Drug Interactions between Salutensin and Symbicort

MONITOR: The hypotensive effects of thiazide diuretics and alpha-adrenergic blockers may be additive. Postural hypotension may occur.

MANAGEMENT: Hemodynamic responses should be monitored during coadministration, especially during the first few weeks of therapy. Patients should be advised to take the alpha-blocker at bedtime and to notify their physician if they experience dizziness or syncope while awake.

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MONITOR: Corticosteroids may antagonize the effects of antihypertensive medications by inducing sodium and fluid retention. These effects may be more common with the natural corticosteroids (cortisone, hydrocortisone) because they have greater mineralocorticoid activity. Conversely, some calcium channel blockers such as diltiazem and verapamil may increase corticosteroid plasma levels and effects by inhibiting their clearance via CYP450 3A4 metabolism.

MANAGEMENT: Patients on prolonged (i.e., longer than about a week) or high-dose corticosteroid therapy should have blood pressure, electrolyte levels, and body weight monitored regularly, and be observed for the development of edema and congestive heart failure. The dosages of antihypertensive medications may require adjustment.

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MONITOR: The concomitant use of corticosteroids and agents that deplete potassium (e.g., potassium-wasting diuretics, amphotericin B, cation exchange resins) may result in increased risk of hypokalemia. Corticosteroids can produce hypokalemia and other electrolyte disturbances via mineralocorticoid effects, the degree of which varies with the agent (from most to least potent: fludrocortisone - cortisone/hydrocortisone - prednisolone/prednisone - other glucocorticoids) and route of administration (i.e. systemic vs. local). However, large systemic doses of any corticosteroid can demonstrate these effects, particularly if given for longer than brief periods. When used pharmacologically, adrenocorticotropic agents such as corticotropin have similar mineralocorticoid activities as cortisone and hydrocortisone.

MANAGEMENT: Patients receiving potassium-depleting agents with corticosteroids should be monitored closely for development of hypokalemia, particularly if fludrocortisone or large doses of another corticosteroid or adrenocorticotropic agent is given. Potassium supplementation may be necessary. Patients should be advised to notify their physician if they experience signs of electrolyte disturbances such as weakness, lethargy, and muscle pains or cramps.

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MONITOR: Coadministration with beta-2 adrenergic agonists may potentiate the hypokalemic effects of potassium-wasting diuretics. Beta-2 agonists can cause clinically significant but usually transient decreases in serum potassium concentrations. Since QT prolongation is a possible side effect of beta-2 agonists, exacerbation of hypokalemia may increase the risk of torsade de pointes and other serious arrhythmias. The interaction may be more likely with systemic or nebulized formulations of beta-2 agonists, high dosages of inhaled beta-2 agonists, or concomitant theophylline or corticosteroid therapy.

MANAGEMENT: Caution is advised when beta-2 agonists are used with potassium-wasting diuretics. Serum potassium level and cardiovascular status should be monitored, especially if the beta-2 agonist is administered systemically or by nebulizer. Patients should be advised to notify their physician if they experience potential signs and symptoms of hypokalemia such as fatigue, weakness, myalgia, muscle cramps, numbness, tingling, abdominal pain, constipation, palpitation, and irregular heartbeat.

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Although they are often combined in clinical practice, the concomitant use of beta-2 adrenergic agonists and corticosteroids may result in additive hypokalemic effects. Since beta-2 agonists can sometimes cause QT interval prolongation, the development of hypokalemia may potentiate the risk of ventricular arrhythmias including torsade de pointes. However, clinical data are limited, and the potential significance is unknown. Patients who are receiving systemic or nebulized formulations of beta-2 agonists, high dosages of inhaled beta-2 agonists, or systemic corticosteroid therapy may be at a greater risk of developing hypokalemia.

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