Isolated reports of myasthenia gravis like syndrome or exacerbation of myasthenia gravis have been reported in patients administered propranolol. Beta adrenoreceptor blocking drugs should not be used in untreated phaeochromocytoma See section 4.

When it has been decided to interrupt a beta-blockade in preparation for surgery, therapy should be discontinued for at least 48 hours. Continuation of beta-blockade reduces the risk of arrhythmias during induction and intubation, however the risk of hypotension may be increased as well. If treatment is continued, caution should be observed with the use of certain anaesthetic drugs.

The patient may be protected against vagal reactions by intravenous administration of atropine. The tablets contain lactose. Patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should not take this drug. Non-cardioselective beta-blockers oppose the bronchodilator effects of beta-agonist bronchodilators, propranolol is contraindicated in patients with asthma see section 4. Calcium channel blockers Verapamil,diltiazem or bepridil: Calcium channel blockers and beta-blockers have additive effects on AV conduction and sinus node function and can cause bradycardia and hypotension.

The combination with propranolol should be avoided, especially in patients with cardiac decompensation see section 4. Potentiation of bradycardia effects with possible fatal outcomes. Treatment with Fingolimod should not be initiated in patients receiving beta blockers. In case of combination, appropriate monitoring for treatment initiation, at least overnight monitoring is recommended.

The plasma levels and the effects of beta-blockers are reduced by the barbiturates. Barbiturates are potent liver enzyme inducers which may increase the metabolism of propranolol. This probably was because propranolol is partially metabolized by the same enzyme like propafenone CYP2D6.

This combination is also not advisable because propafenone has negative inotropic effects. Propranolol may cause a reduction in clearance and an increase in plasma concentrations of warfarin. Concomitant use of MAO inhibitors except MAO-B inhibitors with antihypertensive agents may diminish the antihypertensive effect and lead to hypertensive reactions.

Digitalis glycosides, in association with beta-blockers, may increase atrio-ventricular conduction time. Combination to be used with caution, dose adjustment may be required Amiodarone: A few case reports suggest that patients treated with amiodarone can have severe sinus bradycardia when treated concomitantly with propranolol.

Amiodarone has an extremely long half-life about 50 days , which means that interactions may occur long after discontinuation of therapy. Class I antiarrhythmic drugs disopyramide, quinidine: Digitalis glycosides in association with beta-blockers may increase atrioventricular conduction time.

Combined use of beta-blockers and calcium channel blockers with negative inotropic effects e. This may result in severe hypotension, bradycardia and cardiac failure. Neither the beta-blocker nor the calcium channel blocker should be administered intravenously within 48 hours of discontinuing the other.

Concomitant therapy with dihydropyridines calcium channel blockers e. Concomitant use of sympathomimetic agents e. Caution must be exercised in the parenteral administration of preparations containing adrenaline to patients taking beta-blockers as, in rare cases, vasoconstriction, hypertension and bradycardia may result. Care should also be taken with preparations such as isoprenaline and noradrenaline. Patients already receiving Inderal tend to have higher lidocaine levels than controls.

The combination should be avoided. Concomitant use of cimetidine or hydralazine will increase plasma levels of propranolol, and concomitant use of alcohol may increase the plasma levels of propranolol. Beta-blockers may exacerbate the rebound hypertension which can follow the withdrawal of clonidine.

If the two drugs are co-administered, the beta-blocker should be withdrawn several days before discontinuing clonidine. If replacing clonidine by beta-blocker therapy, the introduction of beta-blockers should be delayed for several days after clonidine administration has stopped. A central effect is also possible. Clinical studies have demonstrated that propranolol is of benefit in exaggerated physiological and essential familial tremor.

Peak plasma concentrations occur about 1 to 4 hours after an oral dose. The binding is enantiomer-selective. Propranolol crosses the blood-brain barrier and the placenta, and is distributed into breast milk.

Metabolism and Elimination Propranolol is extensively metabolized with most metabolites appearing in the urine. Propranolol is metabolized through three primary routes: The four major metabolites are propranolol glucuronide, naphthyloxylactic acid and glucuronic acid, and sulfate conjugates of 4-hydroxy propranolol. In vitro studies have indicated that the aromatic hydroxylation of propranolol is catalyzed mainly by polymorphic CYP2D6.

Propranolol is also a substrate of CYP2C19 and a substrate for the intestinal efflux transporter, p-glycoprotein p-gp. Studies suggest however that p-gp is not dose-limiting for intestinal absorption of propranolol in the usual therapeutic dose range. In healthy subjects, no difference was observed between CYP2D6 extensive metabolizers EMs and poor metabolizers PMs with respect to oral clearance or elimination half-life.

Partial clearance of 4-hydroxy propranolol was significantly higher and of naphthyloxyactic acid significantly lower in EMs than PMs.

The plasma half-life of propranolol is from 3 to 6 hours. Special Populations Geriatric In a study of 12 elderly years old and 12 young years old healthy subjects, the clearance of S - -enantiomer of propranolol was decreased in the elderly.

Clearance of propranolol is reduced with aging due to decline in oxidation capacity ring oxidation and side-chain oxidation. Conjugation capacity remains unchanged.

In a study of 32 patients age 30 to 84 years given a single mg dose of propranolol, an inverse correlation was found between age and the partial metabolic clearances to 4-hydroxypropranolol 40HP-ring oxidation and to naphthoxylactic acid NLA-side chain oxidation. No correlation was found between age and the partial metabolic clearance to propranolol glucuronide PPLG-conjugation.

Gender In a study of 9 healthy women and 12 healthy men, neither the administration of testosterone nor the regular course of the menstrual cycle affected the plasma binding of the propranolol enantiomers. In contrast, there was a significant, although non-enantioselective diminution of the binding of propranolol after treatment with ethinyl estradiol. These findings are inconsistent with another study, in which administration of testosterone cypionate confirmed the stimulatory role of this hormone on propranolol metabolism and concluded that the clearance of propranolol in men is dependent on circulating concentrations of testosterone.

In women, none of the metabolic clearances for propranolol showed any significant association with either estradiol or testosterone. Propranolol plasma clearance was also reduced in the patients with chronic renal failure. Studies have reported a delayed absorption rate and a reduced half-life of propranolol in patients with renal failure of varying severity.

Despite this shorter plasma half-life, propranolol peak plasma levels were times higher and total plasma levels of metabolites were up to 3 times higher in these patients than in subjects with normal renal function. Propranolol is not significantly dialyzable. Hepatic Insufficiency Propranolol is extensively metabolized by the liver. In a study conducted in 7 patients with cirrhosis and 9 healthy subjects receiving mg oral propranolol every 8 hours for 7 doses, the steady-state unbound propranolol concentration in patients with cirrhosis was increased 3-fold in comparison to controls.

No interactions were observed with either ranitidine or lansoprazole. Substrates or Inhibitors of CYP2C19 Blood levels and or toxicity of propranolol may be increased by coadministration with substrates or inhibitors of CYP2C19, such as fluconazole, cimetidine, fluoxetine, fluvoxamine, teniposide, and tolbutamide. No interaction was observed with omeprazole.

Inducers of Hepatic Drug Metabolism Blood levels of propranolol may be decreased by co-administration with inducers such as rifampin, ethanol, phenytoin, and phenobarbital.

The metabolism of propranolol is reduced by co-administration of quinidine, leading to a two-three fold increased blood concentration and greater degrees of clinical beta-blockade.

Propranolol does not affect the pharmacokinetics of verapamil and norverapamil. Verapamil does not affect the pharmacokinetics of propranolol. Benzodiazepines Propranolol can inhibit the metabolism of diazepam, resulting in increased concentrations of diazepam and its metabolites. Diazepam does not alter the pharmacokinetics of propranolol. The pharmacokinetics of oxazepam, triazolam, lorazepam, and alprazolam are not affected by co-administration of propranolol.

Co-administration with aluminum hydroxide gel mg may result in a decrease in propranolol concentrations. Propranolol did not have an effect on the pharmacokinetics of fluvastatin. Warfarin Concomitant administration of propranolol and warfarin has been shown to increase warfarin bioavailability and increase prothrombin time. Alcohol Concomitant use of alcohol may increase plasma levels of propranolol. Propranolol contributed to control of diastolic blood pressure, but the magnitude of the effect of propranolol on blood pressure cannot be ascertained.

Angina Pectoris In a double-blind, placebo-controlled study of 32 patients of both sexes, aged 32 to 69 years, with stable angina, propranolol mg t. Atrial Fibrillation In a report examining the long-term months efficacy of propranolol, 10 patients, aged 27 to 80, with atrial fibrillation and ventricular rate greater than beats per minute despite digitalis, received propranolol up to 30 mg t.

Propranolol was administered at either 60 or 80 mg t. Therapy with propranolol, begun 5 to 21 days following infarction, was shown to reduce overall mortality up to 39 months, the longest period of follow-up. This was primarily attributable to a reduction in cardiovascular mortality. The protective effect of propranolol was consistent regardless of age, sex, or site of infarction. The Norwegian Multicenter Trial in which propranolol was administered at 40 mg q.

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