Digoxin with thiazide diuretics

Drugs that can precipitate lactic acidosis in patients taking metformin include ACE inhibitors, thiazide diuretics, NSAIDs, and drugs such as furosemide, nifedipine, cimetidine, amiloride, triamterene, trimethoprim, and digoxin, which are all secreted in the renal tubules, compete with metformin, and can contribute to increased plasma metformin concentrations (76). 

Metolazone occupies an intermediate position between the thiazide diuretics and the more potent loop diuretics (1). It is more effective than the thiazides in moderate to advanced renal insufficiency (SED-8, 488) (SED-9, 355). In patients with normal renal function its antihypertensive effect compares favorably with that of bendroflumethia-zide. When severe heart failure is refractory to conventional triple therapy (high-dose loop diuretic, digoxin, and angiotensin-converting enzyme inhibitor) metolazone can restore diuresis, with weight loss and clinical improvement. 

With long-term use hypokalemia due to intestinal potassium loss could occur (Blumenthal, 1998). Thiazide diuretics, corticosteroids, and licorice could exacerbate hypokalemia. The effects of digoxin can be potentiated by hypokalemia. 

Quinidine and thiazide diuretics can both enhance the toxicity of digitalis. The action of quini-dine is attributed to phtirmacokinetic mechanisms, especially inhibition of its clearance. The plasma concentration of digoxin predictably increases when quinidine is added. The enhancement of digitalis toxicity by thiazides is due to a pharmacodynamic mechanism, namely, the action of these diuretics to reduce extracellular potassium. Sulfasalazine decreases plasma levels of digitalis by interfering with gut absorption of the drug. The answer is (D). 

Diuretics. Hypercalcaemia may develop in patients administered thiazide diuretics with either calcium or vitamin D supplements, leading to a need to monitor plasma or serum calcium levels. The concurrent use of potassium-sparing diuretics, and other potassium supplements or potassium-containing salt substitutes, could lead to serious hyperkalaemia. Hyperkalaemia is known to interfere with the absorption of vitamin B12. There is a need to warn patients and monitor serum potassium levels. The risk of hypokalaemia is minimal with low doses of thiazides, for example 5 mg of bendroflumethiazide. Hypokalaemia is a concern in patients receiving treatment with drugs such as digoxin, amiodarone, disopyramide or flecainide (drugs used to treat cardiac disorders). 

No interactions are expected at standard therapeutic doses. At higher doses or with long-term use, licorice may potentiate potassium depletion of high-ceiling loop diuretics and thiazide diuretics, stimulant laxatives (Mills and Bone 2005), and corticosteroids such as prednisolone (Cheng et al. 2004 De Smet 1993), and may potentiate the action of cardiac glycosides such as digoxin (Kelly 1990). 

Concomitant use of diuretic herbs with prescription loop diuretics, thiazide diuretics, osmotic diuretics, and potassium-sparing diuretics may cause excessive fluid loss. Reductions in potassium levels caused by diuretics may increase the toxicity of cardiac glycosides, such as digoxin, and their combination should be avoided (Anon 2010). 

Digoxin and Diuretics. One of the problems associated with the use of most of the commonly employed diuretics [e.g., the thiazides furosemide (e.g.,Lasix)], is excessive loss of potassium. Particular caution is necessary in patients also being treated with digoxin, many of whom are also candidates for diuretic therapy. If potassium depletion remains uncorrected, the heart may become more sensitive to the effects of digoxin and arrhythmia may result. 

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