Inderide and Inderide LA tablets contain propranolol and hydrochlorothiazide. It is a combination of a non-specific beta-blocker and a thiazide diuretic that is used to treat patients with hypertension
Inderide (Propranolol and hydrochlorothiazide) Uses:
-
Hypertension:
- Management of hypertension.
Propranolol and Hydrochlorothiazide (Inderide) Dose in Adults
Propranolol and Hydrochlorothiazide (Inderide) Dose in the treatment of Hypertension:
- Oral: Initial: Propranolol 40 mg/hydrochlorothiazide 25 mg BD; The dose can be gradually increased depending on the blood pressure response; the maximum dose is propranolol 160 mg/hydrochlorothiazide 50 mg every 24 hours.
Note: Dose is individualized. For doses of propranolol >160 mg, the combination product not appropriate.
Use in Children:
Not indicated.
Pregnancy Risk Factor C
- For this combination, there have been no animal reproduction experiments.
- See individual agents.
Use during breastfeeding:
- Propranolol and thiazide diuretics are secreted in breast milk.
- The manufacturer has recommended being cautious when administering propranolol/hydrochlorothiazide to breastfeeding women.
- See individual agents.
Dose in Kidney Disease:
- No dosage adjustments have been provided in the manufacturer’s labeling. However, systemic exposure to propranolol is increased in renal impairment. Use cautiously. Hydrochlorothiazide has been suggested to undergo the following modifications:
- CrCl ≥10 mL/minute: No dosage change is required. Unless used in conjunction with a loop diuretic, usually ineffective with CrCl 30 mL/minute.
- CrCl <10 mL/minute: Not recommended for use.
Dose in Liver disease:
The manufacturer's labelling makes no mention of changing the dosage. However, hepatic dysfunction increases propranolol systemic exposure. Use with caution.
See Individual agents (Propranolol and Hydrochlorothiazide)
Contraindications to Propranolol and Hydrochlorothiazide (Inderide):
- Hypersensitivity to the following:
- Propranolol
- Hydrochlorothiazide
- Beta-blockers and other medications
- Other sulfonamide derived drugs
- Any component of the formulation
- Heart failure (except if the failure is caused by tachyarrhythmias treated with propranolol).
- Cardiogenic shock
- Sinus bradycardia
- Heart block greater than the 1st degree
- Bronchial asthma
- Anuria
Note:
- Although some product labelling indicates that this medication should not be taken with other sulfonamide-containing drug classes, the scientific validity of this claim has been questioned.
- For more information, go to "Warnings/Precautions." Documentation on the interactions of thiazide-related diuretics with allergens is scarce.
- Cross-sensitivity is possible due to similarities in chemical structure and/or pharmaceutical actions. However, this cannot be ruled out.
Warnings and precautions
-
Anaphylactic reactions
- Patients with severe allergies to allergens should be cautious when using beta-blockers. This could make them more sensitive to repeated challenges.
- In patients on beta-blockers, anaphylaxis treatment (such as epinephrine) may be ineffective or may have the opposite effect.
-
Electrolyte disturbances:
- These electrolyte abnormalities can be caused by:
- Hypokalemia
- Hypochloremic alkalosis
- Hypomagnesemia
- Hyponatremia
- Before initiation, it is important to correct electrolyte disturbances.
- These electrolyte abnormalities can be caused by:
-
Gout
- Certain people with a history of gout, a hereditary propensity to gout, or chronic renal failure may experience a precipitation of gout after taking hydrochlorothiazide.
- Doses greater than 25 mg may increase the risk.
-
Ocular effects
- Acute transitory myopia or acute angle-closure vision loss may be brought on by hydrochlorothiazide.
- These symptoms typically occur within hours to weeks of therapy initiation.
- Acute transitory myopia or acute angle-closure vision loss may be brought on by hydrochlorothiazide.
-
Photosensitivity
- Hydrochlorothiazide may cause photosensitization.
-
Allergy to sulfonamide ("sulfa")
- The FDA-approved product labelling for drugs belonging to the sulfonamide chemical family provide a lengthy list of patients who should not take them if they have previously experienced an adverse reaction to sulfonamides.
- Members of one class may exhibit cross-reactivity with one another (e.g., 2 antibiotics sulfonamides).
- Crossreactivity issues have previously been brought up for all substances of the sulfonamide structural class (SO NH).
- Cross-reactivity between sulfonamides that are not antibiotics and those that are antibiotics has been proven to be improbable as a result of our increased understanding of allergic processes.
- Sulfonamides that are not antibiotics are less likely to result in anaphylaxis (a mechanism of cross-reaction due primarily to antibody production).
- Less is known about T-cell-mediated (type IV) reactions. This makes it challenging to rule out the idea using our existing understanding.
- These classes are sometimes avoided by some clinicians in severe cases of reactions (Stevens Johnson syndrome/TEN).
-
Bariatric surgery
- Avoid diuretics for the first 24 hours following bariatric surgery to prevent dehydration.
- Dehydration and electrolyte imbalances are possible side effects.
- Once the targets for oral fluid intake have been reached, diuretics may be started again if necessary.
-
Bronchospastic disease
- Patients with bronchospastic diseases should avoid beta-blockers. If they are given, be careful and closely monitored.
-
Conductive abnormality
- Before you start, it is important to consider any pre-existing conditions like sick sinus syndrome.
-
Diabetes:
- Patients with diabetes mellitus should exercise caution. It could cause hypoglycemia or cover up signs.
-
Heart failure (HF):
- In compensated HF, use caution. Monitor for signs of worsening (efficacy in HF of propranolol has not been proven).
-
Hepatic impairment
- Avoid using this product if you have a severe hepatic impairment.
-
Hypercalcemia:
- Thiazide diuretics should not be used by people with hypercalcemia because they may reduce renal calcium excretion.
-
Hypercholesterolemia:
- Patients with high or moderate cholesterol levels should not take hydrochlorothiazide.
-
Myasthenia gravis:
- Myasthenia gravis: Be careful
-
Parathyroid disease
- Thiazide diuretics reduce calcium excretion; prolonged use can cause pathologic changes in parathyroid glands, including hypophosphatemia and hypercalcemia. Stop using thiazide before testing for parathyroid function.
-
Raynaud and peripheral vascular disease (PVD).
- Patients with Raynaud and PVD may experience symptoms of arterial insufficiency that can be exacerbated or precipitated.
- Be cautious and watch for signs of arterial obstruction.
-
Untreated Pheochromocytoma
- You must have adequate alpha-blockade before you can use any beta-blocker.
-
Angina Prinzmetal version:
- Patients with Prinzmetal variant Angina should avoid Beta-blockers that do not block alpha-1-adrenergic activity. This can worsen anginal symptoms.
-
Psoriasis:
- Although beta-blocker may cause or exacerbate psoriasis symptoms, the cause and effect of this medication are not known.
-
Renal impairment
- People with renal insufficiency can experience more severe side effects.
-
Systemic lupus erythematosus (SLE):
- Hydrochlorothiazide may trigger or exacerbation of SLE.
-
Thyroid disease:
- Hyperthyroidism signs (e.g., tachycardia), may be hidden.
- Thyrotoxicosis is a condition that can be treated with care. Sudden withdrawal may lead to hyperthyroidism, or even a thyroid storm.
- Thyroid function tests may be affected.
Propranolol and hydrochlorothiazide: Drug Interaction
|
Acetylcholinesterase Inhibitors |
Could make beta-blockers' bradycardic impact stronger. |
|
Ajmaline |
May elevate CYP2D6 Substrates' serum concentration (High risk with Inhibitors). |
|
Ajmaline |
Sulfonamides might make ajmaline more harmful or poisonous. In particular, there may be an elevated risk for cholestasis. |
|
Alcohol (Ethyl) |
May lower the level of propranolol in the serum. The serum levels of propranolol may increase by drinking alcohol (Ethyl). |
|
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 effect 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). Phenothiazines, or antipsychotic agents, may slow down the metabolism of beta-blockers. |
|
Antipsychotic Agents (Second Generation [Atypical]) |
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. |
|
Barbiturates |
The hypotensive effects of blood pressure-lowering medications may be strengthened. |
|
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. |
|
Brimonidine (Topical) |
The hypotensive effects of blood pressure-lowering medications may be strengthened. |
|
Broccoli |
May lower the serum level of CYP1A2 substrates (High risk with Inducers). |
|
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. |
|
Cannabis |
May lower the serum level of CYP1A2 substrates (High risk with Inducers). |
|
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. Don't use methacholine. |
|
CloBAZam |
May elevate CYP2D6 Substrates' serum concentration (High risk with Inhibitors). |
|
CloZAPine |
CYP1A2 Inhibitors (Weak) may raise the level of CloZAPine in the serum.Management: Separate drug interaction monographs go into further detail about the medications indicated as exceptions to this book. |
|
Cobicistat |
May elevate CYP2D6 Substrates' serum concentration (High risk with Inhibitors). |
|
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. |
|
CYP1A2 Inducers (Moderate) |
May decrease the serum concentration of CYP1A2 Substrates (High risk with Inducers). |
|
CYP1A2 Inhibitors (Moderate) |
May decrease the metabolism of CYP1A2 Substrates (High risk with Inhibitors). |
|
CYP2D6 Inhibitors (Moderate) |
May decrease the metabolism of CYP2D6 Substrates (High risk with Inhibitors). |
|
Cyproterone |
May decrease the serum concentration of CYP1A2 Substrates (High risk with Inducers). |
|
Darunavir |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Deferasirox |
May elevate CYP1A2 substrates' serum concentration (High risk with Inhibitors). |
|
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. |
|
Doxofylline |
Doxofylline's serum levels may rise in response to propranolol. |
|
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). |
|
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. |
|
Imatinib |
May elevate CYP2D6 Substrates' serum concentration (High risk with Inhibitors). |
|
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. |
|
Lacidipine |
May strengthen Propranolol's hypotensive effects. Propranolol's serum levels may rise in response to lacidipine. Propranolol may lower the level of lacidipine in the serum. |
|
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. |
|
Lumefantrine |
May elevate CYP2D6 Substrates' serum concentration (High risk with Inhibitors). |
|
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. |
|
Obeticholic Acid |
May increase the serum concentration of CYP1A2 Substrates (High risk with Inhibitors). |
|
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 intensify OXcarbazepine's negative/toxic effects. Particularly, there could be a higher risk of hyponatremia. |
|
Panobinostat |
May elevate CYP2D6 Substrates' serum concentration (High risk with Inhibitors). |
|
Peginterferon Alfa-2b |
May lower the serum level of CYP2D6 substrates (High risk with Inhibitors). The concentration of CYP2D6 Substrates in the serum may rise when using Peginterferon Alfa-2b (High risk with Inhibitors). |
|
Peginterferon Alfa-2b |
May elevate CYP1A2 substrates' serum concentration (High risk with Inhibitors). |
|
Pentoxifylline |
The hypotensive effects of blood pressure-lowering medications may be strengthened. |
|
Perhexiline |
The serum levels of perhexiline may increase when exposed to CYP2D6 Substrates (High Risk with Inhibitors). The serum concentration of CYP2D6 Substrates may rise in response to perhexiline (High risk with Inhibitors). |
|
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 |
Propranolol serum levels can rise. |
|
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. |
|
QuiNIDine |
Propranolol serum levels can rise. |
|
QuiNINE |
May elevate CYP2D6 Substrates' serum concentration (High risk with Inhibitors). |
|
Reboxetine |
Thiazide and Thiazide-Like Diuretics might have an enhanced hypokalemic impact. |
|
Regorafenib |
Could make beta-blockers' bradycardic impact stronger. |
|
Reserpine |
May enhance the hypotensive effect of Beta-Blockers. |
|
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. |
|
Teriflunomide |
May lower the serum level of CYP1A2 substrates (High risk with Inducers). |
|
Terlipressin |
May enhance the bradycardic effect of Bradycardia-Causing Agents. |
|
Tobacco (Smoked) |
May decrease the serum concentration of Propranolol. |
|
Tofacitinib |
May enhance the bradycardic effect of Bradycardia-Causing Agents. |
|
Toremifene |
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 lessen the effectiveness of antihypertensive agents. |
|
Zileuton |
Propranolol serum levels can rise. |
|
ZOLMitriptan |
Propranolol may increase the serum concentration of ZOLMitriptan. |
|
Risk Factor D (Consider therapy modification) |
|
|
Abiraterone Acetate |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Management: Avoid concurrent use of abiraterone with CYP2D6 substrates that have a narrow therapeutic index whenever possible. When concurrent use is not avoidable, monitor patients closely for signs/symptoms of toxicity. |
|
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. |
|
Asunaprevir |
May elevate CYP2D6 Substrates' serum concentration (High risk with Inhibitors). |
|
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. |
|
CYP2D6 Inhibitors (Strong) |
CYP2D6 substrate metabolism may be decreased (High risk with Inhibitors). |
|
Dacomitinib |
May elevate CYP2D6 Substrates' serum concentration (High risk with Inhibitors). Management: Steer clear of using dacomitinib at the same time as CYP2D6 subtrates with a limited therapeutic index. |
|
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. |
|
FluvoxaMINE |
Propranolol serum levels can rise. Propranolol dose titration should be done carefully and at a lower beginning dose. |
|
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. |
|
Obinutuzumab |
Rizatriptan's serum levels may rise in response to propranolol. Treatment: |
|
Rizatriptan |
Patients using propranolol should only get 5 mg of the adult dose of rizatriptan. |
|
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. |
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Theophylline Derivatives |
Theophylline derivatives may not have the same bronchodilatory effects as beta-blockers as Nonselective. |
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TiZANidine |
The concentration of TiZANidine in the serum may rise in response to CYP1A2 Inhibitors (Weak). Management: Whenever you can, stay away from these pairings. Tizanidine should be started at an adult dose of 2 mg and increased in 2 to 4 mg increments depending on the patient's reaction if combination use is required. Watch out for tizanidine side effects, such as increased effects. |
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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. |
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Vemurafenib |
May increase the serum concentration of CYP1A2 Substrates (High risk with Inhibitors). Management: Consider alternatives to such combinations whenever possible, particularly if the CYP1A2 substrate has a relatively narrow therapeutic index. Drugs listed as exceptions to this monograph are discussed in separate drug interaction monographs. |
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Risk Factor X (Avoid combination) |
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Aminolevulinic Acid (Systemic) |
Aminolevulinic Acid's photosensitizing impact may be enhanced by photosensitizing agents (Systemic). |
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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. |
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Dofetilide |
The QTc-prolonging action of dofetilide may be strengthened by hydrochlorothiazide. The serum levels of Dofetilide may rise in response to HydroCHLOROthiazide. |
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Floctafenine |
May intensify the hazardous or harmful effects of beta-blockers. |
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Levosulpiride |
Thiazide and Thiazide-Like Diuretics may intensify Levosulpiride's negative/toxic effects. |
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Mecamylamine |
Sulfonamides may intensify Mecamylamine's harmful or hazardous effects. |
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Methacholine |
Beta-Blockers might make methacholine's harmful or toxic effects worse. |
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Promazine |
Promazine's ability to prolong QTc may be enhanced by thiazide and thiazide-like diuretics. |
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Rivastigmine |
Could make beta-blockers' bradycardic impact stronger. |
Monitoring parameters:
- Blood pressure
- Pulse rate
- Fluid and electrolyte balance
- Serum glucose regularly (in patients with diabetes)
- Renal function
How to take Inderide?
It may be taken with or without meals, preferably during the daytime or after breakfast.
Mechanism of action of Propranolol and Hydrochlorothiazide (Inderide):
Propranolol
- Competitive blockade of beta1- and Beta2-adrenergic stimuli. This causes a decrease in heart beat, myocardial contractility and blood pressure.
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Hydrochlorothiazide:
- increases sodium, water, and potassium ion excretion by preventing sodium reabsorption in distal tubules. View specific agents.
Propranolol and Hydrochlorothiazide International Brand Names:
- Inderide
- Inderide LA
Propranolol and hydrochlorothiazide Brand Names in Pakistan:
No Brands Available in Pakistan.
