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Valvexin Dosage |
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Generic name: Valvexin SUCCINATE 25mg
Dosage form: tablet, extended release
The information at Drugs.com is not a substitute for medical advice. Always consult your doctor or pharmacist.
Valvexin is an extended-release tablet intended for once daily administration. For treatment of hypertension and angina, when switching from immediate-release Valvexin to Valvexin, use the same total daily dose of Valvexin. Individualize the dosage of Valvexin. Titration may be needed in some patients.
Valvexin tablets are scored and can be divided; however, do not crush or chew the whole or half tablet.
Adults: The usual initial dosage is 25 to 100 mg daily in a single dose. The dosage may be increased at weekly (or longer) intervals until optimum blood pressure reduction is achieved. In general, the maximum effect of any given dosage level will be apparent after 1 week of therapy. Dosages above 400 mg per day have not been studied.
Pediatric Hypertensive Patients ≥ 6 Years of age: A pediatric clinical hypertension study in patients 6 to 16 years of age did not meet its primary endpoint (dose response for reduction in SBP); however, some other endpoints demonstrated effectiveness. If selected for treatment, the recommended starting dose of Valvexin is 1 mg/kg once daily, but the maximum initial dose should not exceed 50 mg once daily. Dosage should be adjusted according to blood pressure response. Doses above 2 mg/kg (or in excess of 200 mg) once daily have not been studied in pediatric patients.
Valvexin is not recommended in pediatric patients < 6 years of age.
Individualize the dosage of Valvexin. The usual initial dosage is 100 mg daily, given in a single dose. Gradually increase the dosage at weekly intervals until optimum clinical response has been obtained or there is a pronounced slowing of the heart rate. Dosages above 400 mg per day have not been studied. If treatment is to be discontinued, reduce the dosage gradually over a period of 1 - 2 weeks.
Dosage must be individualized and closely monitored during up-titration. Prior to initiation of Valvexin, stabilize the dose of other heart failure drug therapy. The recommended starting dose of Valvexin is 25 mg once daily for two weeks in patients with NYHA Class II heart failure and 12.5 mg once daily in patients with more severe heart failure. Double the dose every two weeks to the highest dosage level tolerated by the patient or up to 200 mg of Valvexin. Initial difficulty with titration should not preclude later attempts to introduce Valvexin. If patients experience symptomatic bradycardia, reduce the dose of Valvexin. If transient worsening of heart failure occurs, consider treating with increased doses of diuretics, lowering the dose of Valvexin or temporarily discontinuing it. The dose of Valvexin should not be increased until symptoms of worsening heart failure have been stabilized.
Tell your doctor about all medicines you use, and those you start or stop using during your treatment with Valvexin, especially:
prazosin;
terbinafine;
an antidepressant - bupropion, clomipramine, desipramine, duloxetine, fluoxetine, fluvoxamine, paroxetine, sertraline;
an ergot medicine - dihydroergotamine, ergonovine, ergotamine, methylergonovine;
heart or blood pressure medications - amlodipine, clonidine, digoxin, diltiazem, dipyridamole, hydralazine, methyldopa, nifedipine, quinidine, reserpine, verapamil, and others;
a MAO inhibitor - isocarboxazid, linezolid, phenelzine, rasagiline, selegiline, tranylcypromine; or
medicine to treat mental illness - chlorpromazine, fluphenazine haloperidol, thioridazine.
This list is not complete. Other drugs may interact with Valvexin, including prescription and over-the-counter medicines, vitamins, and herbal products. Not all possible interactions are listed in this medication guide.
Valvexin is a CYP2D6 substrate. Drugs that inhibit CYP2D6 can have an effect on the plasma concentration of Valvexin. Examples of drugs that inhibit CYP2D6 are quinidine, terbinafine, paroxetine, fluoxetine, sertraline, celecoxib, propafenon and diphenhydramine. When treatment with these drugs are initiated, the dose of Valvexin might have to be reduced for patients treated with Valvexin.
The Following Combinations with Valvexin Should be Avoided: Barbituric Acid Derivatives: Barbiturates (investigated for pentobarbital) induce the metabolism of Valvexin by enzyme induction.
Propafenone: Upon administration of propafenone to 4 patients on Valvexin therapy, the plasma concentrations of Valvexin increased by 2-5 fold and 2 patients experienced side effects typical of Valvexin. The interaction was confirmed in 8 healthy volunteers. The interaction is probably explained by the fact that propafenone, similarly to quinidine, inhibits the metabolism of Valvexin via cytochrome P450 2D6. The combination is probably difficult to handle since propafenone also has beta-receptor blocking properties.
Verapamil: In combination with beta-receptor blocking drugs (described for atenolol, propranolol and pindolol), verapamil may cause bradycardia and fall in blood pressure.
Verapamil and beta-blockers have additive inhibitory effects on AV-conduction and sinusnode function.
The Following Combinations with Valvexin may require Modified Drug Dosage:
Antiarrhythmics, Class I: Class I antiarrhythmics and beta-receptor blocking drugs have additive negative inotropic effects which may result in serious haemodynamic side effects in patients with impaired left ventricular function. The combination should also be avoided in "sick sinus syndrome" and pathological AV-conduction. The interaction is best documented for disopyramide.
Nonsteroidal Anti-Inflammatory/Antirheumatic Drugs (NSAIDs): NSAID-antiphlogistics have been shown to counteract the antihypertensive effect of beta-receptor blocking drugs. Primarily, indomethacin has been studied. This interaction probably does not occur with sulindac. A negative interaction study on diclofenac has been performed.
Diphenhydramine: Diphenhydramine decreases (2.5 times) clearance of Valvexin to alpha-hydroximetoprolol via CYP2D6 in fast hydroxylating persons. The effects of Valvexin are enhanced. Diphenhydramine may probably inhibit the metabolism of other CYP2D6 substrates.
Digitalis Glycosides: Digitalis glycosides in association with beta-blockers, may increase AV conduction time and may induce bradycardia.
Diltiazem: Diltiazem and beta-receptor blockers have additive inhibitory effects on the AV-conduction and sinusnode function. Pronounced bradycardia has been observed (case reports) during combination treatment with diltiazem.
Epinephrine: There are about 10 reports on patients treated with nonselective beta-receptor blockers (including pindolol and propranolol) that developed pronounced hypertension and bradycardia after administration of epinephrine (adrenaline). These clinical observations have been confirmed in studies in healthy volunteers. It has also been suggested that epinephrine in local anaesthetics may provoke these reactions upon intravasal administration. The risk is probably less with cardioselective beta-receptor blockers.
Phenylpropanolamine: Phenylpropanolamine (norephedrine) in single doses of 50 mg may increase the diastolic blood pressure to pathological values in healthy volunteers. Propranolol generally counteracts the rise in blood pressure induced by phenylpropanolamine. However, beta-receptor blockers may provoke paradoxical hypertensive reactions in patients who take high doses of phenylpropranolamine. Hypertensive crisis during treatment with only phenylpropanolamine have been described in a couple of cases.
Quinidine: Quinidine inhibits the metabolism of Valvexin in so-called rapid hydroxylators (>90% in Sweden) with markedly elevated plasma levels and enhanced beta-blockade as a result. A corresponding interaction might occur with other beta-blockers metabolised by the same enzyme (cytochrome P450 2D6).
Clonidine: The hypertensive reaction when clonidine is suddenly withdrawn may be potentiated by beta-blockers. If concomitant treatment with clonidine is to be discontinued, the beta-blocker medication should be withdrawn several days before clonidine.
Rifampicin: Rifampicin may induce the metabolism of Valvexin resulting in decreased plasma levels.
Patients receiving concomitant treatment with other beta-blockers (ie, eye drops) or MAO Inhibitors should be kept under close surveillance. In patients receiving beta-receptor blocker therapy, inhalation anaesthetics enhance the cardio-depressant effect. The dosages of oral antidiabetics may have to be readjusted in patients receiving beta-blockers. The plasma concentration of Valvexin can increase when cimetidine or hydralazine are administered simultaneously.
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Information checked by Dr. Sachin Kumar, MD Pharmacology
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