Quinidine interaction with other drugs

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

The drug most commonly used in clinical practice that can produce immune thrombocytopenic purpura is heparin. Other examples are sulfonamides, thiazide diuretics, chlorpropamide, quinidine, and gold. These types of immune thrombocytopenic purpura are reversed when the drug is withdrawn. Molecular mechanisms for the formation of specific drug-dependent antibodies appear to be very similar. The glycoproteins on the platelet surface interact with the drugs to form neo-epitopes. Subsequent... 

The pharmacokinetics, toxic effects and interactions of quinidine with other drugs have been reviewed (30 ). An important interaction has been reported between quinidine and concurrently administered pheno-barbitone or phenytoin which can lead to large changes in the plasma quinidine concentration (31 ). 

Antipsychotics produce more important pharmacodynamic than pharmacokinetic interactions because of their multiple effects. Additive effects may occur when these drugs are combined with others that have sedative effects, a-adrenoceptor-blocking action, anticholinergic effects, and—for thioridazine and ziprasidone—quinidine-like action. 

Drugs metabolized by CYP that interact with cimetidine include, but are not limited to, the following lidocaine, quinidine, midazolam, triazolam, nifedipine, verapamil, and fentanyl (4). In each instance, inhibition of CYP by cimetidine results in reduced metabolic clearance and increases in serum concentrations of the other drug, which can lead to the expected toxicity and adverse experiences characteristic of the other drug. 

Other experiments have shown that the mutation K76T is not the only factor to modulate the action of PfCRT. The Cooper group [82] demonstrated that mutations in transmembrane domains 1, 4, and 9 altered susceptibility to CQ, quinine, and quinidine. Photoaffinity labeling of PfCRT with a novel perfluorophenylazido CQ [83] provided new information concerning interaction of the drug with the protein. Mutations conferring CQ resistance increased the CQ-associated H+ leak in the... 

Inhibitors of OATP transport are typically ster-ically bulky compounds, including anions, cations, and neutral compounds (95). Various medications have been shown to interact with OATPs, including HMG CoA reductase inhibitors, cyclosporine, quinidine, rifampin, ketoconazole, verapamil, and certain protease inhibitors. Cyclosporine and rifampin have relatively high ratios of plasma concentration to Ki, suggesting the potential for clinically significant drug-drug interactions via modulation of OATP. On the other hand, plasma concentrations of pravastatin are... 

The many drug interactions described with cimetidine are largely attributable to inhibition of CYP isozymes or renal clearance of other drugs. Cimetidine also reduces hepatic blood flow and so can, for example, reduce the clearance of lidocaine. In the kidneys cimetidine interferes with the tubular excretion of procainamide and quinidine. Both effects are small, and the long list of drugs for which interference is demonstrable (Table 1) is out of all proportion to the number for which interference is of chnical significance. 

Interactions of mexiletine with other cardioactive drugs have been reviewed (48). The most important are beneficial interactions with beta-adrenoceptor antagonists, quinidine, and amiodarone in the suppression of ventricular tachydysrhythmias. During these interactions the... 

Information on the possible pharmacokinetic interaction seems to be limited to this report. Both quinidine and procainamide are class la an-tiarrhythmics and prolong the QT interval, an effect that is increased with the combination. Such combinations should generally be avoided because of the increased risk of torsade de pointes. See also Drugs that prolong the QT interval + Other drugs that prolong the QT interval , p.257. 

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