of beta-2 agonists or increased heart rate or blood pressure. DISCUSSION: Many patients with asymptomatic or mild reactive airways disease tolerate beta-blockers well. Most patients with COPD do not have bronchospastic component to their illness and may be given beta-blockers. Heart failure treatment guidelines recommend beta-blockers in the presence of COPD. Non-selective beta-blockers have been shown to have a negative effect on lung function (FEV1) and airway hyperresponsiveness (AHR) in patients with asthma and COPD.(1) An open-label study using the nonselective beta blocker nadolol showed no effect on salbutamol in 10 patients with mild asthma not on controller therapy.(2) A study in 8 healthy men showed that long acting propranolol (160 mg) only effected airway dilation at the 200 mcg salbutamol dose. The 800 mcg and 1600 mcg dose were unaffected. However, penbutolol prevented any significant airway dilation with all doses of salbutamol.(3) In a double blind, three-way, crossover study, 44% (7/16 patients) of patients taking metoprolol showed a greater than 20% decrease in FEV1 compared to 19% (3 patients) after dilevalol and 6% (1 patient) after placebo. Dilevalol and metoprolol significantly inhibited isoproterenol response compared to placebo.(4) A double-blind, randomized, crossover study in 10 asthmatic patients showed that intravenous propranolol produced marked symptomatic bronchoconstriction. Only a slight but significant inhibition of bronchomotor sensitivity to isoproterenol was noted during esmolol infusion.(5) In 18 patients with reversible bronchial asthma, labetalol caused a significant increase in FEV1 and metoprolol caused a significant decrease in FEV1. Concurrent administration of isoproterenol and labetalol caused a further increase in FEV1. The effect of isoproterenol was decreased by metoprolol (100, 200mg).(6) In one study propranolol (0.06mg/kg IV) was shown to almost completely block the effects of isoproterenol in asthmatics. Metoprolol (0.12mg/kg IV) did not affect isoproterenol.(7) Studies have shown that cardioselective beta-blockers are safe for patients with asthma and COPD.(8,9,10) Nebivolol and celiprolol significantly decreased FEV1. Inhalation of albuterol (up to 800mcg) significantly improved FEV1, but the values after nebivolol and celiprolol administration were lower than the initial values.(11) Administration of metoprolol did not cause any respiratory problems in 9 asthmatic patients. There was no significant difference between the metoprolol and placebo groups in the respiratory response to an isoproterenol aerosol in 24 asthmatic patients.(12) Eight male asthmatic patients were given 10 mg bisoprolol, 20 mg bisoprolol, and 100 mg metoprolol. Both bisoprolol and metoprolol caused bronchoconstriction measured by a significant fall in PEFR (peak expiratory flow rate). Terbutaline was able to reverse bronchoconstriction in all patients.(13) A double blind, placebo-controlled study analyzed the use of atenolol 100mg, metoprolol 100mg, or acebutolol 400 mg in 8 asthmatic patients before and after exercise. All three drugs reduced significantly FEV1 and PEFR. Administration of terbutaline improved all respiratory indices.(14) A double-blind crossover trial in 10 asthmatic patients showed that a single IV dose of atenolol 3mg caused slight impairment of ventilatory function. A dose of salbutamol by inhalation was able to reverse the bronchial effect of atenolol.(15) Propranolol (80mg/day), oxprenolol (80mg/day), atenolol (100mg/day), and celiprolol 200mg/day were given to 10 asthmatic patients in a randomized, crossover design with a two week washout period between each drug. The non-beta 1 selective beta blockers (propranolol, oxprenolol) caused a significant reduction in FEV1 and inhibited the bronchodilator response to inhaled salbutamol. Atenolol and celiprolol (beta1 selective beta blockers) did not significantly affect respiratory function or antagonize salbutamol effects.(16) A double blind, randomized, within patient, placebo-controlled study compared the cardioselective beta-blocker atenolol to the non-selective propranolol. Atenolol caused a significantly less drop in FEV1 compared to propranolol. The effect of isoprenaline plus the beta blockers were also studied. Both atenolol and propranolol effected isoprenaline FEV1 dose response curves but the greatest displacement was seen with propranolol.(17) The pulmonary effects of celiprolol 200 mg, celiprolol 400mg, propranolol 40mg, atenolol 100 mg were evaluated in 34 asthmatic patients. Propranolol and atenolol caused significant reductions in pulmonary function. Propranolol pretreatment caused a significant reduction in the effect of the bronchodilator. Celiprolol did not antagonize the bronchodilators.(18) A double-blind, placebo controlled, randomized, crossover design study studied the effects of propranolol 80mg or celiprolol 200 or 400mg on pulmonary function. Propranolol produced a significant decrease in FEV1 and FVC. Celiprolol and placebo had similar results. The effect of aerosolized terbutaline was also measured. Even at supratherapeutic doses, terbutaline was unable to restore pulmonary function parameters to baseline levels after treatment with propranolol. Terbutaline caused further bronchodilation after administration of celiprolol.(19) Eleven asthmatic patients showed significant bronchoconstriction in small airways after propranolol 40mg and pindolol 2.5mg in a double blind, randomized trial. Large airways only showed bronchoconstriction with propranolol. Terbutaline 0.5mg subcutaneous was given after pretreatment with propranolol and pindolol. The bronchodilator effect of terbutaline on large airways was diminished after both propranolol and timolol.(20) |
AIRSUPRA, ALBUTEROL SULFATE, ALBUTEROL SULFATE HFA, ANORO ELLIPTA, ARFORMOTEROL TARTRATE, BEVESPI AEROSPHERE, BREO ELLIPTA, BREYNA, BREZTRI AEROSPHERE, BROVANA, BUDESONIDE-FORMOTEROL FUMARATE, COMBIVENT RESPIMAT, DUAKLIR PRESSAIR, DULERA, FLUTICASONE-VILANTEROL, FORMOTEROL FUMARATE, IPRATROPIUM-ALBUTEROL, LEVALBUTEROL CONCENTRATE, LEVALBUTEROL HCL, LEVALBUTEROL TARTRATE HFA, PERFOROMIST, PROAIR DIGIHALER, PROAIR RESPICLICK, STIOLTO RESPIMAT, STRIVERDI RESPIMAT, SYMBICORT, TERBUTALINE SULFATE, TRELEGY ELLIPTA, UMECLIDINIUM-VILANTEROL, VENTOLIN HFA, XOPENEX HFA |
| Iobenguane I 123/Agents that Affect Catecholamines SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Many compounds that reduce catecholamine uptake or that deplete catecholamine stores may interfere with iobenguane uptake into cells.(1) CLINICAL EFFECTS: Compounds that reduce catecholamine uptake or that deplete catecholamine stores may interfere with imaging completed with iobenguane.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Discuss the use of agents that affect catecholamines. Discontinue drugs that reduce catecholamine uptake or deplete catecholamine stores prior to imaging with iobenguane. Before imaging with iobenguane, discontinue agents that affect catecholamines for at least 5 biological half-lives, as clinically tolerated.(1) DISCUSSION: Many agents may reduce catecholamine uptake or deplete catecholamine stores.(1) Examples include: - CNS stimulants or amphetamines (e.g. cocaine, methylphenidate, dextroamphetamine) - norepinephrine and dopamine reuptake inhibitors (e.g. phentermine) - norepinephrine and serotonin reuptake inhibitors (e.g. tramadol) - monoamine oxidase inhibitors (e.g. phenelzine, linezolid) - central monoamine depleting drugs (e.g. reserpine) - non-select beta adrenergic blocking drugs (e.g. labetalol) - alpha agonists or alpha/beta agonists (e.g. pseudoephedrine, phenylephrine, ephedrine, phenylpropanolamine, naphazoline) - tricyclic antidepressants or norepinephrine reuptake inhibitors (e.g. amitriptyline, bupropion, duloxetine, mirtazapine, venlafaxine) - botanicals that may inhibit reuptake of norepinephrine, serotonin or dopamine (e.g. ephedra, ma huang, St. John's Wort, yohimbine) |
ADREVIEW |
| Salmeterol/Non-Cardioselective Beta-Blockers SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Non-cardioselective beta-blockers and beta-2 agonists may antagonize the effects of each other. CLINICAL EFFECTS: Diminished response to either the beta-agonist, beta-blocker, or both may occur. Beta-blockers may also induce bronchospasm. PREDISPOSING FACTORS: Patients receiving beta-2 agonists for the treatment of asthma may be more at risk for bronchospasm. PATIENT MANAGEMENT: If possible, avoid beta-blocker therapy in asthmatic patients requiring beta-2 agonist therapy. If beta-blocker therapy is required, use a cardio-selective beta-blocker. Monitor patients for decreased effects of either agent, such as increased need for/use of beta-2 agonists or increased heart rate or blood pressure. DISCUSSION: Many patients with asymptomatic or mild reactive airways disease tolerate beta-blockers well. Most patients with COPD do not have bronchospastic component to their illness and may be given beta-blockers. Heart failure treatment guidelines recommend beta-blockers in the presence of COPD. Non-selective beta-blockers have been shown to have a negative effect on lung function (FEV1) and airway hyperresponsiveness (AHR) in patients with asthma and COPD.(1) An open-label study using the nonselective beta blocker nadolol showed no effect on salbutamol in 10 patients with mild asthma not on controller therapy.(2) A study in 8 healthy men showed that long acting propranolol (160 mg) only effected airway dilation at the 200 mcg salbutamol dose. The 800 mcg and 1600 mcg dose were unaffected. However, penbutolol prevented any significant airway dilation with all doses of salbutamol.(3) In a double blind, three-way, crossover study, 44% (7/16 patients) of patients taking metoprolol showed a greater than 20% decrease in FEV1 compared to 19% (3 patients) after dilevalol and 6% (1 patient) after placebo. Dilevalol and metoprolol significantly inhibited isoproterenol response compared to placebo.(4) A double-blind, randomized, crossover study in 10 asthmatic patients showed that intravenous propranolol produced marked symptomatic bronchoconstriction. Only a slight but significant inhibition of bronchomotor sensitivity to isoproterenol was noted during esmolol infusion.(5) In 18 patients with reversible bronchial asthma, labetalol caused a significant increase in FEV1 and metoprolol caused a significant decrease in FEV1. Concurrent administration of isoproterenol and labetalol caused a further increase in FEV1. The effect of isoproterenol was decreased by metoprolol (100, 200mg).(6) In one study propranolol (0.06mg/kg IV) was shown to almost completely block the effects of isoproterenol in asthmatics. Metoprolol (0.12mg/kg IV) did not affect isoproterenol.(7) Studies have shown that cardioselective beta-blockers are safe for patients with asthma and COPD.(8,9,10) Nebivolol and celiprolol significantly decreased FEV1. Inhalation of albuterol (up to 800mcg) significantly improved FEV1, but the values after nebivolol and celiprolol administration were lower than the initial values.(11) Administration of metoprolol did not cause any respiratory problems in 9 asthmatic patients. There was no significant difference between the metoprolol and placebo groups in the respiratory response to an isoproterenol aerosol in 24 asthmatic patients.(12) Eight male asthmatic patients were given 10 mg bisoprolol, 20 mg bisoprolol, and 100 mg metoprolol. Both bisoprolol and metoprolol caused bronchoconstriction measured by a significant fall in PEFR (peak expiratory flow rate). Terbutaline was able to reverse bronchoconstriction in all patients.(13) A double blind, placebo-controlled study analyzed the use of atenolol 100mg, metoprolol 100mg, or acebutolol 400 mg in 8 asthmatic patients before and after exercise. All three drugs reduced significantly FEV1 and PEFR. Administration of terbutaline improved all respiratory indices.(14) A double-blind crossover trial in 10 asthmatic patients showed that a single IV dose of atenolol 3mg caused slight impairment of ventilatory function. A dose of salbutamol by inhalation was able to reverse the bronchial effect of atenolol.(15) Propranolol (80mg/day), oxprenolol (80mg/day), atenolol (100mg/day), and celiprolol 200mg/day were given to 10 asthmatic patients in a randomized, crossover design with a two week washout period between each drug. The non-beta 1 selective beta blockers (propranolol, oxprenolol) caused a significant reduction in FEV1 and inhibited the bronchodilator response to inhaled salbutamol. Atenolol and celiprolol (beta1 selective beta blockers) did not significantly affect respiratory function or antagonize salbutamol effects.(16) A double blind, randomized, within patient, placebo-controlled study compared the cardioselective beta-blocker atenolol to the non-selective propranolol. Atenolol caused a significantly less drop in FEV1 compared to propranolol. The effect of isoprenaline plus the beta blockers were also studied. Both atenolol and propranolol effected isoprenaline FEV1 dose response curves but the greatest displacement was seen with propranolol.(17) The pulmonary effects of celiprolol 200 mg, celiprolol 400mg, propranolol 40mg, atenolol 100 mg were evaluated in 34 asthmatic patients. Propranolol and atenolol caused significant reductions in pulmonary function. Propranolol pretreatment caused a significant reduction in the effect of the bronchodilator. Celiprolol did not antagonize the bronchodilators.(18) A double-blind, placebo controlled, randomized, crossover design study studied the effects of propranolol 80mg or celiprolol 200 or 400mg on pulmonary function. Propranolol produced a significant decrease in FEV1 and FVC. Celiprolol and placebo had similar results. The effect of aerosolized terbutaline was also measured. Even at supratherapeutic doses, terbutaline was unable to restore pulmonary function parameters to baseline levels after treatment with propranolol. Terbutaline caused further bronchodilation after administration of celiprolol.(19) Eleven asthmatic patients showed significant bronchoconstriction in small airways after propranolol 40mg and pindolol 2.5mg in a double blind, randomized trial. Large airways only showed bronchoconstriction with propranolol. Terbutaline 0.5mg subcutaneous was given after pretreatment with propranolol and pindolol. The bronchodilator effect of terbutaline on large airways was diminished after both propranolol and timolol.(20) |
ADVAIR DISKUS, ADVAIR HFA, AIRDUO DIGIHALER, FLUTICASONE-SALMETEROL, FLUTICASONE-SALMETEROL HFA, SEREVENT DISKUS, WIXELA INHUB |
There are 5 moderate interactions.
The clinician should assess the patient’s characteristics and take action as needed. Actions required for moderate interactions include, but are not limited to, discontinuing one or both agents, adjusting dosage, altering administration.
| Drug Interaction | Drug Names |
|---|---|
| Selected Beta-Blockers/Theophyllines SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Certain beta-blockers may inhibit theophylline metabolism. In addition, beta-blockers, especially non-selective agents, can antagonize the pharmacologic effects of theophylline. CLINICAL EFFECTS: Even though theophylline concentrations may increase leading to increased possibility of theophylline toxicity, beta-blockers decrease theophylline's therapeutic effects. PREDISPOSING FACTORS: Cigarette smoking may exacerbate this interaction. PATIENT MANAGEMENT: Avoid the use of non-selective beta-blockers with theophylline. If a beta-blocker must be used, a cardioselective agent that does not decrease the clearance of theophylline (e.g., atenolol) should be considered. However, since cardioselectivity is not absolute and is less selective at higher doses, cardioselective beta-blockers should be used with caution in patients with bronchospastic disease. DISCUSSION: Inhibition of theophylline metabolism is greatest with lipophilic beta-blockers undergoing hepatic metabolism (e.g., propranolol). Additionally, the decrease in theophylline clearance appears to be dose dependent as the higher the beta-blocker dose, the greater the decrease in theophylline clearance. If the patient is on both drugs and the beta-blocker is discontinued, serum theophylline concentrations may decrease. In these cases, monitor for a decrease in theophylline therapeutic effect and adjust the dose as needed. |
AMINOPHYLLINE, DYPHYLLINE, THEO-24, THEOPHYLLINE, THEOPHYLLINE ANHYDROUS, THEOPHYLLINE ER, THEOPHYLLINE ETHYLENEDIAMINE |
| Selected Beta-blockers/Selected Calcium Channel Blockers SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Synergistic pharmacologic activity. CLINICAL EFFECTS: May see an increase in the therapeutic and toxic effects of both drugs. Concurrent use in patients with low heart rates may unmask sick sinus syndrome. PREDISPOSING FACTORS: Preexisting left ventricular dysfunction and high doses of the beta-blocking agent may predispose patients to adverse responses to this drug combination. Other possible factors include parenteral administration and concurrent administration of other cardio-depressant drugs such as antiarrhythmics. PATIENT MANAGEMENT: Monitor the patient for signs of increased cardio-depressant effects and hypotension. Adjust the dose accordingly. DISCUSSION: Coadministration of these classes of drugs may be effective in the treatment of angina pectoris and hypertension. Patients should be screened in order to determine who should receive this combination of agents. The concurrent use of mibefradil and beta-blockers in patients with low heart rates may unmask underlying sick sinus syndrome. One or more of the drug pairs linked to this monograph have been included in a list of interactions that could be considered for classification as "non-interruptive" in EHR systems. This DDI subset was vetted by an expert panel commissioned by the U.S. Office of the National Coordinator (ONC) for Health Information Technology. |
CARDIZEM, CARDIZEM CD, CARDIZEM LA, CARTIA XT, DILT-XR, DILTIAZEM 12HR ER, DILTIAZEM 24HR ER, DILTIAZEM 24HR ER (CD), DILTIAZEM 24HR ER (LA), DILTIAZEM 24HR ER (XR), DILTIAZEM HCL, DILTIAZEM HCL-0.7% NACL, DILTIAZEM HCL-0.9% NACL, DILTIAZEM HCL-NACL, DILTIAZEM-D5W, MATZIM LA, NIFEDIPINE, NIFEDIPINE ER, NIFEDIPINE MICRONIZED, PROCARDIA XL, TIADYLT ER, TIAZAC, TRANDOLAPRIL-VERAPAMIL ER, VERAPAMIL ER, VERAPAMIL ER PM, VERAPAMIL HCL, VERAPAMIL SR |
| Selected Beta-Blockers/Selected Alpha-Blockers SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Alpha-blockers may cause syncope with sudden loss of consciousness secondary to excessive postural hypotension. Following the first dose of an alpha-blocker, compensatory tachycardia helps to prevent or limit syncope. Beta-blockers may inhibit this tachycardia, thereby worsening alpha-blocker induced hypotension. CLINICAL EFFECTS: The hypotensive effects of an alpha-blocker may be increased in patients on concurrent beta-blocker therapy. PREDISPOSING FACTORS: Patients may be at increased risk of postural hypotension with concurrent diuretic therapy and those on low-sodium diets. PATIENT MANAGEMENT: When starting alpha-blocker therapy in patients receiving beta-blockers, consider initiating treatment with a reduced dose of the alpha-blocker. If syncope occurs, provide supportive treatment as necessary. The adverse effect is self limiting and in most cases does not recur after the initial period of therapy or during subsequent dose titration with the alpha-blocker. DISCUSSION: Beta-blockers increase the acute postural hypotension that frequently follows the first dose of an alpha-blocker. Initiation of beta-blocker therapy in patients that have started taking an alpha-blocker would not be expected to produce acute postural hypotension. Alpha-blockers linked to this interaction include alfuzosin, doxazosin, prazosin, and terazosin. Beta-blockers linked to this interaction include acebutolol, atenolol, betaxolol, bevantolol, levobunolol, metoprolol, nadolol, pindolol, pronethalol, propranolol, and timolol. |
ALFUZOSIN HCL ER, CARDURA, CARDURA XL, DOXAZOSIN MESYLATE, PRAZOSIN HCL, TERAZOSIN HCL, TEZRULY, UROXATRAL |
| Clonidine/Beta-Blockers SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Withdrawal of clonidine triggers increased catecholamine release. Beta-blockers inhibit the vasodilation mediated by the beta 2 receptor, leaving the vasoconstriction mediated by the alpha 2 receptor unopposed. In addition, concurrent use is expected to produce additive effects on blood pressure and heart rate requiring standard monitoring precautions. CLINICAL EFFECTS: Severe hypertension may occur upon abrupt discontinuation of clonidine in patients receiving both clonidine and beta-blockers. In addition, concurrent use is expected to produce additive effects on blood pressure and heart rate requiring standard monitoring precautions. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: In a patient receiving both drugs, discontinuation of the beta-blocker prior to clonidine may decrease the occurrence of rebound hypertension. If clonidine is discontinued first, rebound hypertension can be treated by restarting the clonidine or by the IV administration of phentolamine, phenoxybenzamine or prazosin. When adding either of these agents to the drug regimen of the patient, monitor blood pressure. Since labetalol has both alpha and beta activity, administration of labetalol may prevent rebound hypertension in patients undergoing clonidine withdrawal, although conflicting reports exist. In addition, concurrent use is expected to produce additive effects on blood pressure and heart rate requiring standard monitoring precautions. DISCUSSION: Increased blood pressure has been observed in patients following: 1) the discontinuation of clonidine in patients receiving beta-blockers, 2) the replacement of clonidine therapy with beta-blockers, 3) the simultaneous discontinuation of both drugs. Conflicting reports exist on the development of increased blood pressure after clonidine withdrawal in patients receiving labetalol. Patients receiving labetalol who are being withdrawn from clonidine should still be closely monitored. |
CATAPRES-TTS 1, CATAPRES-TTS 2, CATAPRES-TTS 3, CLONIDINE, CLONIDINE HCL, CLONIDINE HCL ER, DURACLON, JAVADIN, NEXICLON XR, ONYDA XR, R.E.C.K.(ROPIV-EPI-CLON-KETOR), ROPIVACAINE-CLONIDINE-KETOROLC |
| Antidiabetics/Selected Ophthalmic Non-Cardioselective Beta-Blockers SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Not fully established. Probably blockade of a variety of beta-adrenergic responses to hypoglycemia.(1,2) CLINICAL EFFECTS: Diminished response to sulfonylureas and insulin may occur. Frequency and severity of hypoglycemic episodes may be increased, while warning symptoms of low blood sugar may be masked.(1,2) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Try to avoid beta-blocker therapy, particularly in diabetics prone to hypoglycemic attacks. One of the cardioselective agents may decrease risk of hypertensive attacks and allow more rapid glucose recovery from hypoglycemia. Patients should be counseled not to rely on tachycardia to diagnose hypoglycemia, since it is masked by beta-blocker therapy. Diaphoresis is unaffected by beta-blockade and can be used by the diabetic to recognize hypoglycemia. DISCUSSION: A double blind, randomized, 12 month study of 39 patients tested the metabolic effects of pindolol (5mg BID) compared to control group on insulin sensitivity. The patient's insulin sensitivity index decreased 17% when on pindolol treatment compared to placebo (p<0.01). Insulin mediated glucose uptake was significantly lower (p<0.05) with propranolol treatment than with placebo.(3) A study of 26 patients with chronic heart failure showed that carvedilol (average daily dose 27.5mg/d) caused a significant decrease in fasting insulin levels (17.09 to 10.77 microU/ml, p <0.05) compared to pre-treatment levels. This trial also showed that patients on carvedilol had significantly (p=0.015) lower fasting insulin levels (10.77 microU/ml) compared to the fasting insulin levels (20.72 microU/ml) of patients on bisoprolol treatment (5.9mg/d).(4) There have been case reports of hypoglycemia following the addition of ophthalmic timolol to a diabetic regimen.(5-7) Studies have shown that ophthalmic beta-blockers, especially the aqueous solution, have significant systemic absorption and do not undergo first-pass metabolism.(8,9) |
ADMELOG, ADMELOG SOLOSTAR, AFREZZA, APIDRA, APIDRA SOLOSTAR, BASAGLAR KWIKPEN U-100, DUETACT, FIASP, FIASP FLEXTOUCH, FIASP PENFILL, FIASP PUMPCART, GLIMEPIRIDE, GLIPIZIDE, GLIPIZIDE ER, GLIPIZIDE XL, GLIPIZIDE-METFORMIN, GLYBURIDE, GLYBURIDE-METFORMIN HCL, HUMALOG, HUMALOG JUNIOR KWIKPEN, HUMALOG KWIKPEN U-100, HUMALOG KWIKPEN U-200, HUMALOG MIX 50-50 KWIKPEN, HUMALOG MIX 75-25, HUMALOG MIX 75-25 KWIKPEN, HUMALOG TEMPO PEN U-100, HUMULIN R U-500 KWIKPEN, INSULIN GLARGINE MAX SOLOSTAR, INSULIN GLARGINE SOLOSTAR, INSULIN GLARGINE-YFGN, INSULIN LISPRO, INSULIN LISPRO JUNIOR KWIKPEN, INSULIN LISPRO KWIKPEN U-100, INSULIN LISPRO PROTAMINE MIX, KIRSTY, KIRSTY PEN, LANTUS, LANTUS SOLOSTAR, LYUMJEV, LYUMJEV KWIKPEN U-100, LYUMJEV KWIKPEN U-200, LYUMJEV TEMPO PEN U-100, MERILOG, MERILOG SOLOSTAR, MYXREDLIN, NATEGLINIDE, NOVOLOG, NOVOLOG FLEXPEN, NOVOLOG MIX 70-30, NOVOLOG MIX 70-30 FLEXPEN, NOVOLOG PENFILL, PIOGLITAZONE-GLIMEPIRIDE, REZVOGLAR KWIKPEN, SEMGLEE (YFGN), SEMGLEE (YFGN) PEN, SOLIQUA 100-33, TOUJEO MAX SOLOSTAR, TOUJEO SOLOSTAR, TRESIBA, TRESIBA FLEXTOUCH U-100, TRESIBA FLEXTOUCH U-200, XULTOPHY 100-3.6 |
The following contraindication information is available for TIMOLOL MALEATE (timolol maleate/pf):
Drug contraindication overview.
No enhanced Contraindications information available for this drug.
No enhanced Contraindications information available for this drug.
There are 6 contraindications.
Absolute contraindication.
| Contraindication List |
|---|
| Acute decompensated heart failure |
| Asthma |
| Cardiogenic shock |
| Complete atrioventricular block |
| Incomplete AV heart block |
| Sinus bradycardia |
There are 2 severe contraindications.
Adequate patient monitoring is recommended for safer drug use.
| Severe List |
|---|
| Chronic obstructive pulmonary disease |
| Hyperthyroidism |
There are 3 moderate contraindications.
Clinically significant contraindication, where the condition can be managed or treated before the drug may be given safely.
| Moderate List |
|---|
| Diabetes mellitus |
| Hypoglycemic disorder |
| Myasthenia gravis |
The following adverse reaction information is available for TIMOLOL MALEATE (timolol maleate/pf):
Adverse reaction overview.
No enhanced Common Adverse Effects information available for this drug.
No enhanced Common Adverse Effects information available for this drug.
There are 19 severe adverse reactions.
| More Frequent | Less Frequent |
|---|---|
| None. | None. |
| Rare/Very Rare |
|---|
|
Acute myocardial infarction Acute respiratory failure Anaphylaxis Angioedema Bradycardia Bronchospastic pulmonary disease Cardiac arrhythmia Cerebrovascular accident Choroidal detachment Cystoid macular edema Decreased corneal sensitivity Heart block Heart failure Hypertension Hypotension Keratitis Muscle weakness Peyronie's disease Systemic lupus erythematosus |
There are 58 less severe adverse reactions.
| More Frequent | Less Frequent |
|---|---|
|
Eyelid erythema Ocular itching |
Conjunctivitis Dizziness Ocular discharge Ocular pain Upper respiratory infection |
| Rare/Very Rare |
|---|
|
Acute cognitive impairment Alopecia Angina Anorexia Behavioral disorders Blepharitis Blepharoptosis Blurred vision Chest pain Cough Delirium Depression Diarrhea Diplopia Drowsy Dry eye Dyspepsia Dyspnea Dysuria Erectile dysfunction Erythema Eye tearing Fatigue Foreign body sensation of eye General weakness Hallucinations Headache disorder Insomnia Libido changes Memory impairment Nasal congestion Nausea Nervousness Nightmares Ocular irritation Ocular redness Palpitations Paresthesia Pruritus of skin Psoriasiform eruption Raynaud's phenomenon Sensation of cold Skin pigmentation enhancement Skin rash Symptoms of anxiety Tinnitus Urticaria Vertigo Visual changes Vomiting Xerostomia |
The following precautions are available for TIMOLOL MALEATE (timolol maleate/pf):
No enhanced Pediatric Use information available for this drug.
Contraindicated
Severe Precaution
Management or Monitoring Precaution
Contraindicated
| None |
Severe Precaution
| None |
Management or Monitoring Precaution
| None |
Reproduction studies in mice, rats, and rabbits using oral timolol dosages up to 50 mg/kg daily (7000 times the systemic exposure following the maximum recommended human ophthalmic dosage) have not revealed evidence of harm to the fetus. Although delayed fetal ossification was observed at this dosage in rats, no adverse effects on postnatal development occurred in this species. Oral timolol dosages of 1 g/kg daily (142,000 times the systemic exposure following the maximum recommended human ophthalmic dosage) were maternotoxic and resulted in an increased number of fetal resorptions in mice.
Increased fetal resorptions were also observed in rabbits receiving oral timolol dosages 14,000 times the systemic exposure following the maximum recommended human ophthalmic dosage. There are no adequate and controlled studies to date using timolol ophthalmic solution in pregnant women, and the drug should be used during pregnancy only when the potential benefits justify the possible risks to the fetus.
Increased fetal resorptions were also observed in rabbits receiving oral timolol dosages 14,000 times the systemic exposure following the maximum recommended human ophthalmic dosage. There are no adequate and controlled studies to date using timolol ophthalmic solution in pregnant women, and the drug should be used during pregnancy only when the potential benefits justify the possible risks to the fetus.
Timolol is distributed into milk following oral or topical ophthalmic administration. Because of the potential for serious adverse reactions from timolol in nursing infants, a decision should be made whether to discontinue nursing or the drug, taking into account the importance of the drug to the woman.
No enhanced Geriatric Use information available for this drug.
The following prioritized warning is available for TIMOLOL MALEATE (timolol maleate/pf):
No warning message for this drug.
No warning message for this drug.
The following icd codes are available for TIMOLOL MALEATE (timolol maleate/pf)'s list of indications:
| Ocular hypertension | |
| H40.05 | Ocular hypertension |
| H40.051 | Ocular hypertension, right eye |
| H40.052 | Ocular hypertension, left eye |
| H40.053 | Ocular hypertension, bilateral |
| H40.059 | Ocular hypertension, unspecified eye |
| Open angle glaucoma | |
| H40.1 | Open-angle glaucoma |
| H40.10 | Unspecified open-angle glaucoma |
| H40.10x0 | Unspecified open-angle glaucoma, stage unspecified |
| H40.10x1 | Unspecified open-angle glaucoma, mild stage |
| H40.10x2 | Unspecified open-angle glaucoma, moderate stage |
| H40.10x3 | Unspecified open-angle glaucoma, severe stage |
| H40.10x4 | Unspecified open-angle glaucoma, indeterminate stage |
| H40.11 | Primary open-angle glaucoma |
| H40.111 | Primary open-angle glaucoma, right eye |
| H40.1110 | Primary open-angle glaucoma, right eye, stage unspecified |
| H40.1111 | Primary open-angle glaucoma, right eye, mild stage |
| H40.1112 | Primary open-angle glaucoma, right eye, moderate stage |
| H40.1113 | Primary open-angle glaucoma, right eye, severe stage |
| H40.1114 | Primary open-angle glaucoma, right eye, indeterminate stage |
| H40.112 | Primary open-angle glaucoma, left eye |
| H40.1120 | Primary open-angle glaucoma, left eye, stage unspecified |
| H40.1121 | Primary open-angle glaucoma, left eye, mild stage |
| H40.1122 | Primary open-angle glaucoma, left eye, moderate stage |
| H40.1123 | Primary open-angle glaucoma, left eye, severe stage |
| H40.1124 | Primary open-angle glaucoma, left eye, indeterminate stage |
| H40.113 | Primary open-angle glaucoma, bilateral |
| H40.1130 | Primary open-angle glaucoma, bilateral, stage unspecified |
| H40.1131 | Primary open-angle glaucoma, bilateral, mild stage |
| H40.1132 | Primary open-angle glaucoma, bilateral, moderate stage |
| H40.1133 | Primary open-angle glaucoma, bilateral, severe stage |
| H40.1134 | Primary open-angle glaucoma, bilateral, indeterminate stage |
| H40.119 | Primary open-angle glaucoma, unspecified eye |
| H40.1190 | Primary open-angle glaucoma, unspecified eye, stage unspecified |
| H40.1191 | Primary open-angle glaucoma, unspecified eye, mild stage |
| H40.1192 | Primary open-angle glaucoma, unspecified eye, moderate stage |
| H40.1193 | Primary open-angle glaucoma, unspecified eye, severe stage |
| H40.1194 | Primary open-angle glaucoma, unspecified eye, indeterminate stage |
| H40.12 | Low-tension glaucoma |
| H40.121 | Low-tension glaucoma, right eye |
| H40.1210 | Low-tension glaucoma, right eye, stage unspecified |
| H40.1211 | Low-tension glaucoma, right eye, mild stage |
| H40.1212 | Low-tension glaucoma, right eye, moderate stage |
| H40.1213 | Low-tension glaucoma, right eye, severe stage |
| H40.1214 | Low-tension glaucoma, right eye, indeterminate stage |
| H40.122 | Low-tension glaucoma, left eye |
| H40.1220 | Low-tension glaucoma, left eye, stage unspecified |
| H40.1221 | Low-tension glaucoma, left eye, mild stage |
| H40.1222 | Low-tension glaucoma, left eye, moderate stage |
| H40.1223 | Low-tension glaucoma, left eye, severe stage |
| H40.1224 | Low-tension glaucoma, left eye, indeterminate stage |
| H40.123 | Low-tension glaucoma, bilateral |
| H40.1230 | Low-tension glaucoma, bilateral, stage unspecified |
| H40.1231 | Low-tension glaucoma, bilateral, mild stage |
| H40.1232 | Low-tension glaucoma, bilateral, moderate stage |
| H40.1233 | Low-tension glaucoma, bilateral, severe stage |
| H40.1234 | Low-tension glaucoma, bilateral, indeterminate stage |
| H40.129 | Low-tension glaucoma, unspecified eye |
| H40.1290 | Low-tension glaucoma, unspecified eye, stage unspecified |
| H40.1291 | Low-tension glaucoma, unspecified eye, mild stage |
| H40.1292 | Low-tension glaucoma, unspecified eye, moderate stage |
| H40.1293 | Low-tension glaucoma, unspecified eye, severe stage |
| H40.1294 | Low-tension glaucoma, unspecified eye, indeterminate stage |
| H40.13 | Pigmentary glaucoma |
| H40.131 | Pigmentary glaucoma, right eye |
| H40.1310 | Pigmentary glaucoma, right eye, stage unspecified |
| H40.1311 | Pigmentary glaucoma, right eye, mild stage |
| H40.1312 | Pigmentary glaucoma, right eye, moderate stage |
| H40.1313 | Pigmentary glaucoma, right eye, severe stage |
| H40.1314 | Pigmentary glaucoma, right eye, indeterminate stage |
| H40.132 | Pigmentary glaucoma, left eye |
| H40.1320 | Pigmentary glaucoma, left eye, stage unspecified |
| H40.1321 | Pigmentary glaucoma, left eye, mild stage |
| H40.1322 | Pigmentary glaucoma, left eye, moderate stage |
| H40.1323 | Pigmentary glaucoma, left eye, severe stage |
| H40.1324 | Pigmentary glaucoma, left eye, indeterminate stage |
| H40.133 | Pigmentary glaucoma, bilateral |
| H40.1330 | Pigmentary glaucoma, bilateral, stage unspecified |
| H40.1331 | Pigmentary glaucoma, bilateral, mild stage |
| H40.1332 | Pigmentary glaucoma, bilateral, moderate stage |
| H40.1333 | Pigmentary glaucoma, bilateral, severe stage |
| H40.1334 | Pigmentary glaucoma, bilateral, indeterminate stage |
| H40.139 | Pigmentary glaucoma, unspecified eye |
| H40.1390 | Pigmentary glaucoma, unspecified eye, stage unspecified |
| H40.1391 | Pigmentary glaucoma, unspecified eye, mild stage |
| H40.1392 | Pigmentary glaucoma, unspecified eye, moderate stage |
| H40.1393 | Pigmentary glaucoma, unspecified eye, severe stage |
| H40.1394 | Pigmentary glaucoma, unspecified eye, indeterminate stage |
| H40.14 | Capsular glaucoma with pseudoexfoliation of lens |
| H40.141 | Capsular glaucoma with pseudoexfoliation of lens, right eye |
| H40.1410 | Capsular glaucoma with pseudoexfoliation of lens, right eye, stage unspecified |
| H40.1411 | Capsular glaucoma with pseudoexfoliation of lens, right eye, mild stage |
| H40.1412 | Capsular glaucoma with pseudoexfoliation of lens, right eye, moderate stage |
| H40.1413 | Capsular glaucoma with pseudoexfoliation of lens, right eye, severe stage |
| H40.1414 | Capsular glaucoma with pseudoexfoliation of lens, right eye, indeterminate stage |
| H40.142 | Capsular glaucoma with pseudoexfoliation of lens, left eye |
| H40.1420 | Capsular glaucoma with pseudoexfoliation of lens, left eye, stage unspecified |
| H40.1421 | Capsular glaucoma with pseudoexfoliation of lens, left eye, mild stage |
| H40.1422 | Capsular glaucoma with pseudoexfoliation of lens, left eye, moderate stage |
| H40.1423 | Capsular glaucoma with pseudoexfoliation of lens, left eye, severe stage |
| H40.1424 | Capsular glaucoma with pseudoexfoliation of lens, left eye, indeterminate stage |
| H40.143 | Capsular glaucoma with pseudoexfoliation of lens, bilateral |
| H40.1430 | Capsular glaucoma with pseudoexfoliation of lens, bilateral, stage unspecified |
| H40.1431 | Capsular glaucoma with pseudoexfoliation of lens, bilateral, mild stage |
| H40.1432 | Capsular glaucoma with pseudoexfoliation of lens, bilateral, moderate stage |
| H40.1433 | Capsular glaucoma with pseudoexfoliation of lens, bilateral, severe stage |
| H40.1434 | Capsular glaucoma with pseudoexfoliation of lens, bilateral, indeterminate stage |
| H40.149 | Capsular glaucoma with pseudoexfoliation of lens, unspecified eye |
| H40.1490 | Capsular glaucoma with pseudoexfoliation of lens, unspecified eye, stage unspecified |
| H40.1491 | Capsular glaucoma with pseudoexfoliation of lens, unspecified eye, mild stage |
| H40.1492 | Capsular glaucoma with pseudoexfoliation of lens, unspecified eye, moderate stage |
| H40.1493 | Capsular glaucoma with pseudoexfoliation of lens, unspecified eye, severe stage |
| H40.1494 | Capsular glaucoma with pseudoexfoliation of lens, unspecified eye, indeterminate stage |
| H40.15 | Residual stage of open-angle glaucoma |
| H40.151 | Residual stage of open-angle glaucoma, right eye |
| H40.152 | Residual stage of open-angle glaucoma, left eye |
| H40.153 | Residual stage of open-angle glaucoma, bilateral |
| H40.159 | Residual stage of open-angle glaucoma, unspecified eye |
Formulary Reference Tool