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 may be titrated gradually based on blood pressure response; maximum: propranolol 160 mg/hydrochlorothiazide 50 mg per 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
- No animal reproduction studies have been conducted for this combination.
- 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. The following adjustments have been recommended for hydrochlorothiazide:
- CrCl ≥10 mL/minute: Dosage adjustment not necessary. Usually not effective with CrCl <30 mL/minute unless used in combination with a loop diuretic.
- CrCl <10 mL/minute: Not recommended for use.
Dose in Liver disease:
No dosage adjustments have been provided in the manufacturer’s labeling. However, systemic exposure to propranolol is increased with hepatic impairment. Use cautiously.
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 according to some product labeling 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. There is limited documentation on allergenic cross-reactivity between thiazide-related diuretics.
- 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.
- Anaphylaxis treatment (eg, epinephrine) in patients taking beta-blockers may be ineffective or promote undesirable effects.
-
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
- The use of hydrochlorothiazide can precipitate gout in certain patients with a history of gout, a familial predisposition to gout, or chronic renal failure.
- Doses greater than 25 mg may increase the risk.
-
Ocular effects
- Hydrochlorothiazide may cause acute transient myopia or acute angle-closure vision loss.
- These symptoms typically occur within hours to weeks of therapy initiation.
- Therapy should be stopped for patients experiencing acute visual acuity decreases or severe ocular pain.
- Additional treatment may be required if the intraocular pressure is not controlled.
- The risk factors include a history of penicillin allergy or sulfonamide allergy.
-
Photosensitivity
- Hydrochlorothiazide may cause photosensitization.
-
Allergy to sulfonamide ("sulfa")
- FDA-approved product labels for medications that are part of the sulfonamide chemical family include a wide contraindication for patients who have had an allergic reaction to sulfonamides.
- There is a possibility of cross-reactivity between members from a particular class (e.g., 2 antibiotics sulfonamides).
- Crossreactivity concerns have been raised previously for all compounds with the sulfonamide structural (SO NH).
- A deeper understanding of allergic mechanisms has shown that cross-reactivity between non-antibiotic sulfonamides and antibiotic sulfonamides is unlikely.
- Nonantibiotic sulfonamides are less likely to cause anaphylaxis (a mechanism of cross-reaction due primarily to antibody production).
- T-cell-mediated (type IV), reactions are less well understood. This makes it difficult to exclude the possibility based on current knowledge.
- These classes are sometimes avoided by some clinicians in severe cases of reactions (Stevens Johnson syndrome/TEN).
-
Bariatric surgery
- Dehydration: Avoid diuretics in the first 24 hours after bariatric surgery.
- There is a chance of electrolyte disturbances, and dehydration. If necessary, diuretics may be resumed once oral fluid intake goals have been met.
-
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:
- Diabetes mellitus patients should be cautious. It may lead to hypoglycemia, and/or mask symptoms.
-
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 may decrease renal calcium excretion; patients with hypercalcemia should avoid their use.
-
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
- Side effects can be more severe in those with renal impairment.
-
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 |
May enhance the bradycardic effect of Beta-Blockers. |
|
Ajmaline |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Ajmaline |
Sulfonamides may enhance the adverse/toxic effect of Ajmaline. Specifically, the risk for cholestasis may be increased. |
|
Alcohol (Ethyl) |
May decrease the serum concentration of Propranolol. Alcohol (Ethyl) may increase the serum concentration of Propranolol. |
|
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. |
|
Broccoli |
May decrease the serum concentration of CYP1A2 Substrates (High risk with Inducers). |
|
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. |
|
Cannabis |
May decrease the serum concentration of CYP1A2 Substrates (High risk with Inducers). |
|
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. |
|
CloBAZam |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
CloZAPine |
CYP1A2 Inhibitors (Weak) may increase the serum concentration of CloZAPine. Management: Drugs listed as exceptions to this monograph are discussed in further detail in separate drug interaction monographs. |
|
Cobicistat |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
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. |
|
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 increase the serum concentration of CYP1A2 Substrates (High risk with Inhibitors). |
|
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. |
|
Doxofylline |
Propranolol may increase the serum concentration of Doxofylline. |
|
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). |
|
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. |
|
Imatinib |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
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. |
|
Lacidipine |
May enhance the hypotensive effect of Propranolol. Lacidipine may increase the serum concentration of Propranolol. Propranolol may decrease the serum concentration of Lacidipine. |
|
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. |
|
Lumefantrine |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
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. |
|
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 enhance the adverse/toxic effect of OXcarbazepine. Specifically, there may be an increased risk for hyponatremia. |
|
Panobinostat |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Peginterferon Alfa-2b |
May decrease the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Peginterferon Alfa-2b may increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Peginterferon Alfa-2b |
May increase the serum concentration of CYP1A2 Substrates (High risk with Inhibitors). |
|
Pentoxifylline |
May enhance the hypotensive effect of Blood Pressure Lowering Agents. |
|
Perhexiline |
CYP2D6 Substrates (High risk with Inhibitors) may increase the serum concentration of Perhexiline. Perhexiline may increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
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 Propranolol. |
|
Prostacyclin Analogues |
May enhance the hypotensive effect of Blood Pressure Lowering Agents. |
|
Quinagolide |
May enhance the hypotensive effect of Blood Pressure Lowering Agents. |
|
QuiNIDine |
May increase the serum concentration of Propranolol. |
|
QuiNINE |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
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. |
|
Teriflunomide |
May decrease the serum concentration 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 |
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. |
|
Zileuton |
May increase the serum concentration of Propranolol. |
|
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 increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Bile Acid Sequestrants |
May decrease the absorption of Thiazide and Thiazide-Like Diuretics. The diuretic response is likewise decreased. |
|
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) |
May decrease the metabolism of CYP2D6 Substrates (High risk with Inhibitors). |
|
Dacomitinib |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Management: Avoid concurrent use of dacomitinib with CYP2D6 subtrates that have a narrow 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 |
May increase the serum concentration of Propranolol. Management: Use a lower initial propranolol dose and be cautious with propranolol dose titration. |
|
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. |
|
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. |
|
Rizatriptan |
Propranolol may increase the serum concentration of Rizatriptan. Management: Rizatriptan adult dose should be reduced to 5 mg in patients who are also being treated with propranolol. |
|
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. |
|
Theophylline Derivatives |
Beta-Blockers (Nonselective) may diminish the bronchodilatory effect of Theophylline Derivatives. |
|
TiZANidine |
CYP1A2 Inhibitors (Weak) may increase the serum concentration of TiZANidine. Management: Avoid these combinations when possible. If combined use is necessary, initiate tizanidine at an adult dose of 2 mg and increase in 2 to 4 mg increments based on patient response. Monitor for increased effects of tizanidine, including adverse reactions. |
|
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. |
|
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. |
|
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:
- 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.
-
Hydrochlorothiazide:
- Inhibits sodium reabsorption in distal tubules, increasing excretion of sodium, water, as well as potassium ions. See individual agents.
Propranolol and Hydrochlorothiazide International Brand Names:
- Inderide
- Inderide LA
Propranolol and hydrochlorothiazide Brand Names in Pakistan:
No Brands Available in Pakistan.
.png)
