Interactions, drug quinidine

Antacids also have clinically significant drug interactions with tetracycline, ferrous sulfate, isoniazid, quinidine, sul-fonylureas, and quinolone antibiotics. Antacid-drug interactions are influenced by antacid composition, dose, dosage schedule, and formulation. 

Preliminary studies [241, 249, 250] of the cardiovascular and sympatholytic properties of prenylamine demonstrated that coronary blood flow and oxygenation could be increased under experimental conditions (in dogs) and that the drug interacted in complex fashion with sympathetically innervated organs, but the picture presented was someudiat confused because of the many uncontrolled variables and limitations of the actual techniques used. Anti-arrhythmic activity of potency comparable with that of quinidine, plus local anaesthetic properties, were also demonstrated [251] but the same worker was notable to reproduce these effects in intact live animals with any consistency. Large doses of the drug actually provoked cardiac fibrillation in some cases. 

Hypersensitivity to any component of the product. Coadministration of nelfinavir is contraindicated with drugs that are highly dependent on CYP3A for clearance and for which elevated plasma concentrations are associated with serious and/or life-threatening events (eg, amiodarone, quinidine, ergot derivatives, pimozide, midazolam, triazolam, lovastatin, simvastatin see Drug Interactions). 

Drug interactions Serious and/or life-threatening drug interactions could occur between amprenavir and amiodarone, lidocaine (systemic), tricyclic antidepressants, and quinidine. Concentration monitoring of these agents is recommended if these agents are used concomitantly with amprenavir. 

Several drug interactions involving amantadine and rimantadine are clinically significant. Anticholinergic drugs can potentiate the toxicity of amantadine. Thiazide-triamterene, trimethoprim-sulfamethoxazole, quinine, and quinidine increase plasma amantadine levels. Cimetidine decreases rimantadine clearance, and aspirin and acetaminophen decrease rimantadine plasma levels. 

The drug has a half-life of 6-8 hours. It is extensively metabolized in the liver, and stereoselective metabolism of its two isomers is observed. Since metabolism of ( R)-carvedilol is influenced by polymorphisms in CYP2D6 activity and by drugs that inhibit this enzyme s activity (such as quinidine and fluoxetine, see Chapter 4), drug interactions may occur. Carvedilol also appears to attenuate oxygen free radical-initiated lipid peroxidation and to inhibit vascular smooth muscle mitogenesis independently of adrenoceptor blockade. These effects may contribute to the clinical benefits of the drug in chronic heart failure (see Chapter 13). 

Drug Interactions Other antihypertensive agents Carbamazepine (vasodilators, ACE inhibitors, Rifampin diuretics, and beta-blockers) Phenobarbital Digoxin Cyclosporine Disopyramide Theophylline Flecainide Inhalation anesthetics Quinidine Neuromuscular blocking agents Cimetidine Lithium ... 

Dextromethorphan is known to interact with quini-dine and terbinafine. In both cases, there is a reduction in the metabolism of dextromethorphan by the liver. Terbinafine is a drug used to treat fungal infections. Quinidine is used for the treatment of malarial infections and heart rhythm problems. There has been a case report of a drug interaction between the use of fluoxetine (Prozac) and dextromethorphan. Fluoxetine is an antidepressant in the class of drugs called serotonin reuptake inhibitors. 

Drug interactions Catecholamine-depleting drugs such as reserpine may have an additive effect in combination with betablockers. Drugs that inhibit CYP2D6 (quinidine, fluoxetine, paroxetine, and propafenone) increase metoprolol concentration. 

Multiple drug interactions have been discribed (decreased serum concentrations of phenobarbital, phenytoin, sulfinpyrazone and rifampin, increased serum concentrations of quinidine, carbamazepine, cyclosporin). Important in this setting is that a marked interaction exists between digoxin and verapamil, increasing the serum concentrations of the former due to decreased renal excretion,... 

Drug interactions are multiple but of special interest is the interaction with other AADs such as quinidine and verapamil, both increasing the serum concentration. 

Koley AP, Robinson RC, Markowitz A, et al. Drug-drug interactions effect of quinidine on nifedipine binding to human cytochrome-P450 3A4. Biochem Pharmacol 1997 53 455 160. 

Over the past decade there has been a substantial improvement in the ability to predict metabolism-based in vivo drug interactions from kinetic data obtained in vitro. This advance has been most evident for interactions that occur at the level of cytochrome P450 (CYP)-catalyzed oxidation and reflects the availability of human tissue samples, cDNA-expressed CYPs, and well-defined substrates and inhibitors of individual enzymes. The most common paradigm in the prediction of in vivo drug interactions has been first to determine the enzyme selectivity of a suspected inhibitor and subsequently to estimate the constant that quantifies the potency of reversible inhibition in vitro. This approach has been successful in identifying clinically important potent competitive inhibitors, such as quinidine, fluoxetine, and itraconazole. However, there is a continuing concern that a number of well-established and clinically important CYP-mediated drug interactions are not predictable from the classical approach that assumes reversible mechanisms of inhibition are ubiquitous. 

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