Viskazide is a combination of a non-selective beta-blocker - Pindolol, and a thiazide diuretic (Hydrochlorothiazide). It is used to treat patients with hypertension.
Indications of Viskazide (Pindolol and hydrochlorothiazide):
-
Hypertension:
- It is indicated for the management of hypertension, not for initial therapy.
- Note: Not approved in the US.
Viskazide (Pindolo and hydrochlorothiazide) dose in adults:
The treatment dose of Viskazide in Hypertension:
- Dosage should be individualized and depends on titration and the combination product substituted based upon the daily requirements.
- Usual dose: Pindolol 10 to 20 mg and hydrochlorothiazide 25 to 100 mg per oral once daily.
- Maximum daily dose: Pindolol: 20 mg/hydrochlorothiazide 100 mg.
Note: Individual drugs should be used if higher doses or dosage adjustments are needed.
Viskazide Use in Children:
Not indicated in children.
Dose adjustment in pregnancy and lactation:
- Pindolol and thiazide diuretics have the ability to cross the placenta.
- See individual agents.
Pindolol and hydrochlorothiazide use during breastfeeding:
- Pindolol and thiazide diuretics are secreted in breast milk.
- Breastfeeding is not recommended by the manufacturer.
- See individual agents.
Viskazide Dose adjustment in renal disease:
- Mild to moderate impairment:
- Dosage adjustment is not required. Use with caution.
- Severe impairment:
- There are no dosage adjustments provided in the manufacturer’s labeling. However, dosage reduction and caution is needed. Contraindicated with anuria.
Viskazide Dose adjustment in liver disease:
- Mild to moderate impairment:
- Dosage adjustment is not required. Use with caution.
- Severe impairment:
- There are no dosage adjustments provided in the manufacturer’s labeling. However, dosage reduction and caution are needed.
Side effects of Viskazide (Pindolol and hydrochlorothiazide):
See individual agents (Pindolol and Hydrochlorothiazide)
Contraindications to Viskazide (Pindolol and hydrochlorothiazide):
- Hypersensitivity to pindolol or hydrochlorothiazide, any component of the formulation or sulfonamide derived drugs.
- Bronchial asthma and severe COPD
- Anuria
- Sinus bradycardia (=50 beats per minute), cardiomegaly (prinzmetal angina), sick sinus syndrome, right ventricular failure secondary pulmonary hypertension, second/third-degree atrioventricular block, cardiogenic shock
- Myocardial depression caused by severe peripheral arterial circulation disorders
- Untreated Pheochromocytoma
- Cross-reactivity with other beta-blockers
- Hydrochlorothiazide's manufacturer also warns against increasing azotemia or oliguria in the treatment of severe progressive kidney disease.
- Breastfeeding
Notice: Although the product labeling states this medication is contraindicated with other sulfonamide-containing drug classes, the scientific basis of this statement has been challenged. See "Warnings/Precautions" for more detail.
Warnings and precautions
-
Acute renal failure:
- Patients with volume depletion and heart failure are at greater risk for acute renal failure when taking hydrochlorothiazide.
-
Anaphylactic reactions
- Patients taking beta-blockers could experience severe anaphylaxis to allergens. They may also become more sensitive to repeated challenges.
- Patients taking beta-blockers may experience anaphylaxis (eg epinephrine) that is ineffective or has undesirable side effects.
- Individuals who have never had bronchial asthma or allergies may be hypersensitive to thiazides.
-
Bradycardia
- Pindolol can cause bradycardia. Therefore, dose adjustment is necessary for severe bradycardia.
-
Electrolyte disturbances:
- Hypokalemia, hypochloremic acidosis, hypomagnesemia and hyponatremia can all be caused by hydrochlorothiazide.
- The risk of electrolyte imbalance can be reduced by combining it with electrolyte sparing medications such as ACE inhibitors and angiotensin receptor blocking agents.
- Long-term thiazide therapy can lead to hypercalcemia and hypophosphatemia. Parathyroid testing should be avoided.
-
Gout
- Higher doses of hydrochlorothiazide >25 mg may cause gout. Risk factors include a family history of gout or chronic renal disease.
-
Hypersensitivity reactions
- Hypersensitivity reactions can be caused by hydrochlorothiazide
- Patients with a history or bronchial asthma or allergy are at greater risk.
-
Ocular:
- Beta-blockers can cause dryness of the eye surface (conjunctival conjunctivalxerosis) and should be stopped in severe cases.
- Hydrochlorothiazide therapy can lead to acute transient myopia or acute angle-closure blindness.
- Therapy should be stopped immediately if there is an acute decrease in visual acuity and/or ocular pain
- It is important to treat persistently elevated intraocular pressure.
- A history of penicillin allergy or sulfonamide allergy could be a risk factor.
-
Photosensitivity
- Photosensitization can be a result of therapy.
-
Allergy to sulfonamide ("sulfa")
- FDA-approved product labels for medications that contain a sulfonamide chemical groups include a wide contraindication for patients who have had an allergic reaction to sulfonamides in the past.
- Cross-reactivity is possible between members of one class (eg two antibiotic sulfonamides).
- Cross-reactivity concerns have been raised previously for all compounds with the sulfonamide structural (SO NH).
- A better understanding of allergy mechanisms suggests that there are very few cross-reactivity opportunities between antibiotic sulfonamides, and non-antibiotic sulfonamides.
- Cross-reactions due to antibody production (anaphylaxis) are less likely with non-antibiotic sulfuramides.
- T-cell-mediated (type IV), reactions (eg maculopapular skin rash) are less understood. It is difficult to exclude this possibility based on current knowledge.
- For severe reactions such as Stevens-Johnson syndrome and toxic epidermal necrolysis, these drugs should not be used.
-
Bariatric surgery
- In the immediate postoperative period following bariatric surgery, diuretics can cause electrolyte disturbances or dehydration.
- Therapy can be resumed once fluid levels have returned to normal.
-
Conductive abnormality
- Patients with second- or third-degree atrioventricular block (AV), sick sinus syndrome, and other conditions are contraindicated.
-
Diabetes:
- It is possible to see changes in glucose control, hypoglycemia, or masking signs and symptoms. Therefore it should be treated with caution.
-
Heart failure (HF):
- Before starting treatment, patients should be stabilized with the heart failure protocol.
- Patients with compensated HF require careful monitoring. A reduction in pindolol dosage or withdrawal of therapy might be necessary.
- Beta-blocker therapy should be administered in low doses and titrated slowly.
- It may be necessary to adjust other medications (ACE inhibitors or diuretics).
- It has not been shown that beta-blockers with intrinsic sympathomimetic activities (eg, pindolol), are of any value in HF.
-
Hepatic impairment
- Pindolol can cause an increase in liver impairment so it is important to be cautious when using this drug.
- It is possible to have electrolyte or acid/base imbalances that can lead to hepatic dysfunction/coma. Therefore, it is important to be cautious when giving therapy.
-
Hypercholesterolemia:
- Patients with high or moderate cholesterol should be cautious.
-
Myasthenia gravis:
- Patients with myasthenia gravis should be careful when taking beta-blockers.
-
Parathyroid disease
- Long-term therapy with thiazides may cause changes in parathyroid glands, including hypophosphatemia and hypercalcemia.
- Before testing for parathyroid function, it is important to stop taking any medication.
-
Raynaud's Disease and Peripheral Vascular Disease (PVD).
- Therapy can make arterial insufficiency worse in patients suffering from Raynaud’s disease and PVD.
- It is important to monitor the progression of arterial blockage.
- Use of this product is not recommended for severe peripheral arterial circulation disorders.
-
Psoriasis:
- Beta-blockers can be used to treat psoriasis.
-
Renal impairment
- It is possible for thiazides to cause azotemia. Therefore, caution should be taken when using it with renal impairment
- In severe cases of impairment, therapy should be stopped.
- Anuria is not recommended.
-
Respiratory disease
- It is not recommended for bronchospasm, including bronchial asthma, or severe chronic obstructive lung disease.
- It should not be used in the case of non-allergic bronchitis (eg, emphysema or chronic bronchitis).
-
Systemic lupus erythematosus (SLE):
- SLE activation and exacerbation can be caused by Thiazides.
-
Thyroid disease:
- Therapy can mask the symptoms of hyperthyroidism, such as tachycardia.
- Thyrotoxicosis requires careful monitoring.
- Sudden withdrawal can be a sign of thyroid storm or hyperthyroidism.
Pindolol and hydrochlorothiazide (United States: Not available): Drug Interaction
|
Acetylcholinesterase Inhibitors |
May enhance the bradycardic effect of Beta-Blockers. |
|
Ajmaline |
Sulfonamides may enhance the adverse/toxic effect of Ajmaline. Specifically, the risk for cholestasis may be increased. |
|
Alcohol (Ethyl) |
May enhance the orthostatic hypotensive effect of Thiazide and Thiazide-Like Diuretics. |
|
Alfuzosin |
May enhance the hypotensive effect of Blood Pressure Lowering Agents. |
|
Allopurinol |
Thiazide and Thiazide-Like Diuretics may enhance the potential for allergic or hypersensitivity reactions to Allopurinol. Thiazide and Thiazide-Like Diuretics may increase the serum concentration of Allopurinol. Specifically, Thiazide Diuretics may increase the concentration of Oxypurinol, an active metabolite of Allopurinol. |
|
Alpha1-Blockers |
Beta-Blockers may enhance the orthostatic hypotensive effect of Alpha1Blockers. The risk associated with ophthalmic products is probably less than systemic products. |
|
Aminolevulinic Acid (Topical) |
Photosensitizing Agents may enhance the photosensitizing effect of Aminolevulinic Acid (Topical). |
|
Aminoquinolines (Antimalarial |
May decrease the metabolism of Beta-Blockers. |
|
Amiodarone |
May enhance the bradycardic effect of Beta-Blockers. Possibly to the point of cardiac arrest. Amiodarone may increase the serum concentration of Beta-Blockers. |
|
Amphetamines |
May diminish the antihypertensive effect of Antihypertensive Agents. |
|
Angiotensin-Converting Enzyme Inhibitors |
Thiazide and Thiazide-Like Diuretics may enhance the hypotensive effect of Angiotensin-Converting Enzyme Inhibitors. Thiazide and Thiazide-Like Diuretics may enhance the nephrotoxic effect of Angiotensin-Converting Enzyme Inhibitors. |
|
Anticholinergic Agents |
May increase the serum concentration of Thiazide and Thiazide-Like Diuretics. |
|
Antidiabetic Agents |
Thiazide and Thiazide-Like Diuretics may diminish the therapeutic effect of Antidiabetic Agents. |
|
Antidiabetic Agents |
Hyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents. |
|
Antipsychotic Agents (Phenothiazines) |
May enhance the hypotensive effect of Beta-Blockers. Beta-Blockers may decrease the metabolism of Antipsychotic Agents (Phenothiazines). Antipsychotic Agents (Phenothiazines) may decrease the metabolism of Beta-Blockers. |
|
Antipsychotic Agents (Second Generation [Atypical]) |
Blood Pressure Lowering Agents may enhance the hypotensive effect of Antipsychotic Agents (Second Generation [Atypical]). |
|
Barbiturates |
May decrease the serum concentration of Beta-Blockers. |
|
Barbiturates |
May enhance the orthostatic hypotensive effect of Thiazide and Thiazide-Like Diuretics. |
|
Barbiturates |
May enhance the hypotensive effect of Blood Pressure Lowering Agents. |
|
Benazepril |
HydroCHLOROthiazide may enhance the hypotensive effect of Benazepril. HydroCHLOROthiazide may enhance the nephrotoxic effect of Benazepril. Benazepril may decrease the serum concentration of HydroCHLOROthiazide. |
|
Benperidol |
May enhance the hypotensive effect of Blood Pressure Lowering Agents. |
|
Bradycardia-Causing Agents |
May enhance the bradycardic effect of other Bradycardia-Causing Agents. |
|
Bretylium |
May enhance the bradycardic effect of Bradycardia-Causing Agents. Bretylium may also enhance atrioventricular (AV) blockade in patients receiving AV blocking agents. |
|
Brigatinib |
May diminish the antihypertensive effect of Antihypertensive Agents. Brigatinib may enhance the bradycardic effect of Antihypertensive Agents. |
|
Brimonidine (Topical) |
May enhance the hypotensive effect of Blood Pressure Lowering Agents. |
|
Bupivacaine |
Beta-Blockers may increase the serum concentration of Bupivacaine. |
|
Calcium Channel Blockers (Nondihydropyridine) |
May enhance the hypotensive effect of BetaBlockers. Bradycardia and signs of heart failure have also been reported. Calcium Channel Blockers (Nondihydropyridine) may increase the serum concentration of Beta-Blockers. Exceptions: Bepridil. |
|
Calcium Salts |
Thiazide and Thiazide-Like Diuretics may decrease the excretion of Calcium Salts. Continued concomitant use can also result in metabolic alkalosis. |
|
CarBAMazepine |
Thiazide and Thiazide-Like Diuretics may enhance the adverse/toxic effect of CarBAMazepine. Specifically, there may be an increased risk for hyponatremia. |
|
Cardiac Glycosides |
Beta-Blockers may enhance the bradycardic effect of Cardiac Glycosides. |
|
Cardiac Glycosides |
Thiazide and Thiazide-Like Diuretics may enhance the adverse/toxic effect of Cardiac Glycosides. Specifically, cardiac glycoside toxicity may be enhanced by the hypokalemic and hypomagnesemic effect of thiazide diuretics. |
|
Cholinergic Agonists |
Beta-Blockers may enhance the adverse/toxic effect of Cholinergic Agonists. Of particular concern are the potential for cardiac conduction abnormalities and bronchoconstriction. Management: Administer these agents in combination with caution, and monitor for conduction disturbances. Avoid methacholine with any beta blocker due to the potential for additive bronchoconstriction. |
|
Corticosteroids (Orally Inhaled) |
May enhance the hypokalemic effect of Thiazide and ThiazideLike Diuretics. |
|
Corticosteroids (Systemic) |
May enhance the hypokalemic effect of Thiazide and Thiazide-Like Diuretics. |
|
Cyclophosphamide |
Thiazide and Thiazide-Like Diuretics may enhance the adverse/toxic effect of Cyclophosphamide. Specifically, granulocytopenia may be enhanced. |
|
Dexketoprofen |
May enhance the adverse/toxic effect of Sulfonamides. |
|
Dexmethylphenidate |
May diminish the therapeutic effect of Antihypertensive Agents. |
|
Diacerein |
May enhance the therapeutic effect of Diuretics. Specifically, the risk for dehydration or hypokalemia may be increased. |
|
Diazoxide |
Thiazide and Thiazide-Like Diuretics may enhance the adverse/toxic effect of Diazoxide. |
|
Diazoxide |
May enhance the hypotensive effect of Blood Pressure Lowering Agents. |
|
Dipyridamole |
May enhance the bradycardic effect of Beta-Blockers. |
|
Disopyramide |
May enhance the bradycardic effect of Beta-Blockers. Beta-Blockers may enhance the negative inotropic effect of Disopyramide. |
|
DULoxetine |
Blood Pressure Lowering Agents may enhance the hypotensive effect of DULoxetine. |
|
EPINEPHrine (Nasal) |
Beta-Blockers (Nonselective) may enhance the hypertensive effect of EPINEPHrine (Nasal). |
|
EPINEPHrine (Oral Inhalation |
Beta-Blockers (Nonselective) may enhance the hypertensive effect of EPINEPHrine (Oral Inhalation). |
|
Epinephrine (Racemic) |
Beta-Blockers (Nonselective) may enhance the hypertensive effect of Epinephrine (Racemic). |
|
EPINEPHrine (Systemic) |
Beta-Blockers (Nonselective) may enhance the hypertensive effect of EPINEPHrine (Systemic). |
|
Erdafitinib |
May increase the serum concentration of OCT2 Substrates. |
|
Flecainide |
May enhance the bradycardic effect of Pindolol. The negative inotropic effects of Pindolol may also be enhanced. |
|
Herbs (Hypertensive Properties) |
May diminish the antihypertensive effect of Antihypertensive Agents. |
|
Herbs (Hypotensive Properties |
May enhance the hypotensive effect of Blood Pressure Lowering Agents. |
|
Hypotension-Associated Agents |
Blood Pressure Lowering Agents may enhance the hypotensive effect of Hypotension-Associated Agents. |
|
Insulins |
Beta-Blockers may enhance the hypoglycemic effect of Insulins. |
|
Ipragliflozin |
May enhance the adverse/toxic effect of Thiazide and Thiazide-Like Diuretics. Specifically, the risk for intravascular volume depletion may be increased. |
|
Ivabradine |
Thiazide and Thiazide-Like Diuretics may enhance the arrhythmogenic effect of Ivabradine. |
|
Ivabradine |
Bradycardia-Causing Agents may enhance the bradycardic effect of Ivabradine. |
|
Lacosamide |
Bradycardia-Causing Agents may enhance the AV-blocking effect of Lacosamide. |
|
Levodopa-Containing Products |
Blood Pressure Lowering Agents may enhance the hypotensive effect of Levodopa-Containing Products. |
|
Licorice |
May enhance the hypokalemic effect of Thiazide and Thiazide-Like Diuretics. |
|
Lidocaine (Systemic) |
Beta-Blockers may increase the serum concentration of Lidocaine (Systemic). |
|
Lidocaine (Topical) |
Beta-Blockers may increase the serum concentration of Lidocaine (Topical). |
|
Lormetazepam |
May enhance the hypotensive effect of Blood Pressure Lowering Agents. |
|
Mepivacaine |
Beta-Blockers may increase the serum concentration of Mepivacaine. |
|
Methoxyflurane |
May enhance the hypotensive effect of Beta-Blockers. |
|
Methylphenidate |
May diminish the antihypertensive effect of Antihypertensive Agents. |
|
Midodrine |
May enhance the bradycardic effect of Bradycardia-Causing Agents. |
|
Molsidomine |
May enhance the hypotensive effect of Blood Pressure Lowering Agents. |
|
Multivitamins/Fluoride (with ADE) |
May enhance the hypercalcemic effect of Thiazide and Thiazide-Like Diuretics. |
|
Multivitamins/Minerals (with ADEK, Folate, Iron) |
Thiazide and Thiazide-Like Diuretics may enhance the hypercalcemic effect of Multivitamins/Minerals (with ADEK, Folate, Iron). |
|
Multivitamins/Minerals (with AE, No Iron |
Thiazide and Thiazide-Like Diuretics may increase the 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. |
|
Naftopidil |
May enhance the hypotensive effect of Blood Pressure Lowering Agents. |
|
Neuromuscular-Blocking Agents (Nondepolarizing) |
Thiazide and Thiazide-Like Diuretics may enhance the neuromuscular-blocking effect of Neuromuscular-Blocking Agents (Nondepolarizing). |
|
Nicergoline |
May enhance the hypotensive effect of Blood Pressure Lowering Agents. |
|
Nicorandil |
May enhance the hypotensive effect of Blood Pressure Lowering Agents. |
|
NIFEdipine |
May enhance the hypotensive effect of Beta-Blockers. NIFEdipine may enhance the negative inotropic effect of Beta-Blockers. |
|
Nitroprusside |
Blood Pressure Lowering Agents may enhance the hypotensive effect of Nitroprusside. |
|
Nonsteroidal Anti-Inflammatory Agents |
May diminish the antihypertensive effect of BetaBlockers. |
|
Nonsteroidal Anti-Inflammatory Agents |
Thiazide and Thiazide-Like Diuretics may enhance the nephrotoxic effect of Nonsteroidal Anti-Inflammatory Agents. Nonsteroidal Anti-Inflammatory Agents may diminish the therapeutic effect of Thiazide and Thiazide-Like Diuretics. |
|
Opioid Agonists |
May enhance the adverse/toxic effect of Diuretics. Opioid Agonists may diminish the therapeutic effect of Diuretics. |
|
Opioids (Anilidopiperidine) |
May enhance the bradycardic effect of Beta-Blockers. Opioids (Anilidopiperidine) may enhance the hypotensive effect of Beta-Blockers. |
|
Oxcarbazepine |
Thiazide and Thiazide-Like Diuretics may enhance the adverse/toxic effect of OXcarbazepine. Specifically, there may be an increased risk for hyponatremia. |
|
Pentoxifylline |
May enhance the hypotensive effect of Blood Pressure Lowering Agents. |
|
Pholcodine |
Blood Pressure Lowering Agents may enhance the hypotensive effect of Pholcodine. |
|
Phosphodiesterase 5 Inhibitors |
May enhance the hypotensive effect of Blood Pressure Lowering Agents. |
|
Porfimer |
Photosensitizing Agents may enhance the photosensitizing effect of Porfimer. |
|
Propafenone |
May increase the serum concentration of Beta-Blockers. Propafenone possesses some independent beta blocking activity. |
|
Prostacyclin Analogues |
May enhance the hypotensive effect of Blood Pressure Lowering Agents. |
|
Quinagolide |
May enhance the hypotensive effect of Blood Pressure Lowering Agents. |
|
Reboxetine |
May enhance the hypokalemic effect of Thiazide and Thiazide-Like Diuretics. |
|
Regorafenib |
May enhance the bradycardic effect of Beta-Blockers. |
|
Reserpine |
May enhance the hypotensive effect of Beta-Blockers. |
|
Rifamycin Derivatives |
May decrease the serum concentration of Beta-Blockers. Exceptions: Rifabutin. |
|
Ruxolitinib |
May enhance the bradycardic effect of Bradycardia-Causing Agents. Management: Ruxolitinib Canadian product labeling recommends avoiding use with bradycardia-causing agents to the extent possible. |
|
Selective Serotonin Reuptake Inhibitors |
May increase the serum concentration of Beta-Blockers. Exceptions: Citalopram; Escitalopram; FluvoxaMINE. |
|
Selective Serotonin Reuptake Inhibitors |
May enhance the hyponatremic effect of Thiazide and Thiazide-Like Diuretics. |
|
Sulfonylureas |
Beta-Blockers may enhance the hypoglycemic effect of Sulfonylureas. Cardioselective beta-blockers (eg, acebutolol, atenolol, metoprolol, and penbutolol) may be safer than nonselective beta-blockers. All beta-blockers appear to mask tachycardia as an initial symptom of hypoglycemia. Ophthalmic beta-blockers are probably associated with lower risk than systemic agents. |
|
Terlipressin |
May enhance the bradycardic effect of Bradycardia-Causing Agents. |
|
Tofacitinib |
May enhance the bradycardic effect of Bradycardia-Causing Agents. |
|
Toremifene |
Thiazide and Thiazide-Like Diuretics may enhance the hypercalcemic effect of Toremifene. |
|
Valsartan |
HydroCHLOROthiazide may enhance the hypotensive effect of Valsartan. Valsartan may increase the serum concentration of HydroCHLOROthiazide. |
|
Verteporfin |
Photosensitizing Agents may enhance the photosensitizing effect of Verteporfin. |
|
Vitamin D Analogs |
Thiazide and Thiazide-Like Diuretics may enhance the hypercalcemic effect of Vitamin D Analogs. |
|
Yohimbine |
May diminish the antihypertensive effect of Antihypertensive Agents. |
|
Risk Factor D (Consider therapy modification) |
|
|
Alpha2-Agonists |
May enhance the AV-blocking effect of Beta-Blockers. Sinus node dysfunction may also be enhanced. Beta-Blockers may enhance the rebound hypertensive effect of Alpha2Agonists. This effect can occur when the Alpha2-Agonist is abruptly withdrawn. 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. Exceptions: Apraclonidine. |
|
Amifostine |
Blood Pressure Lowering Agents may enhance the hypotensive effect of Amifostine. Management: When amifostine is used at chemotherapy doses, blood pressure lowering medications should be withheld for 24 hours prior to amifostine administration. If blood pressure lowering therapy cannot be withheld, amifostine should not be administered. |
|
Bile Acid Sequestrants |
|
|
Ceritinib |
Bradycardia-Causing Agents may enhance the bradycardic effect 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. Exceptions are discussed in separate monographs. |
|
Dronedarone |
May enhance the bradycardic effect of Beta-Blockers. Dronedarone may increase the 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 betablocker dose. |
|
Ergot Derivatives |
Beta-Blockers may enhance the vasoconstricting effect of Ergot Derivatives. Exceptions: Nicergoline. |
|
Fingolimod |
Beta-Blockers may enhance the bradycardic effect of Fingolimod. Management: Avoid the concomitant use of fingolimod and beta-blockers if possible. If coadministration is necessary, patients should have overnight continuous ECG monitoring conducted after the first dose of fingolimod. Monitor patients for bradycardia. |
|
Grass Pollen Allergen Extract (5 Grass Extract) |
Beta-Blockers may enhance the adverse/toxic effect 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. |
|
Lithium |
Thiazide and Thiazide-Like Diuretics may decrease the excretion of Lithium. |
|
Monoamine Oxidase Inhibitors |
May enhance the hypotensive effect of Pindolol. Management: Canadian labeling for pindolol states that concurrent use with a monoamine oxidase inhibitor is not recommended. |
|
Obinutuzumab |
May enhance the hypotensive effect 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. |
|
Siponimod |
Bradycardia-Causing Agents may enhance the bradycardic effect of Siponimod. Management: Avoid coadministration of siponimod with drugs that may cause bradycardia. |
|
Sodium Phosphates |
Diuretics may enhance the nephrotoxic effect of Sodium Phosphates. Specifically, the risk of acute phosphate nephropathy may be enhanced. Management: Consider avoiding this combination by temporarily suspending treatment with diuretics, or seeking alternatives to oral sodium phosphate bowel preparation. If the combination cannot be avoided, hydrate adequately and monitor fluid and renal status. |
|
Tafenoquine |
May increase the serum concentration of OCT2 Substrates. 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. |
|
Theophylline Derivatives |
Beta-Blockers (Nonselective) may diminish the bronchodilatory effect of Theophylline Derivatives. |
|
Topiramate |
Thiazide and Thiazide-Like Diuretics may enhance the hypokalemic effect of Topiramate. Thiazide and Thiazide-Like Diuretics may increase the serum concentration of Topiramate. Management: Monitor for increased topiramate levels/adverse effects (e.g., hypokalemia) with initiation/dose increase of a thiazide diuretic. Closely monitor serum potassium concentrations with concomitant therapy. Topiramate dose reductions may be necessary. |
|
Risk Factor X (Avoid combination) |
|
|
Aminolevulinic Acid (Systemic) |
Photosensitizing Agents may enhance the photosensitizing effect of Aminolevulinic Acid (Systemic). |
|
Beta2-Agonists |
Beta-Blockers (Nonselective) may diminish the bronchodilatory effect of Beta2Agonists. |
|
Bromperidol |
Blood Pressure Lowering Agents may enhance the hypotensive effect of Bromperidol. Bromperidol may diminish the hypotensive effect of Blood Pressure Lowering Agents. |
|
Dofetilide |
HydroCHLOROthiazide may enhance the QTc-prolonging effect of Dofetilide. HydroCHLOROthiazide may increase the serum concentration of Dofetilide. |
|
Floctafenine |
May enhance the adverse/toxic effect of Beta-Blockers. |
|
Levosulpiride |
Thiazide and Thiazide-Like Diuretics may enhance the adverse/toxic effect of Levosulpiride. |
|
Mecamylamine |
Sulfonamides may enhance the adverse/toxic effect of Mecamylamine. |
|
Methacholine |
Beta-Blockers may enhance the adverse/toxic effect of Methacholine. |
|
Promazine |
Thiazide and Thiazide-Like Diuretics may enhance the QTc-prolonging effect of Promazine. |
|
Rivastigmine |
May enhance the bradycardic effect of Beta-Blockers. |
Monitoring parameters:
- BP
- Pulse
- Serum electrolytes,
- Serum creatinine, BUN
How to administer Viskazide (Pindolol and hydrochlorothiazide)?
It should be taken orally with food or milk early in the day to avoid nocturia.
Mechanism of action of Pindolol and hydrochlorothiazide (Viskazide):
Pindolol:
- It blocks beta-1 and beta-2 receptors, which makes it mildly sympathomimetic.
- This causes slow AV nodal conduction because of negative inotropic or chronotropic effects.
- Antagonism of the serotonin 1A autoreceptor can result in augmentative antidepressant action.
Hydrochlorothiazide:
- It increases sodium excretion, water, potassium and hydrogen ions, by inhibiting sodium absorption in the distal tubules.
See individual agents (Pindolol and Hydrocholorothiazide)
International Brands of Pindolol and hydrochlorothiazide:
- Viskazide 10/25
- Viskazide 10/50
Pindolol and hydrochlorothiazide Brand Names in Pakistan:
No Brands Available in Pakistan.
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