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Pharmacokinetic interactions: The metabolism of budesonide is primarily mediated by the enzyme CYP3A4. Inhibitors of this enzyme, eg ketoconazole, may therefore increase systemic exposure to budesonide. This is of limited clinical importance for short-term (1 to 2 weeks) treatment with ketoconazole, but should be taken into consideration during long-term treatment with ketoconazole or other potent CYP3A4 inhibitors.
Pharmacodynamic interactions: Neither budesonide nor formoterol have been observed to interact with any other drug used in the treatment of asthma or COPD.
β-receptor blocking agents: β-receptor blocking agents, especially those that are non-selective, may partially or totally inhibit the effect of β2-agonists. These drugs may also increase airway resistance, therefore the use of these drugs in asthma patients is not recommended.
Other sympathomimetic agents: Other β-adrenergic stimulants or sympathomimetic amines such as ephedrine should not be given concomitantly with formoterol, since the effects will be cumulative. Patients who have already received large doses of sympathomimetic amines should not be given formoterol.
Xanthine derivatives, mineralocorticosteroids, and diuretics: Hypokalaemia may result from β2-agonist therapy and may be potentiated by concomitant treatment with xanthine derivatives, mineralocorticosteroids, and diuretics (see Hypokalaemia under Precautions).
Monoamine oxidase inhibitors, tricyclic antidepressants, quinidine, disopyramide, procainamide, phenothiazines, and antihistamines: The adverse cardiovascular effects of formoterol may be exacerbated by concurrent administration of drugs associated with QT-interval prolongation and increased risk of ventricular arrhythmia. For this reason, caution is advised when formoterol is administered to patients already taking monoamine oxidase inhibitors, tricyclic antidepressants, quinidine, disopyramide, procainamide, phenothiazines, or antihistamines associated with QT-interval prolongation (eg terfenadine, astemizole).
