Drug Interactions between ephedrine / potassium iodide and fosinopril / hydrochlorothiazide

MONITOR CLOSELY: Concomitant use of angiotensin converting enzyme (ACE) inhibitors and potassium salts may increase the risk of hyperkalemia. Inhibition of ACE results in decreased aldosterone secretion, which in turn causes potassium retention. In one report, a significant increase in serum potassium level (3.88 +/- 0.41 to 4.84 +/- 0.45 mEq/L) was observed within one or two days following the addition of captopril in five patients who were treated with regimens that included potassium supplements or potassium-sparing diuretics. Three patients had laboratory-diagnosed hyperkalemia, including one patient receiving potassium supplementation who had a 66% increase in serum potassium. Levels remained elevated until potassium supplementation or captopril therapy was reduced or discontinued. In a postmarketing survey of patients who were prescribed enalapril in England between April and December 1985, researchers identified ten cases where enalapril appeared to have contributed to a deterioration in renal function and subsequent death. All ten patients had hyperkalemia, and seven were also receiving moderate to high dosages of potassium-sparing diuretics and/or potassium supplements. Hyperkalemia was felt to be the immediate cause of death in two of them. Risk factors for developing severe or life-threatening hyperkalemia may include renal impairment, diabetes, old age, severe or worsening heart failure, dehydration, and concomitant use of other agents that block the renin-angiotensin-aldosterone system or otherwise increase serum potassium levels.

MANAGEMENT: Caution is advised if ACE inhibitors must be used concurrently with potassium salts, particularly in patients with renal impairment, diabetes, old age, severe or worsening heart failure, dehydration, or concomitant therapy with other agents that increase serum potassium such as nonsteroidal anti-inflammatory drugs, beta-blockers, cyclosporine, heparin, tacrolimus, trimethoprim, and licorice. The combination should generally be avoided in these patients unless absolutely necessary and the benefits outweigh the potential risks. Serum potassium and renal function should be checked prior to initiating therapy and regularly thereafter. Patients should be given counseling on the appropriate levels of potassium and fluid intake, and advised to seek medical attention if they experience signs and symptoms of hyperkalemia such as nausea, vomiting, weakness, listlessness, tingling of the extremities, paralysis, confusion, weak pulse, and a slow or irregular heartbeat.

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MONITOR: Although they are frequently combined in clinical practice, diuretics and angiotensin converting enzyme (ACE) inhibitors may have additive effects. Coadministration makes hypotension and hypovolemia more likely than does either drug alone. Some ACE inhibitors may attenuate the increase in the urinary excretion of sodium caused by some loop diuretics. Some patients on diuretics, especially those on dialysis or a dietary salt restriction, may experience acute hypotension with lightheadedness and dizziness after receiving the first dose of the ACE inhibitor. In addition, ACE inhibitors may cause renal insufficiency or acute renal failure in patients with sodium depletion or renal artery stenosis.

MANAGEMENT: Monitoring of blood pressure, diuresis, electrolytes, and renal function is recommended during coadministration. The possibility of first-dose hypotensive effects may be minimized by initiating therapy with small doses of the ACE inhibitor, or either discontinuing the diuretic temporarily or increasing the salt intake approximately one week prior to initiating an ACE inhibitor. Alternatively, the patient may remain under medical supervision for at least two hours after the first dose of the ACE inhibitor, or until blood pressure has stabilized.

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