• Digoxin
  

Digoxin increases the renal excretion of magnesium (Schwinger and Erdmann 1992). Low magnesium concentrations increase cardiac glycoside toxicity.

Magnesium deficiency affects calcium and vitamin D metabolism and is primarily associated with hypocalcemia (Cashman and Flynn 1999). Clinically, neuromuscular hyperexcitability may be the first symptom manifested in patients with hypomagnesemia (reflected in a serum concentration of 17 mg/L or less). Recent evidence supports a possible connection between chronically low magnesium levels and various illnesses such as cardiovascular disease, hypertension, diabetes, and osteoporosis.

The current recommended dietary allowance (RDA) for magnesium ranges from 30 to 420 mg/day, depending upon age and gender (Cashman and Flynn 1999). For replacement therapy, doses should be tailored to the patient's clinical condition, taking into account serum magnesium levels, dietary habits, and medication regimen.

Digoxin inhibits thiamine uptake by cardiac cells; chronic use may cause a deficiency of this nutrient (Zangen et al. 1998).

Early nonspecific manifestations of depleted thiamine levels include weakness, fatigue, anorexia, constipation, nystagmus, and mental status changes such as memory loss, confusion, and depression (Covington 1999). Beriberi is the classic condition associated with thiamine deficiency. Symptoms include polyneuritis, cardiac disturbances (bradycardia, heart failure, hypertrophy), and possibly edema. Thiamine deficiency rarely occurs alone; it is usually accompanied by deficiencies in other B vitamins.

Although the recommended daily allowance (RDA) for this nutrient ranges from 1.1 to 1.5 mg for adults depending on gender, treatment of beriberi requires oral doses as high as 5 to 10 mg/day for one month to achieve tissue saturation and replenish body stores of thiamine (Covington 1999). Treatment of deficiency secondary to alcoholism may require up to 40 mg/day of thiamine orally; cardiovascular disease may warrant a total daily intake of 90 mg (Marcus and Coulston 1996). Replacement therapy should be tailored to the patient's needs depending on age, gender, clinical presentation, serum vitamin B1 levels, dietary habits, and medication regimen.

This information is intended to serve as a concise reference for healthcare professionals to identify substances that may be depleted by many commonly prescribed medications. Depletion of these substances depends upon a number of factors including medical history, lifestyle, dietary habits, and duration of treatment with a particular medication. The signs and symptoms associated with deficiency may be nonspecific and could be indicative of clinical conditions other than deficiency. The material presented in these monographs should not in any event be construed as specific instructions for individual patients.

Cashman K, Flynn A. Optimal nutrition: calcium, magnesium and phosphorus. Proc Nutr Soc. 1999;58:477-487.

Covington T, ed. Nonprescription Drug Therapy Guiding Patient Self-Care. St Louis, MO: Facts and Comparisons; 1999:467-545.

Marcus R, Coulston AM. Water-soluble vitamins. In: Hardman JG, Limbird LE, et al, eds. Goodman & Gilman's The Pharmacological Basis of Therapeutics. 9^th ed. New York, NY: McGraw-Hill Health Professions Division; 1996:1557-1558.

Schwinger RH, Erdmann E. Heart failure and electrolyte disturbances. Methods Find Exp Clin Pharmacol. 1992;14(4);315-325.

Zangen A, Botzer D, Zangen R, Shainberg A. Furosemide and digoxin inhibit thiamine uptake in cardiac cells. Eur J Pharmacol. 1998;61(1):151-155.