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Pindolol and hydrochlorothiazide (United States: Not available): Drug information

Pindolol and hydrochlorothiazide (United States: Not available): Drug information
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For additional information see "Pindolol and hydrochlorothiazide (United States: Not available): Patient drug information"

For abbreviations, symbols, and age group definitions show table
Brand Names: Canada
  • Viskazide 10/25;
  • Viskazide 10/50
Pharmacologic Category
  • Antihypertensive;
  • Beta-Blocker With Intrinsic Sympathomimetic Activity;
  • Diuretic, Thiazide
Dosing: Adult

Note: When higher doses or dosage adjustments are needed, use individual agents.

Hypertension

Hypertension: Oral: Dosage should be determined by titration of the individual agents and the combination product substituted based upon the daily requirements.

Usual dose: Pindolol 10 to 20 mg and hydrochlorothiazide 25 to 100 mg once daily. Maximum daily dose: Pindolol: 20 mg/hydrochlorothiazide: 100 mg

Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Dosing: Kidney Impairment: Adult

Mild to moderate impairment: No dosage adjustment necessary. Use with caution.

Severe impairment: There are no dosage adjustments provided in the manufacturer’s labeling. However, dosage reduction may be necessary; use with caution. Contraindicated with anuria.

Dosing: Liver Impairment: Adult

Mild to moderate impairment: No dosage adjustment necessary. Use with caution.

Severe impairment: There are no dosage adjustments provided in the manufacturer’s labeling. However, dosage reduction may be necessary; use with caution.

Dosing: Older Adult

Refer to adult dosing; use with caution.

Adverse Reactions

See individual agents.

Contraindications

Hypersensitivity to pindolol, hydrochlorothiazide, any other component of the formulation, or sulfonamide-derived drugs; or cross-sensitivity to other beta blockers; decompensated heart failure, right ventricular failure secondary to pulmonary hypertension, significant cardiomegaly, sinus bradycardia (≤50 bpm), second/third degree atrioventricular (AV) block; sick sinus syndrome; cardiogenic shock; prinzmetal angina (variant angina); severe peripheral arterial circulatory disorders; bronchospasm (including bronchial asthma) or severe chronic obstructive pulmonary disease (COPD); anesthetic agents producing myocardial depression; anuria; pheochromocytoma (untreated)

Additionally, the manufacturer of hydrochlorothiazide contraindicates use for increasing azotemia and oliguria during treatment of severe progressive renal disease; breastfeeding

Note: Although the FDA-approved product labeling states this medication is contraindicated in patients with hypersensitivity to sulfonamide-containing drugs, the scientific basis of this cross-sensitivity has been challenged.

Warnings/Precautions

Concerns related to adverse effects:

• Anaphylactic reactions: Use caution with history of severe anaphylaxis to allergens; patients taking beta-blockers may become more sensitive to repeated challenges. Treatment of anaphylaxis (eg, epinephrine) in patients taking beta-blockers may be ineffective or promote undesirable effects.

• Bradycardia: Pindolol may cause bradycardia; dose reduction may be necessary if excessive bradycardia occurs.

• Electrolyte disturbances: Hypokalemia, hypochloremic alkalosis, hypomagnesemia, and hyponatremia may occur with hydrochlorothiazide. Development of electrolyte disturbances can be minimized when used in combination with other electrolyte sparing antihypertensives (eg, ACE inhibitors or angiotensin receptor blockers) (Sica 2011). Hypercalcemia and hypophosphatemia have been observed with prolonged thiazide therapy; discontinue use prior to parathyroid testing.

• Gout: In certain patients with a history of gout, a familial predisposition to gout, or chronic renal failure, gout can be precipitated by hydrochlorothiazide. This risk may be increased with doses ≥25 mg (Gurwitz 1997).

• Hypersensitivity reactions: Hypersensitivity reactions may occur with hydrochlorothiazide. Risk is increased in patients with a history of allergy or bronchial asthma.

• Ocular: Conjunctival xerosis (dryness of eye surface) has been reported with use of beta blockers. Hydrochlorothiazide may cause acute transient myopia and acute angle-closure glaucoma, typically occurring within hours to weeks following initiation. Discontinue therapy immediately in patients with acute decreases in visual acuity or ocular pain; additional treatments may be needed if uncontrolled intraocular pressure persists. Risk factors may include a history of sulfonamide or penicillin allergy.

• Photosensitivity: Photosensitization may occur.

• Skin cancer, nonmelanoma: Prolonged use (≥3 years) may increase the risk for squamous cell carcinoma up to 4 times and increase the risk for basal cell carcinoma up to 1.25 times compared to patients not treated with hydrochlorothiazide (Pedersen 2018; Pottegård 2017).

• Sulfonamide (“sulfa”) allergy: The FDA-approved product labeling for many medications containing a sulfonamide chemical group includes a broad contraindication in patients with a prior allergic reaction to sulfonamides. There is a potential for cross-reactivity between members of a specific class (eg, two antibiotic sulfonamides). However, concerns for cross-reactivity have previously extended to all compounds containing the sulfonamide structure (SO2NH2). An expanded understanding of allergic mechanisms indicates cross-reactivity between antibiotic sulfonamides and nonantibiotic sulfonamides may not occur or at the very least this potential is extremely low (Brackett 2004; Johnson 2005; Slatore 2004; Tornero 2004). In particular, mechanisms of cross-reaction due to antibody production (anaphylaxis) are unlikely to occur with nonantibiotic sulfonamides. T-cell-mediated (type IV) reactions (eg, maculopapular rash) are less well understood and it is not possible to completely exclude this potential based on current insights. In cases where prior reactions were severe (Stevens-Johnson syndrome/TEN), some clinicians choose to avoid exposure to these classes.

Disease-related concerns:

• Bariatric surgery: Dehydration: Avoid diuretics in the immediate postoperative period after bariatric surgery; electrolyte disturbances and dehydration may occur. Diuretics may be resumed, if indicated, once oral fluid intake goals are met (Ziegler 2009).

• Conduction abnormality: Consider preexisting conditions before initiating.

• Diabetes: Use with caution in patients with diabetes mellitus; may potentiate hypoglycemia and/or mask signs and symptoms, also may see a change in glucose control

• Heart failure (HF): Use with caution in patients with compensated HF and monitor for a worsening of the condition. If condition worsens, consider temporary discontinuation or dosage reduction of pindolol. Patients should be stabilized on heart failure regimen prior to initiation of beta-blocker. Beta-blocker therapy should be initiated at very low doses with gradual and very careful titration. Adjustment of other medications (ACE inhibitors and/or diuretics) may be required. Beta-blockers with intrinsic sympathomimetic activity (eg, pindolol) have not been demonstrated to be of value in HF.

• Hepatic impairment: Use with caution in patients with hepatic impairment; pindolol levels may increase significantly with hepatic impairment. In progressive or severe liver disease, avoid electrolyte and acid/base imbalances that might lead to hepatic encephalopathy/coma

• Hypercholesterolemia: Use with caution in patients with moderate or high cholesterol concentrations.

• Myasthenia gravis: Use beta blockers with caution in patients with myasthenia gravis.

• Parathyroid disease: Thiazide diuretics reduce calcium excretion; pathologic changes in the parathyroid glands with hypercalcemia and hypophosphatemia have been observed with prolonged use; should be discontinued prior to testing for parathyroid function.

• Peripheral vascular disease (PVD) and Raynaud disease: Can precipitate or aggravate symptoms of arterial insufficiency in patients with PVD and Raynaud's disease. Use with caution and monitor for progression of arterial obstruction.

• Psoriasis: Beta-blocker use has been associated with induction or exacerbation of psoriasis, but cause and effect have not been firmly established.

• Renal impairment: Use with caution in patients with renal impairment; thiazides may precipitate azotemia. Discontinue use with worsening of renal function. Hydrochlorothiazide is ineffective in severe renal disease.

• Respiratory disease: Use with caution in patients prone to nonallergic bronchospasm (eg, emphysema, chronic bronchitis).

• Systemic lupus erythematosus (SLE): Thiazides may cause SLE exacerbation or activation.

• Thyroid disease: May mask signs of hyperthyroidism (eg, tachycardia). If thyrotoxicosis is suspected, carefully manage and monitor; abrupt withdrawal may exacerbate symptoms of hyperthyroidism or precipitate thyroid storm.

Special populations:

• Older adult: Bradycardia may be observed more frequently in older adult patients (>65 years of age); dosage reductions may be necessary.

Other warnings/precautions:

• Abrupt withdrawal: Beta-blocker therapy should not be withdrawn abruptly (particularly in patients with CAD), but gradually tapered over 1 to 2 weeks to avoid acute tachycardia, hypertension, and/or ischemia. Severe exacerbation of angina, ventricular arrhythmias, and myocardial infarction (MI) have been reported following abrupt withdrawal of beta-blocker therapy. Temporary but prompt resumption of beta-blocker therapy may be indicated with worsening of angina or acute coronary insufficiency.

• Major surgery: Chronic beta-blocker therapy should not be routinely withdrawn prior to major surgery (Fleischmann 2009).

Product Availability

Not available in the US

Generic Equivalent Available: US

May be product dependent

Dosage Forms: Canada

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Tablet, Oral:

Viskazide 10/25: Pindolol 10 mg and hydrochlorothiazide 25 mg [contains corn starch]

Viskazide 10/50: Pindolol 10 mg and hydrochlorothiazide 50 mg [contains corn starch]

Administration: Adult

Oral: May be administered with food or milk. Take early in day to avoid nocturia.

Use: Labeled Indications

Note: Not approved in the US.

Hypertension: Management of hypertension; not for initial therapy.

Medication Safety Issues
Sound-alike/look-alike issues:

Viskazide may be confused with hydroCHLOROthiazide, Visken.

Older Adult: High-Risk Medication:

Beers Criteria: Diuretics (hydrochlorothiazide) are identified in the Beers Criteria as potentially inappropriate medications to be used with caution in patients 65 years and older due to the potential to cause or exacerbate syndrome of inappropriate antidiuretic hormone secretion (SIADH) or hyponatremia; monitor sodium concentration closely when initiating or adjusting the dose in older adults (Beers Criteria [AGS 2023]).

Metabolism/Transport Effects

Refer to individual components.

Drug Interactions

Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.

Acetylcholinesterase Inhibitors: May increase bradycardic effects of Beta-Blockers. Risk C: Monitor

Agents with Clinically Relevant Anticholinergic Effects: May increase serum concentration of Thiazide and Thiazide-Like Diuretics. Risk C: Monitor

Ajmaline: Sulfonamides may increase adverse/toxic effects of Ajmaline. Specifically, the risk for cholestasis may be increased. Risk C: Monitor

Alcohol (Ethyl): May increase orthostatic hypotensive effects of Thiazide and Thiazide-Like Diuretics. Risk C: Monitor

Alfuzosin: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Allopurinol: Thiazide and Thiazide-Like Diuretics may increase hypersensitivity effects of Allopurinol. Risk C: Monitor

Alpha2-Agonists: Beta-Blockers may increase rebound hypertensive effects of Alpha2-Agonists. This effect can occur when the Alpha2-Agonist is abruptly withdrawn. Alpha2-Agonists may increase AV-blocking effects of Beta-Blockers. Sinus node dysfunction may also be enhanced. Management: Closely monitor heart rate during treatment with a beta blocker and clonidine. Withdraw beta blockers several days before clonidine withdrawal when possible, and monitor blood pressure closely. Recommendations for other alpha2-agonists are unavailable. Risk D: Consider Therapy Modification

Amifostine: Blood Pressure Lowering Agents may increase hypotensive effects of Amifostine. Management: When used at chemotherapy doses, hold blood pressure lowering medications for 24 hours before amifostine administration. If blood pressure lowering therapy cannot be held, do not administer amifostine. Use caution with radiotherapy doses of amifostine. Risk D: Consider Therapy Modification

Aminolevulinic Acid (Systemic): Photosensitizing Agents may increase photosensitizing effects of Aminolevulinic Acid (Systemic). Risk X: Avoid

Aminolevulinic Acid (Topical): Photosensitizing Agents may increase photosensitizing effects of Aminolevulinic Acid (Topical). Risk C: Monitor

Amiodarone: May increase bradycardic effects of Beta-Blockers. Possibly to the point of cardiac arrest. Amiodarone may increase serum concentration of Beta-Blockers. Risk C: Monitor

Amphetamines: May decrease antihypertensive effects of Antihypertensive Agents. Risk C: Monitor

Angiotensin-Converting Enzyme Inhibitors: Thiazide and Thiazide-Like Diuretics may increase hypotensive effects of Angiotensin-Converting Enzyme Inhibitors. Thiazide and Thiazide-Like Diuretics may increase nephrotoxic effects of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor

Antidiabetic Agents: Beta-Blockers (Nonselective) may increase hypoglycemic effects of Antidiabetic Agents. Beta-Blockers (Nonselective) may increase adverse/toxic effects of Antidiabetic Agents. Specifically, beta-blockers may mask the hypoglycemic symptoms of antidiabetic agents. Risk C: Monitor

Antidiabetic Agents: Hyperglycemia-Associated Agents may decrease therapeutic effects of Antidiabetic Agents. Risk C: Monitor

Antidiabetic Agents: Thiazide and Thiazide-Like Diuretics may decrease therapeutic effects of Antidiabetic Agents. Risk C: Monitor

Antipsychotic Agents (Phenothiazines): May increase hypotensive effects of Beta-Blockers. Beta-Blockers may decrease metabolism of Antipsychotic Agents (Phenothiazines). Antipsychotic Agents (Phenothiazines) may decrease metabolism of Beta-Blockers. Risk C: Monitor

Antipsychotic Agents (Second Generation [Atypical]): Blood Pressure Lowering Agents may increase hypotensive effects of Antipsychotic Agents (Second Generation [Atypical]). Risk C: Monitor

Arginine: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Arimoclomol: May increase serum concentration of OCT2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor

Arsenic Trioxide: Thiazide and Thiazide-Like Diuretics may increase hypotensive effects of Arsenic Trioxide. Thiazide and Thiazide-Like Diuretics may increase QTc-prolonging effects of Arsenic Trioxide. Management: When possible, avoid concurrent use of arsenic trioxide with drugs that can cause electrolyte abnormalities, such as the thiazide and thiazide-like diuretics. Risk D: Consider Therapy Modification

Barbiturates: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Benperidol: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Beta2-Agonists: Beta-Blockers (Nonselective) may decrease bronchodilatory effects of Beta2-Agonists. Risk X: Avoid

Bile Acid Sequestrants: May decrease absorption of Thiazide and Thiazide-Like Diuretics. Management: Separate administration of bile acid sequestrants and oral thiazide diuretics by at least 4 hours. Monitor for decreased therapeutic effects of thiazide diuretics if coadministered with a bile acid sequestrant. Risk D: Consider Therapy Modification

Bradycardia-Causing Agents: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor

Brigatinib: May decrease antihypertensive effects of Antihypertensive Agents. Brigatinib may increase bradycardic effects of Antihypertensive Agents. Risk C: Monitor

Brimonidine (Topical): May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Bromperidol: May decrease hypotensive effects of Blood Pressure Lowering Agents. Blood Pressure Lowering Agents may increase hypotensive effects of Bromperidol. Risk X: Avoid

Cafedrine: May increase bradycardic effects of Beta-Blockers. Beta-Blockers may decrease therapeutic effects of Cafedrine. Risk C: Monitor

Calcium Salts: Thiazide and Thiazide-Like Diuretics may increase serum concentration of Calcium Salts. Risk C: Monitor

Cannabis: Beta-Blockers may increase adverse/toxic effects of Cannabis. Specifically, the risk of hypoglycemia may be increased. Risk C: Monitor

Cardiac Glycosides: Thiazide and Thiazide-Like Diuretics may increase adverse/toxic effects of Cardiac Glycosides. Specifically, cardiac glycoside toxicity may be enhanced by the hypokalemic and hypomagnesemic effect of thiazide diuretics. Risk C: Monitor

Ceritinib: Bradycardia-Causing Agents may increase bradycardic effects of Ceritinib. Management: If this combination cannot be avoided, monitor patients for evidence of symptomatic bradycardia, and closely monitor blood pressure and heart rate during therapy. Risk D: Consider Therapy Modification

Cholinergic Agonists: Beta-Blockers may increase adverse/toxic effects of Cholinergic Agonists. Of particular concern are the potential for cardiac conduction abnormalities and bronchoconstriction. Risk C: Monitor

Corticosteroids (Systemic): May increase hypokalemic effects of Thiazide and Thiazide-Like Diuretics. Risk C: Monitor

CycloPHOSphamide: Thiazide and Thiazide-Like Diuretics may increase adverse/toxic effects of CycloPHOSphamide. Specifically, granulocytopenia may be enhanced. Risk C: Monitor

Desmopressin: Hyponatremia-Associated Agents may increase hyponatremic effects of Desmopressin. Risk C: Monitor

Dexketoprofen: May increase adverse/toxic effects of Sulfonamides. Risk C: Monitor

Dexmethylphenidate: May decrease therapeutic effects of Antihypertensive Agents. Risk C: Monitor

Diacerein: May increase therapeutic effects of Diuretics. Specifically, the risk for dehydration or hypokalemia may be increased. Risk C: Monitor

Diazoxide Choline: May increase adverse/toxic effects of Thiazide and Thiazide-Like Diuretics. Specifically, the hyperglycemic and hyperuricemic effects may be increased. Risk C: Monitor

Diazoxide: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Diazoxide: Thiazide and Thiazide-Like Diuretics may increase adverse/toxic effects of Diazoxide. Risk C: Monitor

Dichlorphenamide: Thiazide and Thiazide-Like Diuretics may increase hypokalemic effects of Dichlorphenamide. Risk C: Monitor

Dipyridamole: May increase bradycardic effects of Beta-Blockers. Risk C: Monitor

Disopyramide: May increase bradycardic effects of Beta-Blockers. Beta-Blockers may increase negative inotropic effects of Disopyramide. Risk C: Monitor

DOBUTamine: Beta-Blockers may decrease therapeutic effects of DOBUTamine. Risk C: Monitor

Dofetilide: HydroCHLOROthiazide may increase QTc-prolonging effects of Dofetilide. HydroCHLOROthiazide may increase serum concentration of Dofetilide. Risk X: Avoid

Dronedarone: May increase bradycardic effects of Beta-Blockers. Dronedarone may increase serum concentration of Beta-Blockers. This likely applies only to those agents that are metabolized by CYP2D6. Management: Use lower initial beta-blocker doses; adequate tolerance of the combination, based on ECG findings, should be confirmed prior to any increase in beta-blocker dose. Increase monitoring for clinical response and adverse effects. Risk D: Consider Therapy Modification

DULoxetine: Blood Pressure Lowering Agents may increase hypotensive effects of DULoxetine. Risk C: Monitor

EPHEDrine (Systemic): Beta-Blockers may decrease therapeutic effects of EPHEDrine (Systemic). Risk C: Monitor

EPINEPHrine (Nasal): Beta-Blockers (Nonselective) may increase hypertensive effects of EPINEPHrine (Nasal). Risk C: Monitor

EPINEPHrine (Oral Inhalation): Beta-Blockers (Nonselective) may increase hypertensive effects of EPINEPHrine (Oral Inhalation). Risk C: Monitor

EPINEPHrine (Systemic): Beta-Blockers (Nonselective) may increase hypertensive effects of EPINEPHrine (Systemic). Risk C: Monitor

EPINEPHrine (Systemic): Diuretics may increase arrhythmogenic effects of EPINEPHrine (Systemic). Diuretics may decrease vasopressor effects of EPINEPHrine (Systemic). Risk C: Monitor

Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates): Beta-Blockers may increase vasoconstricting effects of Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates). Risk C: Monitor

Etilefrine: Beta-Blockers may decrease therapeutic effects of Etilefrine. Etilefrine may increase bradycardic effects of Beta-Blockers. Risk C: Monitor

Etofylline: Beta-Blockers may decrease therapeutic effects of Etofylline. Risk X: Avoid

Etrasimod: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor

Fedratinib: May increase serum concentration of OCT2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor

Fexinidazole: Bradycardia-Causing Agents may increase arrhythmogenic effects of Fexinidazole. Risk X: Avoid

Fingolimod: Bradycardia-Causing Agents may increase bradycardic effects of Fingolimod. Management: Consult with the prescriber of any bradycardia-causing agent to see if the agent could be switched to an agent that does not cause bradycardia prior to initiating fingolimod. If combined, perform continuous ECG monitoring after the first fingolimod dose. Risk D: Consider Therapy Modification

Flecainide: May increase bradycardic effects of Pindolol. The negative inotropic effects of Pindolol may also be enhanced. Risk C: Monitor

Flunarizine: May increase therapeutic effects of Antihypertensive Agents. Risk C: Monitor

Gilteritinib: May increase serum concentration of OCT1 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor

Givinostat: May increase serum concentration of OCT2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor

Grass Pollen Allergen Extract (5 Grass Extract): Beta-Blockers may increase adverse/toxic effects of Grass Pollen Allergen Extract (5 Grass Extract). More specifically, Beta-Blockers may inhibit the ability to effectively treat severe allergic reactions to Grass Pollen Allergen Extract (5 Grass Extract) with epinephrine. Some other effects of epinephrine may be unaffected or even enhanced (e.g., vasoconstriction) during treatment with Beta-Blockers. Management: Consider alternatives to either grass pollen allergen extract (5 grass extract) or beta-blockers in patients with indications for both agents. Canadian product labeling specifically lists this combination as contraindicated. Risk D: Consider Therapy Modification

Herbal Products with Blood Pressure Increasing Effects: May decrease antihypertensive effects of Antihypertensive Agents. Risk C: Monitor

Herbal Products with Blood Pressure Lowering Effects: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Hypotension-Associated Agents: Blood Pressure Lowering Agents may increase hypotensive effects of Hypotension-Associated Agents. Risk C: Monitor

Iloperidone: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Indoramin: May increase hypotensive effects of Antihypertensive Agents. Risk C: Monitor

Insulin: Beta-Blockers (Nonselective) may increase hypoglycemic effects of Insulin. Beta-Blockers (Nonselective) may decrease therapeutic effects of Insulin. Risk C: Monitor

Ipragliflozin: May increase adverse/toxic effects of Thiazide and Thiazide-Like Diuretics. Specifically, the risk for intravascular volume depletion may be increased. Risk C: Monitor

Isocarboxazid: May increase antihypertensive effects of Antihypertensive Agents. Risk X: Avoid

Isocarboxazid: May increase hypotensive effects of Diuretics. Risk X: Avoid

Isoproterenol: Beta-Blockers may decrease therapeutic effects of Isoproterenol. Risk C: Monitor

Ivabradine: Bradycardia-Causing Agents may increase bradycardic effects of Ivabradine. Risk C: Monitor

Ivabradine: Thiazide and Thiazide-Like Diuretics may increase arrhythmogenic effects of Ivabradine. Risk C: Monitor

Lacosamide: Bradycardia-Causing Agents may increase AV-blocking effects of Lacosamide. Risk C: Monitor

Landiolol: Bradycardia-Causing Agents may increase bradycardic effects of Landiolol. Risk X: Avoid

Levodopa-Foslevodopa: Blood Pressure Lowering Agents may increase hypotensive effects of Levodopa-Foslevodopa. Risk C: Monitor

Levosulpiride: Thiazide and Thiazide-Like Diuretics may increase adverse/toxic effects of Levosulpiride. Risk X: Avoid

Licorice: May increase hypokalemic effects of Thiazide and Thiazide-Like Diuretics. Risk C: Monitor

Lithium: Thiazide and Thiazide-Like Diuretics may decrease excretion of Lithium. Management: Reduce the lithium dose if coadministered with thiazide or thiazide-like diuretics. Monitor serum lithium levels during coadministration with thiazide and thiazide-like diuretics. Risk D: Consider Therapy Modification

Loop Diuretics: May increase hypotensive effects of Antihypertensive Agents. Risk C: Monitor

Lormetazepam: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Mavacamten: Beta-Blockers may increase adverse/toxic effects of Mavacamten. Specifically, negative inotropic effects may be increased. Risk C: Monitor

Mecamylamine: Thiazide and Thiazide-Like Diuretics may increase adverse/toxic effects of Mecamylamine. Management: Consider avoiding the use of mecamylamine and thiazide diuretics. If combined, mecamylamine prescribing information suggests reducing the mecamylamine dose by 50% in order to avoid excessive hypotension. Risk D: Consider Therapy Modification

Metergoline: May decrease antihypertensive effects of Blood Pressure Lowering Agents. Blood Pressure Lowering Agents may increase orthostatic hypotensive effects of Metergoline. Risk C: Monitor

Methacholine: Beta-Blockers may increase adverse/toxic effects of Methacholine. Risk C: Monitor

Methenamine: Thiazide and Thiazide-Like Diuretics may decrease therapeutic effects of Methenamine. Risk C: Monitor

Methotrexate: HydroCHLOROthiazide may increase nephrotoxic effects of Methotrexate. Risk C: Monitor

Methoxsalen (Systemic): Photosensitizing Agents may increase photosensitizing effects of Methoxsalen (Systemic). Risk C: Monitor

Methylphenidate: May decrease antihypertensive effects of Antihypertensive Agents. Risk C: Monitor

Midodrine: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor

Mivacurium: Beta-Blockers may increase therapeutic effects of Mivacurium. Risk C: Monitor

Molsidomine: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Multivitamins/Fluoride (with ADE): May increase hypercalcemic effects of Thiazide and Thiazide-Like Diuretics. Risk C: Monitor

Multivitamins/Minerals (with ADEK, Folate, Iron): Thiazide and Thiazide-Like Diuretics may increase hypercalcemic effects of Multivitamins/Minerals (with ADEK, Folate, Iron). Risk C: Monitor

Multivitamins/Minerals (with AE, No Iron): Thiazide and Thiazide-Like Diuretics may increase serum concentration of Multivitamins/Minerals (with AE, No Iron). Specifically, thiazide diuretics may decrease the excretion of calcium, and continued concomitant use can also result in metabolic alkalosis. Risk C: Monitor

Naftopidil: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Neuromuscular-Blocking Agents (Nondepolarizing): Thiazide and Thiazide-Like Diuretics may increase neuromuscular-blocking effects of Neuromuscular-Blocking Agents (Nondepolarizing). Risk C: Monitor

Nicergoline: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Nicorandil: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

NIFEdipine (Topical): May increase adverse/toxic effects of Beta-Blockers. Risk C: Monitor

NIFEdipine: May increase hypotensive effects of Beta-Blockers. NIFEdipine may increase negative inotropic effects of Beta-Blockers. Risk C: Monitor

Nitrendipine: May increase therapeutic effects of Beta-Blockers. Risk C: Monitor

Nitroprusside: Blood Pressure Lowering Agents may increase hypotensive effects of Nitroprusside. Risk C: Monitor

Nonsteroidal Anti-Inflammatory Agents (Topical): May decrease therapeutic effects of Beta-Blockers. Risk C: Monitor

Nonsteroidal Anti-Inflammatory Agents (Topical): May decrease therapeutic effects of Thiazide and Thiazide-Like Diuretics. Risk C: Monitor

Nonsteroidal Anti-Inflammatory Agents: May decrease antihypertensive effects of Beta-Blockers. Risk C: Monitor

Nonsteroidal Anti-Inflammatory Agents: May decrease therapeutic effects of Thiazide and Thiazide-Like Diuretics. Thiazide and Thiazide-Like Diuretics may increase nephrotoxic effects of Nonsteroidal Anti-Inflammatory Agents. Risk C: Monitor

Obinutuzumab: May increase hypotensive effects of Blood Pressure Lowering Agents. Management: Consider temporarily withholding blood pressure lowering medications beginning 12 hours prior to obinutuzumab infusion and continuing until 1 hour after the end of the infusion. Risk D: Consider Therapy Modification

Opioid Agonists: May increase adverse/toxic effects of Diuretics. Opioid Agonists may decrease therapeutic effects of Diuretics. Risk C: Monitor

Opipramol: Beta-Blockers may increase serum concentration of Opipramol. Opipramol may increase serum concentration of Beta-Blockers. Risk C: Monitor

Ozanimod: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor

Palopegteriparatide: Thiazide and Thiazide-Like Diuretics may increase therapeutic effects of Palopegteriparatide. Thiazide and Thiazide-Like Diuretics may decrease therapeutic effects of Palopegteriparatide. Risk C: Monitor

Pentoxifylline: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Perazine: May increase hypotensive effects of Antihypertensive Agents. Risk C: Monitor

Pholcodine: Blood Pressure Lowering Agents may increase hypotensive effects of Pholcodine. Risk C: Monitor

Phosphodiesterase 5 Inhibitors: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Piperacillin: May increase hypokalemic effects of Diuretics. Risk C: Monitor

Polyethylene Glycol-Electrolyte Solution: Diuretics may increase nephrotoxic effects of Polyethylene Glycol-Electrolyte Solution. Risk C: Monitor

Ponesimod: Bradycardia-Causing Agents may increase bradycardic effects of Ponesimod. Management: Avoid coadministration of ponesimod with drugs that may cause bradycardia when possible. If combined, monitor heart rate closely and consider obtaining a cardiology consult. Do not initiate ponesimod in patients on beta-blockers if HR is less than 55 bpm. Risk D: Consider Therapy Modification

Porfimer: Photosensitizing Agents may increase photosensitizing effects of Porfimer. Risk X: Avoid

Prazosin: Antihypertensive Agents may increase hypotensive effects of Prazosin. Risk C: Monitor

Promazine: Thiazide and Thiazide-Like Diuretics may increase QTc-prolonging effects of Promazine. Risk X: Avoid

Prostacyclin Analogues: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Quinagolide: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Reboxetine: May increase hypokalemic effects of Thiazide and Thiazide-Like Diuretics. Risk C: Monitor

Reserpine: May increase hypotensive effects of Beta-Blockers. Reserpine may increase bradycardic effects of Beta-Blockers. Risk C: Monitor

Rivastigmine: May increase bradycardic effects of Beta-Blockers. Risk X: Avoid

Selective Serotonin Reuptake Inhibitor: May increase hyponatremic effects of Thiazide and Thiazide-Like Diuretics. Risk C: Monitor

Silodosin: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Siponimod: Bradycardia-Causing Agents may increase bradycardic effects of Siponimod. Management: Avoid coadministration of siponimod with drugs that may cause bradycardia. If combined, consider obtaining a cardiology consult regarding patient monitoring. Risk D: Consider Therapy Modification

Sodium Phosphates: Diuretics may increase nephrotoxic effects of Sodium Phosphates. Specifically, the risk of acute phosphate nephropathy may be enhanced. Risk C: Monitor

Sotagliflozin: HydroCHLOROthiazide may decrease therapeutic effects of Sotagliflozin. Sotagliflozin may decrease serum concentration of HydroCHLOROthiazide. Risk C: Monitor

Succinylcholine: Beta-Blockers may increase neuromuscular-blocking effects of Succinylcholine. Risk C: Monitor

Sulfonylureas: Beta-Blockers (Nonselective) may increase hypoglycemic effects of Sulfonylureas. Beta-Blockers (Nonselective) may decrease therapeutic effects of Sulfonylureas. Risk C: Monitor

Tafenoquine: May increase serum concentration of OCT2 Substrates (Clinically Relevant with Inhibitors). Management: Avoid use of OCT2 substrates with tafenoquine, and if the combination cannot be avoided, monitor closely for evidence of toxicity of the OCT2 substrate and consider a reduced dose of the OCT2 substrate according to that substrate's labeling. Risk D: Consider Therapy Modification

Tasimelteon: Beta-Blockers may decrease therapeutic effects of Tasimelteon. Management: Consider avoiding nighttime administration of beta-blockers during tasimelteon therapy due to the potential for reduced tasimelteon efficacy. Risk D: Consider Therapy Modification

Terazosin: Antihypertensive Agents may increase hypotensive effects of Terazosin. Risk C: Monitor

Theodrenaline: May increase bradycardic effects of Beta-Blockers. Beta-Blockers may decrease therapeutic effects of Theodrenaline. Risk C: Monitor

Theophylline Derivatives: Beta-Blockers (Nonselective) may decrease bronchodilatory effects of Theophylline Derivatives. Risk C: Monitor

Thioridazine: May increase serum concentration of Pindolol. Pindolol may increase serum concentration of Thioridazine. Risk X: Avoid

Topiramate: Thiazide and Thiazide-Like Diuretics may increase hypokalemic effects of Topiramate. Thiazide and Thiazide-Like Diuretics may increase serum concentration of Topiramate. Risk C: Monitor

Toremifene: Thiazide and Thiazide-Like Diuretics may increase hypercalcemic effects of Toremifene. Risk C: Monitor

Urapidil: Antihypertensive Agents may increase hypotensive effects of Urapidil. Risk C: Monitor

Verteporfin: Photosensitizing Agents may increase photosensitizing effects of Verteporfin. Risk C: Monitor

Vimseltinib: May increase serum concentration of OCT2 Substrates (Clinically Relevant with Inhibitors). Management: Avoid concomitant use of vimseltinib and OCT2 substrates when possible. If combined, monitor for increased effects and toxicities of the OCT2 substrate and consider dose adjustments. Risk D: Consider Therapy Modification

Vitamin D Analogs: Thiazide and Thiazide-Like Diuretics may increase hypercalcemic effects of Vitamin D Analogs. Risk C: Monitor

White Birch Allergen Extract: Beta-Blockers may increase adverse/toxic effects of White Birch Allergen Extract. Specifically, beta-blockers may reduce the effectiveness of beta-agonists that may be required to treat systemic reactions to white birch allergen extract. Risk X: Avoid

Pregnancy Considerations

Pindolol and thiazide diuretics cross the placenta. See individual agents.

Breastfeeding Considerations

Pindolol and thiazide diuretics are present in breast milk. Breastfeeding is not recommended by the manufacturer. See individual agents.

Dietary Considerations

May be taken with food or milk.

Monitoring Parameters

Blood pressure, heart rate; serum electrolytes, BUN, creatinine

Mechanism of Action

Pindolol: Blocks both beta1- and beta2-receptors and has mild intrinsic sympathomimetic activity; has negative inotropic and chronotropic effects and can significantly slow AV nodal conduction. Augmentive action of antidepressants thought to be mediated via a serotonin 1A autoreceptor antagonism.

Hydrochlorothiazide: Inhibits sodium reabsorption in the distal tubules causing increased excretion of sodium and water as well as potassium and hydrogen ions

Pharmacokinetics (Adult Data Unless Noted)

See individual agents.

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