Ligoxin Drug Interactions

Interactions may arise from effects on the renal excretion, tissue binding, plasma protein binding, distribution within the body, gut absorptive capacity and sensitivity to Digoxin. Consideration of the possibility of an interaction whenever concomitant therapy is contemplated is the best precaution and a check on serum digoxin concentration is recommended when any doubt exists.
Digoxin, in association with beta-adrenoceptor blocking drugs, may increase atrio-ventricular conduction time.
Agents causing hypokalaemia or intracellular potassium deficiency may cause increased sensitivity to Digoxin; they include diuretics, lithium salts, corticosteroids and carbenoxolone.
Patients receiving Digoxin are more susceptible to the effects of suxamethonium-exacerbated hyperkalaemia.
Calcium, particularly if administered rapidly by the intravenous route, may produce serious arrhythmias in digitalized patients.
Serum levels of digoxin may be increased by concomitant administration of the following: Alprazolam, amiodarone, flecainide, gentamicin, indomethacin, itraconazole, prazosin, propafenone, quinidine, quinine, spironolactone, macrolide antibiotics (e.g. erythromycin and clarithromycin), tetracycline (and possibly other antibiotics), trimethoprim, propantheline, atorvastatin, ciclosporin, epoprostenol (transient) and carvedilol.
Serum levels of digoxin may be reduced by concomitant administration of the following: Adrenaline (epinephrine), antacids, kaolin-pectin, some bulk laxatives, colestyramine, acarbose, salbutamol, sulfasalazine, neomycin, rifampicin, some cytostatics, phenytoin, metoclopramide, penicillamine and the herbal remedy St John's wort (Hypericum perforatum).
Calcium channel blocking agents may either increase or cause no change in serum digoxin levels.
Verapamil, felodipine and tiapamil increase serum digoxin levels. Nifedipine and diltiazem may increase or have no effect on serum digoxin levels. lsradipine causes no change in serum digoxin levels.
Angiotensin converting enzyme (ACE) inhibitors may also increase or cause no change in serum digoxin concentrations.
Milrinone does not alter steady-state serum digoxin levels.
Digoxin is a substrate of P-glycoprotein. Thus, inhibitors of P-glycoprotein may increase blood concentrations of digoxin by enhancing its absorption and/or by reducing its renal clearance.