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:
- Individual dosage should be determined by titration and substitution of a combination product according to daily needs.
- 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.
- The manufacturer does not advise breastfeeding.
- See individual agents.
Viskazide Dose adjustment in renal disease:
- Mild to moderate impairment:
- No dosage change is necessary. Take care when using.
- Severe impairment:
- The manufacturer's labelling does not mention dosage modifications. But there is a need for caution and dosage decrease. Anuria makes it inappropriate.
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 any ingredient in the formulation, including medications derived from sulfonamides or pindolol or hydrochlorothiazide.
- Bronchial asthma and severe COPD
- Anuria
- Right ventricular failure, second- or third-degree atrioventricular block, ensuing pulmonary hypertension, and cardiogenic shock are all symptoms of cardiomegaly (prinzmetal angina), sick sinus syndrome, sick sinus bradycardia (50 beats per minute), and sick sinus syndrome.
- 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: The scientific validity of the claim that this medication is contraindicated when used with other sulfonamide-containing drug classes has been questioned.
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:
- For more information, go to "Warnings/Precautions."
- Hydrochlorothiazide may result in hypokalemia, hypochloremic acidosis, hypomagnesemia, and hyponatremia.
- 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")
- Wide-ranging contraindications for patients who have previously experienced an adverse reaction to sulfonamides are listed on
- FDA-approved product labels for drugs that contain sulfonamide chemical groups.
- Cross-reactivity between members of a class is conceivable (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.
- With non-antibiotic sulfuramides, there is a lower risk of antibody-induced cross-reactions (anaphylaxis).
- Less is known about type IV T-cell reactions, such as maculopapular skin rash. Based on what is known at the moment, it is difficult to rule out this possibility.
- These medications shouldn't be used for severe reactions including Stevens-Johnson syndrome and toxic epidermal necrolysis.
-
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 sick sinus syndrome, second- or third-degree atrioventricular block, and other disorders 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 medication needs to be started carefully and at low doses.
- It might be essential to change other prescription drugs (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 |
Could make beta-blockers' bradycardic impact stronger. |
|
Ajmaline |
Sulfonamides might make ajmaline more harmful or poisonous. In particular, there may be an elevated risk for cholestasis. |
|
Alcohol (Ethyl) |
Increases the effectiveness of thiazide and thiazide-like diuretics in lowering orthostatic blood pressure. |
|
Alfuzosin |
The hypotensive effects of blood pressure-lowering medications may be strengthened. |
|
Allopurinol |
The possibility of allergic or hypersensitive reactions to allopurinol may be increased by thiazide and thiazide-like diuretics. The serum concentration of Allopurinol may rise in response to thiazides and thiazide-like diuretics. In particular, Thiazide Diuretics may raise Oxypurinol's levels, an active metabolite of Allopurinol. |
|
Alpha1-Blockers |
Alpha1Blockers' orthostatic hypotensive action may be strengthened by beta-blockers. Ophthalmic products likely carry a lower level of risk than systemic ones. |
|
Aminolevulinic Acid (Topical) |
Aminolevulinic Acid's photosensitizing impact may be enhanced by photosensitizing agents (Topical). |
|
Aminoquinolines (Antimalarial |
Beta-Blockers' metabolism might be slowed down. |
|
Amiodarone |
Could make beta-blockers' bradycardic impact stronger. It could have reached the point of cardiac arrest. Beta-Blockers' serum concentration may rise as a result of amiodarone. |
|
Amphetamines |
May lessen the effectiveness of antihypertensive agents. |
|
Angiotensin-Converting Enzyme Inhibitors |
Angiotensin-Converting Enzyme Inhibitors' hypotensive effects may be enhanced by thiazide and thiazide-like diuretics. Angiotensin-Converting Enzyme Inhibitors' nephrotoxic effects may be increased by thiazide and thiazide-like diuretics. |
|
Anticholinergic Agents |
May raise the levels of thiazide and thiazide-like diuretics in the blood. |
|
Antidiabetic Agents |
The therapeutic value of anti-diabetic agents may be diminished by thiazide and thiazide-like diuretics. |
|
Antidiabetic Agents |
The therapeutic benefit of anti-diabetic agents may be reduced by hyperglycemia-associated agents. |
|
Antipsychotic Agents (Phenothiazines) |
May strengthen beta-blockers' hypotensive effects. Antipsychotic Agents' metabolism may be slowed down by beta-blockers (Phenothiazines). |
|
Antipsychotic Agents (Second Generation [Atypical]) |
Phenothiazines, or antipsychotic agents, may slow down the metabolism of beta-blockers. |
|
Barbiturates |
Antipsychotic drugs' hypotensive effects may be enhanced by blood pressure-lowering medications (Second Generation [Atypical]). |
|
Barbiturates |
May lower the level of beta-blockers in the serum. |
|
Barbiturates |
Increases the effectiveness of thiazide and thiazide-like diuretics in lowering orthostatic blood pressure. |
|
Benazepril |
Benazepril's hypotensive impact may be strengthened by hydrochlorothiazide. Benazepril may have a more nephrotoxic effect when combined with hydrochlorothiazide. Benazepril may lower the level of HydroCHLOROthiazide in the blood. |
|
Benperidol |
The hypotensive effects of blood pressure-lowering medications may be strengthened. |
|
Bradycardia-Causing Agents |
May intensify other bradycardia-causing agents' bradycardic effects. |
|
Bretylium |
Bradycardia-Causing Agents' bradycardic effect might be enhanced. In patients taking AV blocking medications, bretylium may also strengthen atrioventricular (AV) blockade. |
|
Brigatinib |
May lessen the effectiveness of antihypertensive agents. Antihypertensive Agents' bradycardic action may be strengthened by brutinib. |
|
Bupivacaine |
Beta-blockers may raise the serum level of buprenorphine. |
|
Calcium Channel Blockers (Nondihydropyridine) |
May strengthen betablockers' hypotensive effects. In addition, reports of bradycardia and heart failure symptoms have been made. The serum concentration of beta-blockers may rise in response to calcium channel blockers (nondihydropyridine). Bepridil is an exception. |
|
Calcium Salts |
The excretion of calcium salts may be decreased by thiazide and thiazide-like diuretics. Metabolic alkalosis can also be brought on by continued concurrent usage. |
|
CarBAMazepine |
Thiazide and Thiazide-Like Diuretics may intensify CarBAMazepine's negative/toxic effects. Particularly, there could be a higher risk of hyponatremia. |
|
Cardiac Glycosides |
Cardiac Glycosides' bradycardic action may be strengthened by beta-blockers. |
|
Cardiac Glycosides |
Cardiac Glycosides may have an increased negative or toxic effect when used with thiazide and thiazide-Like Diuretics. Particularly, the hypokalemic and hypomagnesemic impact of thiazide diuretics may worsen cardiac glycoside toxicity. |
|
Cholinergic Agonists |
Beta-Blockers may make Cholinergic Agonists' harmful or toxic effects worse. The possibilities for bronchoconstriction and aberrant cardiac conduction are of special concern. Management: Use cautious while combining these drugs, and keep an eye out for conduction issues. Because methacholine may cause further bronchoconstriction when used with any beta blocker, avoid using it. |
|
Corticosteroids (Orally Inhaled) |
Thiazide and Thiazide-Like Diuretics might have an enhanced hypokalemic impact. |
|
Corticosteroids (Systemic) |
Thiazide and Thiazide-Like Diuretics might have an enhanced hypokalemic impact. |
|
Cyclophosphamide |
Thiazide and Thiazide-Like Diuretics may intensify Cyclophosphamide's harmful or hazardous effects. Particularly, granulocytopenia could be worsened. |
|
Dexketoprofen |
Sulfonamides' harmful or poisonous effects could be amplified. |
|
Dexmethylphenidate |
Can lessen an antihypertensive drug's therapeutic impact. |
|
Diacerein |
Could make diuretics' therapeutic effects stronger. Particularly, there may be a higher chance of hypokalemia or dehydration. |
|
Diazoxide |
Thiazide and Thiazide-Like Diuretics may intensify Diazoxide's harmful or toxic effects. |
|
Diazoxide |
The hypotensive effects of blood pressure-lowering medications may be strengthened. |
|
Dipyridamole |
Could make beta-blockers' bradycardic impact stronger. |
|
Disopyramide |
Could make beta-blockers' bradycardic impact stronger. Beta-blockers might make Disopyramide's adverse inotropic impact worse |
|
DULoxetine |
The hypotensive impact of DULoxetine may be enhanced by blood pressure lowering medications. |
|
EPINEPHrine (Nasal) |
The hypertensive impact of EPINEPHRINE may be enhanced by beta-blockers like Nonselective (Nasal). |
|
EPINEPHrine (Oral Inhalation |
The hypertensive impact of EPINEPHRINE may be enhanced by beta-blockers like Nonselective (Oral Inhalation). |
|
Epinephrine (Racemic) |
Epinephrine's hypertensive action may be enhanced by beta-blockers like Nonselective (Racemic). |
|
EPINEPHrine (Systemic) |
The hypertensive impact of EPINEPHRINE may be enhanced by beta-blockers like Nonselective (Systemic). |
|
Erdafitinib |
OCT2 Substrates' serum concentration can rise. |
|
Flecainide |
May intensify Pindolol's bradycardic impact. Pindolol's unfavourable inotropic effects might even be exacerbated. |
|
Herbs (Hypertensive Properties) |
May lessen the effectiveness of antihypertensive agents. |
|
Herbs (Hypotensive Properties |
The hypotensive effects of blood pressure-lowering medications may be strengthened. |
|
Hypotension-Associated Agents |
The hypotensive action of hypotension-associated agents may be strengthened by blood pressure lowering medications. |
|
Insulins |
Beta-Blockers might improve insulin's ability to lower blood sugar. |
|
Ipragliflozin |
The toxic and harmful effects of thiazide and thiazide-like diuretics may be increased. In particular, there may be an elevated risk for intravascular volume depletion. |
|
Ivabradine |
The arrhythmogenic impact of ivabradine may be enhanced by thiazide and thiazide-like diuretics. |
|
Ivabradine |
Bradycardia-Causing Agents may intensify Ivabradine's bradycardic impact. |
|
Lacosamide |
Bradycardia-Causing Substances may intensify Lacosamide's AV-blocking effects. |
|
Levodopa-Containing Products |
Levodopa-Containing Products' hypotensive effects may be strengthened by blood pressure-lowering medications. |
|
Licorice |
Thiazide and Thiazide-Like Diuretics might have an enhanced hypokalemic impact. |
|
Lidocaine (Systemic) |
Beta-blockers might boost the level of lidocaine in the blood (Systemic). |
|
Lidocaine (Topical) |
Beta-blockers might boost the level of lidocaine in the blood (Topical). |
|
Lormetazepam |
The hypotensive effects of blood pressure-lowering medications may be strengthened. |
|
Mepivacaine |
Mepivacaine's serum levels may rise after taking beta-blockers. |
|
Methoxyflurane |
May strengthen beta-blockers' hypotensive effects. |
|
Methylphenidate |
May lessen the effectiveness of antihypertensive agents. |
|
Midodrine |
Bradycardia-Causing Agents' bradycardic effect might be enhanced. |
|
Molsidomine |
The hypotensive effects of blood pressure-lowering medications may be strengthened. |
|
Multivitamins/Fluoride (with ADE) |
May intensify the effects of thiazide and thiazide-like diuretics on hypercalcemia. |
|
Multivitamins/Minerals (with ADEK, Folate, Iron) |
The effect of multivitamins and minerals on hypercalcemia may be enhanced by thiazide and thiazide-like diuretics (with ADEK, Folate, Iron). |
|
Multivitamins/Minerals (with AE, No Iron |
The serum concentration of multiple vitamins and minerals may rise after taking thiazide and thiazide-like diuretics (with AE, No Iron). Particularly, thiazide diuretics may reduce calcium excretion, and long-term concurrent usage may result in metabolic alkalosis. |
|
Naftopidil |
The hypotensive effects of blood pressure-lowering medications may be strengthened. |
|
Neuromuscular-Blocking Agents (Nondepolarizing) |
The neuromuscular-blocking action of neuromuscular-blocking agents may be enhanced by thiazide and thiazide-like diuretics (Nondepolarizing). |
|
Nicergoline |
The hypotensive effects of blood pressure-lowering medications may be strengthened. |
|
Nicorandil |
The hypotensive effects of blood pressure-lowering medications may be strengthened. |
|
NIFEdipine |
May strengthen beta-blockers' hypotensive effects. The detrimental inotropic impact of beta-blockers may be amplified by NIFEdipine. |
|
Nitroprusside |
Nitroprusside's hypotensive impact may be strengthened by blood pressure-lowering medications. |
|
Nonsteroidal Anti-Inflammatory Agents |
BetaBlockers' ability to reduce hypertension may be diminished. |
|
Nonsteroidal Anti-Inflammatory Agents |
Nonsteroidal Anti-Inflammatory Agents' nephrotoxic effects may be intensified by thiazide and thiazide-like diuretics. Thiazide and Thiazide-Like Diuretics may have less of a therapeutic impact when used with nonsteroidal anti-inflammatory drugs. |
|
Opioid Agonists |
Could make diuretics' harmful or toxic effects worse. Opioid antagonists may reduce diuretics' therapeutic benefit. |
|
Opioids (Anilidopiperidine) |
Could make beta-blockers' bradycardic impact stronger. Beta-Blockers may have a greater hypotensive impact when combined with opioids (anilidopiperidine). |
|
Oxcarbazepine |
Thiazide and Thiazide-Like Diuretics may intensify OXcarbazepine's negative/toxic effects. Particularly, there could be a higher risk of hyponatremia. |
|
Pentoxifylline |
The hypotensive effects of blood pressure-lowering medications may be strengthened. |
|
Pholcodine |
Pholcodine's hypotensive impact may be strengthened by blood pressure lowering medications. |
|
Phosphodiesterase 5 Inhibitors |
The hypotensive effects of blood pressure-lowering medications may be strengthened. |
|
Porfimer |
The photosensitizing effect of Porfimer may be strengthened by photosensitizing agents. |
|
Propafenone |
May raise the level of beta-blockers in the serum. There is some independent beta-blocking activity in propafenone. |
|
Prostacyclin Analogues |
The hypotensive effects of blood pressure-lowering medications may be strengthened. |
|
Quinagolide |
The hypotensive effects of blood pressure-lowering medications may be strengthened. |
|
Reboxetine |
Thiazide and Thiazide-Like Diuretics might have an enhanced hypokalemic impact. |
|
Regorafenib |
Could make beta-blockers' bradycardic impact stronger. |
|
Reserpine |
May strengthen beta-blockers' hypotensive effects. |
|
Rifamycin Derivatives |
May lower the level of beta-blockers in the serum. Rifabutin is an exception. |
|
Ruxolitinib |
Bradycardia-Causing Agents' bradycardic effect might be enhanced. Management: The Canadian product labelling for roxolitinib advises against using it in conjunction with medications that can cause bradycardia whenever feasible. |
|
Selective Serotonin Reuptake Inhibitors |
May raise the level of beta-blockers in the serum. Citalopram, Escitalopram, and FluvoxaMINE are exceptions. |
|
Selective Serotonin Reuptake Inhibitors |
The hyponatremic effects of thiazide and thiazide-like diuretics may be enhanced. |
|
Sulfonylureas |
Beta-Blockers might make Sulfonylureas' hypoglycemia effect more potent. Beta-blockers that are cardioselective (such penbutolol, acebutolol, atenolol, and metoprolol) may be less dangerous than nonselective beta-blockers. As the initial sign of hypoglycemia, tachycardia seems to be concealed by all beta-blockers. |
|
Terlipressin |
Beta-blockers used intravenously most likely carry a lesser risk than those used systemically. |
|
Tofacitinib |
Bradycardia-Causing Agents' bradycardic effect might be enhanced. |
|
Toremifene |
Bradycardia-Causing Agents' bradycardic effect might be enhanced. Toremifene's hypercalcemic impact may be enhanced by thiazide and thiazide-like diuretics. |
|
Valsartan |
HydroCHLOROthiazide may increase Valsartan's ability to lower blood pressure. The serum concentration of HydroCHLOROthiazide may rise in response to Valsartan. |
|
Verteporfin |
Verteporfin's photosensitizing effect may be strengthened by photosensitizing agents. |
|
Vitamin D Analogs |
The hypercalcemic impact of vitamin D analogues may be enhanced by thiazides and thiazide-like diuretics. |
|
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 |
The absorption of thiazide and thiazide-like diuretics may be reduced. Also reduced is the diuretic reaction. |
|
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 |
The excretion of lithium may be reduced by thiazide and thiazide-like diuretics. |
|
Monoamine Oxidase Inhibitors |
May strengthen Pindolol's hypotensive effects. Management: Pindolol's Canadian labelling warns against using a monoamine oxidase inhibitor at the same time. |
|
Obinutuzumab |
The hypotensive effects of blood pressure-lowering medications may be strengthened. Management: Take into account temporarily stopping blood pressure-lowering drugs 12 hours before the start of the obinutuzumab infusion and keeping them off until 1 hour after the infusion is finished. |
|
Siponimod |
Siponimod's bradycardic action may be enhanced by bradycardia-causing substances. Management: Steer clear of combining siponimod with medications that can slow your heart rate. |
|
Sodium Phosphates |
The nephrotoxic effects of sodium phosphates may be increased by diuretics. In particular, there may be an increased risk of acute phosphate nephropathy. Treatment: You might want to temporarily stop taking diuretics or look for an alternative to the oral sodium phosphate bowel preparation in order to prevent this combo. If the combination cannot be avoided, drink well and keep an eye on your kidney and fluid levels. |
|
Tafenoquine |
OCT2 Substrates' serum concentration can rise. Management: If using OCT2 substrates with tafenoquine cannot be avoided, watch closely for any signs of toxicity and take into account using a lower dose of the OCT2 substrate in accordance with the labelling of that substrate. |
|
Theophylline Derivatives |
Theophylline derivatives may not have the same bronchodilatory effects as beta-blockers as Nonselective. |
|
Topiramate |
The hypokalemic impact of topiramate may be enhanced by thiazide and thiazide-like diuretics. The blood concentration of topiramate may rise in response to thiazide and thiazide-like diuretics. Management: When starting or increasing the dosage of a thiazide diuretic, keep an eye out for elevated topiramate levels and any negative effects (such as hypokalemia). Serum potassium levels should be closely watched when receiving concurrent treatment. There may be a need to lower topiramate dosage. |
|
Risk Factor X (Avoid combination) |
|
|
Aminolevulinic Acid (Systemic) |
Aminolevulinic Acid's photosensitizing impact may be enhanced by photosensitizing agents (Systemic). |
|
Beta2-Agonists |
Beta-Blockers (Nonselective) may diminish the bronchodilatory effect of Beta2Agonists. |
|
Bromperidol |
The hypotensive impact of bromperidol may be enhanced by blood pressure lowering medications. Blood Pressure Lowering Agents' hypotensive effects may be lessened by bromperidol. |
|
Dofetilide |
The QTc-prolonging action of dofetilide may be strengthened by hydrochlorothiazide. The serum levels of Dofetilide may rise in response to HydroCHLOROthiazide. |
|
Floctafenine |
May intensify the hazardous or harmful effects of beta-blockers. |
|
Levosulpiride |
Thiazide and Thiazide-Like Diuretics may intensify Levosulpiride's negative/toxic effects. |
|
Mecamylamine |
Sulfonamides may intensify Mecamylamine's harmful or hazardous effects. |
|
Methacholine |
Promazine's ability to prolong QTc may be enhanced by thiazide and thiazide-like diuretics. |
|
Promazine |
By preventing sodium from being absorbed in the distal tubules, it increases sodium excretion together with water, potassium, and hydrogen ions. |
|
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:
- By preventing sodium from being absorbed in the distal tubules, it increases sodium excretion together with water, potassium, and hydrogen ions.
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.
